Details:
Write a paper (1,250-1,750 words) describing the approach to care of cancer. In addition, include the
following in your paper:
1. Describe the diagnosis and staging of cancer.
2. Describe at least three complications of cancer, the side effects of treatment, and methods to
lessen physical and psychological effects.
3. Prepare this assignment according to the APA guidelines found in the APA Style Guide, located
in the Student Success Center. An abstract is not required.
This assignment uses a grading rubric. Instructors will be using the
rubric to grade the assignment; therefore, students should review the rubric prior to beginning the
assignment to become familiar with the assignment criteria and expectations for successful completion
of the assignment.
Approach to Care
2
1
Less Than
Unsatisfactory 0Satisfactory 7272%
75%
0.00%
75.00%
80.0 %Content
30.0 %Explanation
of the Diagnosis
and Staging of
Cancers is
Provided.
An explanation of
the diagnosis and
staging of cancers
is not provided.
An explanation of
the diagnosis and
staging of cancers
is provided but is
missing relevant
information.
3
Satisfactory 7679%
79.00%
An explanation of
the diagnosis and
staging of cancers
is provided that
meets the
assignment
criteria.
4
Good 80-89%
89.00%
An explanation of
the diagnosis and
staging of cancers
is provided that is
offered in a
detailed manner.
5
Excellent 90100%
100.00%
An explanation of
the diagnosis and
staging of cancers
is provided that is
offered in a
detailed manner,
while
demonstrating
higher level or
critical thinking.
20.0 %At Least
Less than three
At least three
At least three
More than three More than three
Three
complications of complications of complications of complications of complications of
Complications of cancer are
cancer are
cancer are
cancer are
cancer are
Cancer are
identified.
identified but
identified with a identified with a identified with a
Identified With
lacking a
comprehensive
comprehensive
comprehensive
Comprehensive
comprehensive
discussion of
discussion of
discussion of
Discussion of
discussion of
available
available
available
Available
available
treatments.
treatments.
treatments, while
Treatments.
treatments.
demonstrating
higher level or
critical thinking.
30.0 %Provides
Recommendations Recommendations Recommendations Recommendations Recommendations
Recommendations to address
to address
to address
to address
to address
to Address
physiological and physiological and physiological and physiological and physiological and
Physiological and psychological side psychological side psychological side psychological side psychological side
Psychological Side effects of care are effects of care are effects of care
effects of care are effects of care are
Effects of Care.
lacking.
missing relevant meet the
offered in a
offered in a
information.
assignment
detailed manner. detailed manner,
criteria.
while
demonstrating
higher level or
critical thinking.
15.0
%Organization and
Effectiveness
5.0 %Thesis
Paper lacks any
Thesis and/or
Thesis and/or
Thesis and/or
Thesis and/or
Development and discernible overall main claim are
main claim are
main claim are
main claim are
Purpose
purpose or
insufficiently
apparent and
clear and forecast comprehensive;
organizing claim. developed and/or appropriate to
the development contained within
vague; purpose is purpose.
of the paper. It is the thesis is the
not clear.
descriptive and
essence of the
reflective of the paper. Thesis
arguments and
statement makes
appropriate to the the purpose of the
purpose.
paper clear.
5.0 %Paragraph
Paragraphs and
Some paragraphs Paragraphs are
A logical
There is a
Development and transitions
and transitions
generally
progression of
sophisticated
Transitions
consistently lack may lack logical competent, but
ideas between
construction of
unity and
progression of
ideas may show
paragraphs is
paragraphs and
coherence. No
ideas, unity,
some
apparent.
transitions. Ideas
apparent
coherence, and/or inconsistency in Paragraphs exhibit progress and
connections
cohesiveness.
organization
a unity,
relate to each
between
paragraphs are
established.
Transitions are
inappropriate to
purpose and
scope.
Organization is
disjointed.
5.0 %Mechanics of Surface errors are
Writing (includes pervasive enough
spelling,
that they impede
punctuation,
communication of
grammar,
meaning.
language use)
Inappropriate
word choice
and/or sentence
construction are
used.
Some degree of
organization is
evident.
and/or in their
relationships to
each other.
Frequent and
repetitive
mechanical errors
distract the
reader.
Inconsistencies in
language choice
(register),
sentence
structure, and/or
word choice are
present.
Some mechanical Prose is largely
Writer is clearly in
errors or typos are free of mechanical command of
present, but are errors, although a standard, written,
not overly
few may be
academic English.
distracting to the present. A variety
reader. Correct
of sentence
sentence structure structures and
and audienceeffective figures
appropriate
of speech are
language are used. used.
5.0 %Format
2.0 %Paper
Template is not
Template is used,
Format (1- inch
used appropriately but some
margins; 12-point- or documentation elements are
font; doubleformat is rarely
missing or
spaced; Times
followed
mistaken; lack of
New Roman, Arial, correctly.
control with
or Courier)
formatting is
apparent.
3.0 %Research
No reference page Reference page is
Citations (In-text is included. No
present. Citations
citations for
citations are used. are inconsistently
paraphrasing and
used.
direct quotes, and
reference page
listing and
formatting, as
appropriate to
assignment)
100 %Total
Weightage
Template is used,
and formatting is
correct, although
some minor errors
may be present.
coherence, and
cohesiveness.
Topic sentences
and concluding
remarks are
appropriate to
purpose.
other. Paragraph
and transition
construction guide
the reader.
Paragraph
structure is
seamless.
Template is fully All format
used; There are
elements are
virtually no errors correct.
in formatting
style.
Reference page is Reference page is
included and lists present and fully
sources used in
inclusive of all
the paper. Sources cited sources.
are appropriately Documentation is
documented,
appropriate and
although some
GCU style is
errors may be
usually correct.
present.
In-text citations
and a reference
page are
complete. The
documentation of
cited sources is
free of error.
Can use information from here as resources as
well
NRS-410V Lecture 2
Genetic Alterations and Cancer
Introduction
Congenital disorders or birth defects and many common diseases such as cancer are directly
related to alterations in the genetic structure of deoxyribonucleic acid (DNA). A general
knowledge of the principles of inheritance, the cell cycle, and the impact environmental
influences have on the genetic structure are crucial to understanding the disease processes,
ongoing research, and current disease treatments.
Aberrant Chromosomal Numbers
Congenital disorders or birth defects are more common than we realize. Many spontaneous
abortions are due to chromosomal defects, whether it is the number of chromosomes or the
construction of the chromosomes. Down syndrome, or trisomy of chromosome 21 (three copies
instead of two), is the most common chromosomal disorder that occurs during meiosis (Porth,
2007).
Aberrant Chromosomal Structure
During the process of meiosis, chromosomes often exchange blocks of DNA or alleles, causing
variation in the chromosomes. When the exchange is not precise, the alterations may prove fatal
to the gamete. This exchange of chromosomal material can also occur during mitosis and the cell
may die or the mutation may continue in the cell line. This translocation of genetic material is
implicated as the cause of many cancers. One example is the Philadelphia chromosome, in which
the translocation of DNA between chromosome 9 and chromosome 22 causes chronic myeloid
leukemia (CML). The translocation results in a novel protein, tyrosine kinase that promotes
unregulated growth of myeloid cells. A drug being used to treat CML, Gleevec (Novartis),
specifically blocks this tyrosine kinase, slowing the growth of the myeloid cells (McCance &
Heuther, 2006).
Neuroblastoma is associated with duplication of the MYCN gene. This MYCN gene is an
oncogene, meaning that in its nonmutated state, it directs and controls the proliferation of certain
cells. In its mutated state, proliferation is uncontrolled, which leads to tumors.
Single Gene Mutations
During mitosis and meiosis, the chromosomes are copied exactly. If one or more of the base
pairs in the DNA sequence of a gene is altered, there is the possibility of a point mutation in that
gene. This single defective gene on one chromosome may cause serious alterations in the
functioning of the body, such as Marfan's syndrome. This is an autosomal dominant gene and has
a 50% chance of being transmitted to offspring. The BRCA1 and BRCA2 genes are autosomal
dominant and are linked with breast cancer. The BRCA1 is found on chromosome 17, while the
BRCA2 is found on chromosome 13. The HER-2/neu is also implicated in breast cancer. With
overexpression, this gene causes excessive growth signals to the nucleus. The drug trastuzumab
(Herceptin), a monoclonal antibody, is used to treat women who have the HER-2/neu alteration
because it blocks the receptors for growth factor.
Mutations of the ras gene family prevents the breakdown of GTP, which then allows the
cytoplasmic signaling molecules to remain active and stimulate cell growth inappropriately.
Lung cancer, leukemia, colon cancer, and ovarian cancer are all linked to the ras gene (Copstead
& Banasik, 2005). The p53 gene or tumor suppressor gene is responsible for apoptosis–or
programmed cell death–and the repair of damaged DNA. This gene helps maintain the
appropriate number of cells within tissues. A mutation of this gene allows the cells with damaged
DNA to live and become more aggressive. Many breast cancers have one or all of these
mutations, plus a few more. The p53 gene mutation is also linked to colon cancer and lung
cancer.
Autosomal recessive diseases require both copies of the gene to be defective. Cystic fibrosis and
phenylketonuria (PKU) are prime examples of autosomal recessive genes. These disorders relate
to enzymes that are incorrectly made rather than run-away cell growth. Punett squares and
pedigree charts demonstrate the inheritance patterns of either recessive or dominant genes.
Genetics and Common Diseases
Heart disease, hypertension, diabetes, and many psychiatric disorders have a familial tendency
which is linked to genetics. In coronary heart disease, lipids are highly involved in the formation
of atherosclerotic plaques. Twenty or more genes have been identified that play key roles in lipid
formation, transport, coagulation, and hypertension (McCance & Heuther, 2006). An
angiotensinogen gene has been implicated as a cause for hypertension and preeclampsia. These
altered genes along with other environmental and lifestyle risk factors increase the likelihood of
developing the disease.
In type I diabetics, the HLA-DR3 and/or HLA-DR4 allele have been identified. Alterations of
genes around the insulin gene on chromosome 11 also increase the risk of developing type I
diabetes (McCance & Heuther, 2006). For type 2 diabetes, several genes have been identified
that may increase the susceptibility. One gene is involved in adipocyte differentiation and
glucose metabolism, while mutation of the glucokinase gene alters glucose conversion in the
pancreas.
Environmental and Lifestyle Risk Factors
Environmental Risk Factors
With billions and billions of cells replicating, it is amazing that the process does not incur more
errors. Environmental influences increase the risk of errors in replication. Known chemical
carcinogens include benzopyrene, which is found in foods fried in fat. Nitrosamines found in
smoked, salted, and cured foods are also powerful carcinogens. The tars and nicotines in
cigarettes are also cancer promoters. In addition, the ultraviolet (UV) rays of the sun can cause
mutation of the p53 gene, thereby causing squamous cell carcinoma and a mutation in the p16
gene related to melanoma. The UV light also activates tumor necrosis factor-α (TNF-α), which
seems to reduce the immune surveillance system (McCance & Heuther, 2006).
Lifestyle Risk Factors
Obesity has been linked to increasing the risk of cancer. The adipose tissue produces enzymes
that increase the levels of free estradiol and testosterone. The receptors react to the increased
levels by causing cellular proliferation and inhibiting apoptosis (McCance & Huether, 2006),
increasing the risk of tumor development.
Viruses such as human papillomavirus (HPV), hepatitis B virus, and the Epstein-Barr virus have
been associated with cancer. The DNA of HPV becomes integrated into the nucleus of cervical
cells and directs the proliferation of the virus.
Cell Cycle
Now that the chromosomal and gene mutations have been discussed, the process of cell division
and growth as it relates to cancer needs to be understood. Cells that replicate have a five-phase
cell cycle. During the S phase of the cell cycle, chromosomes are replicated. It is during this
phase that environmental factors can affect the exact replication and cause mutations. The end of
the G2 phase allows for a quality control check of the replication. Alterations of the kinases that
control this checkpoint allow mutations to continue rather than be corrected, increasing the
chances of cancer.
Chemotherapy agents have been developed that act on different phases of the cell cycle with the
intent of blocking the replication of the cancerous cell along with normal cells. Methotrexate, an
antimetabolite, enters the cell and inhibits DNA synthesis. Cyclophosphamide, an alkylating
agent, causes the DNA strands to cross-link, preventing normal use of the DNA, as well as its
replication. Tamoxifen blocks the estrogen receptor cells–preventing DNA synthesis–and the
cells remain in the G0 or G1 phase rather than replicating.
Tumor Cell Transformation
Promotion Stage
Once a cell has survived one gene alteration, it must be able to continue to replicate and survive.
Promotion is the stage in which the altered cells proliferate. In the progression stage, cancer cells
often lose their ability to function and are not like the original tissue cells. These cells are
considered anaplastic. Contact inhibition is lost and the cancer cells overwhelm the area in which
they began. These malignant cells secrete proteases that destroy healthy cells and allow space for
the cancerous cells to grow.
Cancer Cell Growth
Continued growth of the cancer cells depends on an adequate blood supply. Tumor cells can
secrete vascular endothelial growth factor (VEGF) along with other growth factors that promote
angiogenesis. As the blood supply increases to the tumor, the metastatic potential increases.
Research is directed toward developing agents that can block the enzymes that support
angiogenesis. Without a good blood supply, cancer cells die.
Cancer Expansion
Cancer cells do not adhere to each other as do the cells in normal tissue. Given a good blood
supply or a lymphatic channel, the cancer cells can break away from the primary site and
metastasize to other areas in the body. It may take years for the cancer cells to overcome the
normal cells in the new site, so they can go undetected.
Cancer Signs and Symptoms
Early Stages
In the early stages of cancer, there are usually not noticeable symptoms. Fatigue-like pain is very
subjective and the reason for the fatigue is being researched. Pain is due to inflammation,
stretching of visceral surfaces, compression of nerve endings, and bone metastasis. In addition,
pain control is an ongoing problem in treating patients with cancer.
Later Stages
Cachexia or severe malnutrition is found in the later stages of cancer and is often the cause of
death. TNF-α produced by macrophages has been implicated as a cause for the depression of
protein synthesis and the increase in protein degradation. Anemia is also a common finding, as
are leucopenia and thrombocytopenia due to suppression of the bone marrow.
Cancer Therapy Research
Throughout the lecture, different treatment therapies have been mentioned. Surgery,
chemotherapy, and radiation continue as mainstay treatments. Immunomodulation therapy uses
interferons, interleukins, monoclonal antibodies, and hematopoietic growth factors to destroy
cancer cells. The interferons inhibit cancer cell proliferation and stimulate NK cells, T cells, and
macrophages. Interleukin 2 stimulates the proliferation of T cells, NK cells, and macrophages,
increasing the number available to destroy cancer cells. Monoclonal antibodies are specific to
certain tumor cell receptors blocking growth factors as well as identifying the cell to the NK cells
as foreign. The hematopoietic growth factors are used to stimulate production of neutrophils,
macrophages, erythrocytes, and platelets in order to support the tissues during the tumor
destruction.
Research into gene therapy involves attempting to alter the genetic structure of the tumor cells,
making them more susceptible to the immune system, or replacing the missing p53 gene by
transporting it into the tumor cell using an inactivated virus. Stem cell transplant involves
harvesting stem cells from the bone marrow of a closely matched donor and transplanting the
stem cells. The therapy serves to restore the function of the once cancerous bone marrow. In
addition, research is being done on vaccines for specific cancers. The HPV vaccine, Gardisil, is a
beginning, whereas another area of research is being studied to inhibit the protelytic enzymes
that allow the cancer cells to expand and metastasize.
Conclusion
Understanding genetics is important for the clinician who works with families who are or wish to
become pregnant in order to explain the risks of birth defects and other genetically linked
diseases. Every nurse needs to be able to educate patients on the environmental and lifestyle risks
associated with cancer along with the genetic link. For those patients who are already being
treated for cancer, the nurse should be able to explain how the medications and radiation help
treat the disease.
References
Copstead, L. E., & Banasik, J. L. (2005). Pathophysiology (3rd ed.). St. Louis, MO: Saunders
Elsevier.
McCance, K. L., & Huether, S. E. (2006). Pathophysiology: The biological basis fordisease in
adults and children (5th ed.). St. Louis, MO: Mosby Elsevier.
Porth, C. M. (2007). Essentials of pathophysiology: Concepts of altered health states (2nd ed.).
Philadelphia, PA: Lippincott Williams & Wilkins.
© 2013. Grand Canyon University. All Rights Reserved.
Details:
Write a paper (1,250-1,750 words) describing the approach to care of cancer. In addition, include the
following in your paper:
1. Describe the diagnosis and staging of cancer.
2. Describe at least three complications of cancer, the side effects of treatment, and methods to
lessen physical and psychological effects.
3. Prepare this assignment according to the APA guidelines found in the APA Style Guide, located
in the Student Success Center. An abstract is not required.
This assignment uses a grading rubric. Instructors will be using the
rubric to grade the assignment; therefore, students should review the rubric prior to beginning the
assignment to become familiar with the assignment criteria and expectations for successful completion
of the assignment.
Approach to Care
2
1
Less Than
Unsatisfactory 0Satisfactory 7272%
75%
0.00%
75.00%
80.0 %Content
30.0 %Explanation
of the Diagnosis
and Staging of
Cancers is
Provided.
An explanation of
the diagnosis and
staging of cancers
is not provided.
An explanation of
the diagnosis and
staging of cancers
is provided but is
missing relevant
information.
3
Satisfactory 7679%
79.00%
An explanation of
the diagnosis and
staging of cancers
is provided that
meets the
assignment
criteria.
4
Good 80-89%
89.00%
An explanation of
the diagnosis and
staging of cancers
is provided that is
offered in a
detailed manner.
5
Excellent 90100%
100.00%
An explanation of
the diagnosis and
staging of cancers
is provided that is
offered in a
detailed manner,
while
demonstrating
higher level or
critical thinking.
20.0 %At Least
Less than three
At least three
At least three
More than three More than three
Three
complications of complications of complications of complications of complications of
Complications of cancer are
cancer are
cancer are
cancer are
cancer are
Cancer are
identified.
identified but
identified with a identified with a identified with a
Identified With
lacking a
comprehensive
comprehensive
comprehensive
Comprehensive
comprehensive
discussion of
discussion of
discussion of
Discussion of
discussion of
available
available
available
Available
available
treatments.
treatments.
treatments, while
Treatments.
treatments.
demonstrating
higher level or
critical thinking.
30.0 %Provides
Recommendations Recommendations Recommendations Recommendations Recommendations
Recommendations to address
to address
to address
to address
to address
to Address
physiological and physiological and physiological and physiological and physiological and
Physiological and psychological side psychological side psychological side psychological side psychological side
Psychological Side effects of care are effects of care are effects of care
effects of care are effects of care are
Effects of Care.
lacking.
missing relevant meet the
offered in a
offered in a
information.
assignment
detailed manner. detailed manner,
criteria.
while
demonstrating
higher level or
critical thinking.
15.0
%Organization and
Effectiveness
5.0 %Thesis
Paper lacks any
Thesis and/or
Thesis and/or
Thesis and/or
Thesis and/or
Development and discernible overall main claim are
main claim are
main claim are
main claim are
Purpose
purpose or
insufficiently
apparent and
clear and forecast comprehensive;
organizing claim. developed and/or appropriate to
the development contained within
vague; purpose is purpose.
of the paper. It is the thesis is the
not clear.
descriptive and
essence of the
reflective of the paper. Thesis
arguments and
statement makes
appropriate to the the purpose of the
purpose.
paper clear.
5.0 %Paragraph
Paragraphs and
Some paragraphs Paragraphs are
A logical
There is a
Development and transitions
and transitions
generally
progression of
sophisticated
Transitions
consistently lack may lack logical competent, but
ideas between
construction of
unity and
progression of
ideas may show
paragraphs is
paragraphs and
coherence. No
ideas, unity,
some
apparent.
transitions. Ideas
apparent
coherence, and/or inconsistency in Paragraphs exhibit progress and
connections
cohesiveness.
organization
a unity,
relate to each
between
paragraphs are
established.
Transitions are
inappropriate to
purpose and
scope.
Organization is
disjointed.
5.0 %Mechanics of Surface errors are
Writing (includes pervasive enough
spelling,
that they impede
punctuation,
communication of
grammar,
meaning.
language use)
Inappropriate
word choice
and/or sentence
construction are
used.
Some degree of
organization is
evident.
and/or in their
relationships to
each other.
Frequent and
repetitive
mechanical errors
distract the
reader.
Inconsistencies in
language choice
(register),
sentence
structure, and/or
word choice are
present.
Some mechanical Prose is largely
Writer is clearly in
errors or typos are free of mechanical command of
present, but are errors, although a standard, written,
not overly
few may be
academic English.
distracting to the present. A variety
reader. Correct
of sentence
sentence structure structures and
and audienceeffective figures
appropriate
of speech are
language are used. used.
5.0 %Format
2.0 %Paper
Template is not
Template is used,
Format (1- inch
used appropriately but some
margins; 12-point- or documentation elements are
font; doubleformat is rarely
missing or
spaced; Times
followed
mistaken; lack of
New Roman, Arial, correctly.
control with
or Courier)
formatting is
apparent.
3.0 %Research
No reference page Reference page is
Citations (In-text is included. No
present. Citations
citations for
citations are used. are inconsistently
paraphrasing and
used.
direct quotes, and
reference page
listing and
formatting, as
appropriate to
assignment)
100 %Total
Weightage
Template is used,
and formatting is
correct, although
some minor errors
may be present.
coherence, and
cohesiveness.
Topic sentences
and concluding
remarks are
appropriate to
purpose.
other. Paragraph
and transition
construction guide
the reader.
Paragraph
structure is
seamless.
Template is fully All format
used; There are
elements are
virtually no errors correct.
in formatting
style.
Reference page is Reference page is
included and lists present and fully
sources used in
inclusive of all
the paper. Sources cited sources.
are appropriately Documentation is
documented,
appropriate and
although some
GCU style is
errors may be
usually correct.
present.
In-text citations
and a reference
page are
complete. The
documentation of
cited sources is
free of error.
Can use information from here as resources as
well
NRS-410V Lecture 2
Genetic Alterations and Cancer
Introduction
Congenital disorders or birth defects and many common diseases such as cancer are directly
related to alterations in the genetic structure of deoxyribonucleic acid (DNA). A general
knowledge of the principles of inheritance, the cell cycle, and the impact environmental
influences have on the genetic structure are crucial to understanding the disease processes,
ongoing research, and current disease treatments.
Aberrant Chromosomal Numbers
Congenital disorders or birth defects are more common than we realize. Many spontaneous
abortions are due to chromosomal defects, whether it is the number of chromosomes or the
construction of the chromosomes. Down syndrome, or trisomy of chromosome 21 (three copies
instead of two), is the most common chromosomal disorder that occurs during meiosis (Porth,
2007).
Aberrant Chromosomal Structure
During the process of meiosis, chromosomes often exchange blocks of DNA or alleles, causing
variation in the chromosomes. When the exchange is not precise, the alterations may prove fatal
to the gamete. This exchange of chromosomal material can also occur during mitosis and the cell
may die or the mutation may continue in the cell line. This translocation of genetic material is
implicated as the cause of many cancers. One example is the Philadelphia chromosome, in which
the translocation of DNA between chromosome 9 and chromosome 22 causes chronic myeloid
leukemia (CML). The translocation results in a novel protein, tyrosine kinase that promotes
unregulated growth of myeloid cells. A drug being used to treat CML, Gleevec (Novartis),
specifically blocks this tyrosine kinase, slowing the growth of the myeloid cells (McCance &
Heuther, 2006).
Neuroblastoma is associated with duplication of the MYCN gene. This MYCN gene is an
oncogene, meaning that in its nonmutated state, it directs and controls the proliferation of certain
cells. In its mutated state, proliferation is uncontrolled, which leads to tumors.
Single Gene Mutations
During mitosis and meiosis, the chromosomes are copied exactly. If one or more of the base
pairs in the DNA sequence of a gene is altered, there is the possibility of a point mutation in that
gene. This single defective gene on one chromosome may cause serious alterations in the
functioning of the body, such as Marfan's syndrome. This is an autosomal dominant gene and has
a 50% chance of being transmitted to offspring. The BRCA1 and BRCA2 genes are autosomal
dominant and are linked with breast cancer. The BRCA1 is found on chromosome 17, while the
BRCA2 is found on chromosome 13. The HER-2/neu is also implicated in breast cancer. With
overexpression, this gene causes excessive growth signals to the nucleus. The drug trastuzumab
(Herceptin), a monoclonal antibody, is used to treat women who have the HER-2/neu alteration
because it blocks the receptors for growth factor.
Mutations of the ras gene family prevents the breakdown of GTP, which then allows the
cytoplasmic signaling molecules to remain active and stimulate cell growth inappropriately.
Lung cancer, leukemia, colon cancer, and ovarian cancer are all linked to the ras gene (Copstead
& Banasik, 2005). The p53 gene or tumor suppressor gene is responsible for apoptosis–or
programmed cell death–and the repair of damaged DNA. This gene helps maintain the
appropriate number of cells within tissues. A mutation of this gene allows the cells with damaged
DNA to live and become more aggressive. Many breast cancers have one or all of these
mutations, plus a few more. The p53 gene mutation is also linked to colon cancer and lung
cancer.
Autosomal recessive diseases require both copies of the gene to be defective. Cystic fibrosis and
phenylketonuria (PKU) are prime examples of autosomal recessive genes. These disorders relate
to enzymes that are incorrectly made rather than run-away cell growth. Punett squares and
pedigree charts demonstrate the inheritance patterns of either recessive or dominant genes.
Genetics and Common Diseases
Heart disease, hypertension, diabetes, and many psychiatric disorders have a familial tendency
which is linked to genetics. In coronary heart disease, lipids are highly involved in the formation
of atherosclerotic plaques. Twenty or more genes have been identified that play key roles in lipid
formation, transport, coagulation, and hypertension (McCance & Heuther, 2006). An
angiotensinogen gene has been implicated as a cause for hypertension and preeclampsia. These
altered genes along with other environmental and lifestyle risk factors increase the likelihood of
developing the disease.
In type I diabetics, the HLA-DR3 and/or HLA-DR4 allele have been identified. Alterations of
genes around the insulin gene on chromosome 11 also increase the risk of developing type I
diabetes (McCance & Heuther, 2006). For type 2 diabetes, several genes have been identified
that may increase the susceptibility. One gene is involved in adipocyte differentiation and
glucose metabolism, while mutation of the glucokinase gene alters glucose conversion in the
pancreas.
Environmental and Lifestyle Risk Factors
Environmental Risk Factors
With billions and billions of cells replicating, it is amazing that the process does not incur more
errors. Environmental influences increase the risk of errors in replication. Known chemical
carcinogens include benzopyrene, which is found in foods fried in fat. Nitrosamines found in
smoked, salted, and cured foods are also powerful carcinogens. The tars and nicotines in
cigarettes are also cancer promoters. In addition, the ultraviolet (UV) rays of the sun can cause
mutation of the p53 gene, thereby causing squamous cell carcinoma and a mutation in the p16
gene related to melanoma. The UV light also activates tumor necrosis factor-α (TNF-α), which
seems to reduce the immune surveillance system (McCance & Heuther, 2006).
Lifestyle Risk Factors
Obesity has been linked to increasing the risk of cancer. The adipose tissue produces enzymes
that increase the levels of free estradiol and testosterone. The receptors react to the increased
levels by causing cellular proliferation and inhibiting apoptosis (McCance & Huether, 2006),
increasing the risk of tumor development.
Viruses such as human papillomavirus (HPV), hepatitis B virus, and the Epstein-Barr virus have
been associated with cancer. The DNA of HPV becomes integrated into the nucleus of cervical
cells and directs the proliferation of the virus.
Cell Cycle
Now that the chromosomal and gene mutations have been discussed, the process of cell division
and growth as it relates to cancer needs to be understood. Cells that replicate have a five-phase
cell cycle. During the S phase of the cell cycle, chromosomes are replicated. It is during this
phase that environmental factors can affect the exact replication and cause mutations. The end of
the G2 phase allows for a quality control check of the replication. Alterations of the kinases that
control this checkpoint allow mutations to continue rather than be corrected, increasing the
chances of cancer.
Chemotherapy agents have been developed that act on different phases of the cell cycle with the
intent of blocking the replication of the cancerous cell along with normal cells. Methotrexate, an
antimetabolite, enters the cell and inhibits DNA synthesis. Cyclophosphamide, an alkylating
agent, causes the DNA strands to cross-link, preventing normal use of the DNA, as well as its
replication. Tamoxifen blocks the estrogen receptor cells–preventing DNA synthesis–and the
cells remain in the G0 or G1 phase rather than replicating.
Tumor Cell Transformation
Promotion Stage
Once a cell has survived one gene alteration, it must be able to continue to replicate and survive.
Promotion is the stage in which the altered cells proliferate. In the progression stage, cancer cells
often lose their ability to function and are not like the original tissue cells. These cells are
considered anaplastic. Contact inhibition is lost and the cancer cells overwhelm the area in which
they began. These malignant cells secrete proteases that destroy healthy cells and allow space for
the cancerous cells to grow.
Cancer Cell Growth
Continued growth of the cancer cells depends on an adequate blood supply. Tumor cells can
secrete vascular endothelial growth factor (VEGF) along with other growth factors that promote
angiogenesis. As the blood supply increases to the tumor, the metastatic potential increases.
Research is directed toward developing agents that can block the enzymes that support
angiogenesis. Without a good blood supply, cancer cells die.
Cancer Expansion
Cancer cells do not adhere to each other as do the cells in normal tissue. Given a good blood
supply or a lymphatic channel, the cancer cells can break away from the primary site and
metastasize to other areas in the body. It may take years for the cancer cells to overcome the
normal cells in the new site, so they can go undetected.
Cancer Signs and Symptoms
Early Stages
In the early stages of cancer, there are usually not noticeable symptoms. Fatigue-like pain is very
subjective and the reason for the fatigue is being researched. Pain is due to inflammation,
stretching of visceral surfaces, compression of nerve endings, and bone metastasis. In addition,
pain control is an ongoing problem in treating patients with cancer.
Later Stages
Cachexia or severe malnutrition is found in the later stages of cancer and is often the cause of
death. TNF-α produced by macrophages has been implicated as a cause for the depression of
protein synthesis and the increase in protein degradation. Anemia is also a common finding, as
are leucopenia and thrombocytopenia due to suppression of the bone marrow.
Cancer Therapy Research
Throughout the lecture, different treatment therapies have been mentioned. Surgery,
chemotherapy, and radiation continue as mainstay treatments. Immunomodulation therapy uses
interferons, interleukins, monoclonal antibodies, and hematopoietic growth factors to destroy
cancer cells. The interferons inhibit cancer cell proliferation and stimulate NK cells, T cells, and
macrophages. Interleukin 2 stimulates the proliferation of T cells, NK cells, and macrophages,
increasing the number available to destroy cancer cells. Monoclonal antibodies are specific to
certain tumor cell receptors blocking growth factors as well as identifying the cell to the NK cells
as foreign. The hematopoietic growth factors are used to stimulate production of neutrophils,
macrophages, erythrocytes, and platelets in order to support the tissues during the tumor
destruction.
Research into gene therapy involves attempting to alter the genetic structure of the tumor cells,
making them more susceptible to the immune system, or replacing the missing p53 gene by
transporting it into the tumor cell using an inactivated virus. Stem cell transplant involves
harvesting stem cells from the bone marrow of a closely matched donor and transplanting the
stem cells. The therapy serves to restore the function of the once cancerous bone marrow. In
addition, research is being done on vaccines for specific cancers. The HPV vaccine, Gardisil, is a
beginning, whereas another area of research is being studied to inhibit the protelytic enzymes
that allow the cancer cells to expand and metastasize.
Conclusion
Understanding genetics is important for the clinician who works with families who are or wish to
become pregnant in order to explain the risks of birth defects and other genetically linked
diseases. Every nurse needs to be able to educate patients on the environmental and lifestyle risks
associated with cancer along with the genetic link. For those patients who are already being
treated for cancer, the nurse should be able to explain how the medications and radiation help
treat the disease.
References
Copstead, L. E., & Banasik, J. L. (2005). Pathophysiology (3rd ed.). St. Louis, MO: Saunders
Elsevier.
McCance, K. L., & Huether, S. E. (2006). Pathophysiology: The biological basis fordisease in
adults and children (5th ed.). St. Louis, MO: Mosby Elsevier.
Porth, C. M. (2007). Essentials of pathophysiology: Concepts of altered health states (2nd ed.).
Philadelphia, PA: Lippincott Williams & Wilkins.
© 2013. Grand Canyon University. All Rights Reserved.
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Record: 1
Title: Cancer.
Authors: Hosick, Howard L., Ph.D.
Rizzo, Connie, M.D., Ph.D.
Campanella, James J., Ph.D.
Alder, Richard, Ph.D.
Source: Magill’s Medical Guide (Online Edition), January, 2017. 5p.
Document Type: Article
Subject Terms: CANCER
TUMORS
CELLULAR growth
Abstract: Cancer is a disease of abnormal cellular growth. Growth is a
feature of all living things, but it must be precisely regulated for
development to occur properly. All growing cells pass through a
strictly regulated series of events called the cell cycle, where
most cellular structures are duplicated. At the end of the cycle,
one cell is separated into two “daughter cells,” each receiving
one copy of the duplicated structures. The most important
structures to be duplicated are the genes, which govern all
cellular activities.
Full Text Word Count: 3367
Accession Number: 86193961
Database: Research Starters
Cancer
Last reviewed: January 2017
Anatomy or system affected: All
Definition: Inappropriate and uncontrollable cell growth within one of the specialized tissues of the
body, threatening normal cell and organ function and in serious cases traveling via the bloodstream to
other areas of the body.
Causes: Genetic, environmental, or lifestyle factors; viruses
Symptoms: Varies widely; may include tumor growth, headaches, lethargy, fever, bloating, pain,
swelling
Duration: Chronic, possibly recurrent
Treatments: Surgery, chemotherapy, radiation
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Causes and Symptoms
Cancer is a disease of abnormal cellular growth. Growth is a feature of all living things, but it must be
precisely regulated for development to occur properly. All growing cells pass through a strictly regulated
series of events called the cell cycle, where most cellular structures are duplicated. At the end of the
cycle, one cell is separated into two “daughter cells,” each receiving one copy of the duplicated
structures. The most important structures to be duplicated are the genes, which govern all cellular
activities.
Cancer cells are fast-growing, irregular cells; normally, the body releases killer T cells that
interact with antigens on the surface of the cancer cell, releasing lymphokines that are toxic
to the cancer cell.
Human life begins as a fertilized egg which divides again and again; the adult human body is composed
of a trillion cells, each with a specific job to perform. At adulthood, most cells stop duplicating. Some
cells, however, must continue dividing to replace worn-out cells in places like the blood, skin, and
intestine. Such growth is accurately controlled so excess cells are not produced. Sometimes, however,
a mutation arises in one or more genes, resulting in needless cell duplication and ultimately loss of
growth control: a malignant transformation. This is the start of cancer.
At first, these cells resemble their neighbors. For example, newly altered blood cells look like normal
blood cells, and in most respects are. However, cancer cells differ in a number of ways from “normal”
cells. First, cancer cells grow uncontrollably. They may or may not grow faster than normal cells, but
cancer cells do not cease growth. If placed in a laboratory cell culture dish, cancer cells will pile upon
one another in a manner analogous to the formation of a tumor. By contrast, normal cells grow in a
single layer (monolayer) and stop replicating when they reach the edges of their dish when cellular
signals instruct them to halt. Second, cancer cells often grow independently of hormones and growth
factors, like insulin, required by other cells. They become “growth factor independent.” Third, cancer
cells are immortal. Normal cells are able to replicate themselves a regulated number of times, usually
approximately fifty divisions, while cancer cells have no such limit. For example, HeLa cells, originally
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obtained from a woman with cervical cancer in the mid-1950s, have been cultured in laboratories ever
since. Fourth, cancer cells in later stages change shape and size compared to normal cells. They may
look very different. Oncologists (cancer specialists) use this information to identify cancer types and
make prognoses.
The first event triggering cancer is initiation, precipitated by a mutation in one of the genes controlling
some feature of the cell cycle. There are several hundred such genes regulating different aspects of the
cell cycle and cellular growth. These genes have mundane jobs governing the life of the cell until they
become damaged. When there is a mutation in a controlling gene, it functions improperly. It does not
govern the cell cycle correctly, and the cell cycle proceeds when it should be halted. Such cancercausing genes are called oncogenes.
After initiation, additional mutations and defects begin to accumulate, and the defective cells become
increasingly abnormal. Tumor-suppressor genes, normally functioning to keep cell division from
becoming disorganized, are the site of these second-stage mutations. Those cells whose division and
growth genes have mutated (oncogenes) and whose division and growth inhibitor genes (tumorsuppressor genes) have also mutated will become cancer cells. Typically, a further change, “promotion,”
must take place before cancer cells begin growing freely. Promotion allows cells to escape the
monitoring activity of the body. For example, various hormones instruct cells how to behave; a change
of the promotion type may allow a cell to ignore such instructions. Both initiation and promotion occur
randomly. Many initiated cells fail to grow into tumors. It is only those few cells that happen to acquire
both defects that cause a problem. Fortunately, few cells have both their oncogenes turned “on” and
their tumor suppressor genes turned “off.”
At this point in the process, the new cancer cell is dividing and producing larger numbers. These cells
grow into a mass called a tumor—except in blood and lymph tissues, where cancer cells circulate
individually. Nevertheless, these cells look normal at this early stage and are relatively easy to control
with surgery. The excess cells may not cause much harm. Warts, for example, result from underlying
skin cells exhibiting abnormal growth control. Such harmless tumors are called benign.
Unfortunately, as cells continue to replicate uncontrollably, more mutations develop. The most harmful
changes result in complete loss of growth control. Cancer cells spread, resulting in damage to other
parts of the body. For example, cancer cells may acquire the ability to digest their way through nearby
tissues, a process called invasion. Eventually, the functioning of organs containing such cells becomes
impaired. Other cancer cells may break loose from the tumor and travel to other parts of the body in the
circulatory or lymphatic systems. This process is called metastasis. In advanced stages, a cancer
patient may actually have dozens or hundreds of tumors, all of which developed from a single tumor
cell. Cells that can invade or metastasize are called malignant. It becomes increasingly difficult to
eradicate cancer cells as they become more malignant. Because each event leading to tumor
development is rare, it may take years for the several acquired mistakes to aggregate in a single cell,
resulting in a malignant tumor.
Cancer-causing mutations occur when outside forces cause oncogenes and tumor suppressor genes to
function abnormally. For example, genes may be chemically damaged by a number of highly active and
dangerous chemicals known as carcinogens. Additionally, several kinds of radiation can damage genes:
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ultraviolet radiation, gamma radiation, nuclear radiation, and possibly electromagnetic field radiation.
Finally, several kinds of viruses, including certain strains of the human papillomavirus (HPV) or human
herpesviruses, can cause oncogenes to function improperly. In most cancers, however, the origin of the
disease is unknown and may result simply from a genetic mistake that takes place during gene
duplication.
Treatment and Therapy
The most common cancer treatments fall into three categories: surgery, chemotherapy, and
radiotherapy. The oldest treatment, going back several hundred years, is the surgical removal of
tumors. If performed at an early stage, before metastasis, this method can be highly successful. Even
so, surgery is much easier and less dangerous for some cancers (like that of the skin) than others (like
that of the brain, which can be difficult to reach and remove). Surgery is not an option for blood and
lymph cancers that are widely distributed.
The second most common type of cancer treatment for tumors is radiation therapy or radiotherapy. The
radiation of choice is X-rays, which can penetrate the body to reach a tumor in very high dosages using
modern equipment. X-rays can be focused on a specific small area or be administered over the whole
body in the case of metastasized cancer. Therapeutic radiation damages genes to such an extent that
they become physically fragmented and nonfunctional, ending the life of the target cell.
Radiotherapy has major drawbacks. The most serious problem is that normal cells in the path of the
radiation will also be killed. Bone marrow, the source of blood cells, is destroyed with whole-body
cancer treatments. This problem can be overcome after radiotherapy by transplanting new bone
marrow into the patient, so that a treated patient can begin to manufacture new blood cells. Ironically,
radiation designed to kill cancer cells can also cause malignant mutations in normal cells. Recent
innovations in radiotherapy include instrumentation such as the gamma knife, a method to direct
radiation precisely into the center of a tumor. In this manner, damage to surrounding cells may be
minimized.
If a patient has metastasized tumor cells, radiation and surgery are not the treatments of choice.
Neither of these therapies acts systemically. The most common systemic treatment used that can reach
everywhere in the body is chemotherapy. Patients are treated with chemicals that prevent cells from
duplicating or slow the process. Such drugs reach all parts of the body much more effectively than
surgery when cancer has reached a later stage of distribution.
Different kinds of chemicals work in different ways to achieve this result. These chemicals can be
divided into four major categories. First are chemicals that react directly with the substances required
for cells to survive and function. Many such agents directly attack a cell’s genes, preventing them from
passing along information required for a cancer cell to stay alive; these are known as alkylating agents.
Second are antimetabolites, which prevent the chemical reactions that allow cells to produce the energy
needed to live. The third category consists of steroid hormones. Cancer cells in some tissues respond
to these hormones, which can therefore be used to regulate growth. Thus, estrogens, the female
steroid hormones, are often used for treatment of breast cancer, while the male steroids, androgens,
may influence prostate cancer. Fourth are miscellaneous drugs that affect cancer cells in various ways.
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For example, drugs called vinca alkaloids (one type of the category known as antimicrotubule agents)
stop the mechanical process of cell division and prevent growth. A derivative of the insecticide DDT
(dichloro-diphenyl-tricholorethane) prevents unwanted steroid-hormone production and has been useful
for treating tumors of the adrenal gland Other drug types include topoisomerase inhibitors and cytotoxic
antibiotics.
The newest class of anticancer drugs is known as taxanes, another type of antimicrotubule agent.
Taxol, isolated from the bark of the yew tree, is the best known of these drugs. Taxanes are active,
poisonous constituents that can induce tumor cell death. This class of drug promotes the polymerization
of the tubulin protein, which is needed to move chromosomes during cell division. By stabilizing the
tubulin in the cancer cells, the equilibrium in the cell is disrupted, leading ultimately to cell death. The
drugs paclitaxel and docetaxel are used frequently in ovarian and breast cancer and often in
conjunction with one another.
The most common and difficult problem with the chemotherapeutic approach to cancer management is
that normal cells are also affected by the same drugs that halt the growth of cancer cells. This reaction
causes many difficulties for patients. Probably the most serious problems are with the immune system.
Growth of the white blood cells that make antibodies is necessary to fight an infectious disease.
Chemotherapy often depresses the immune system so it functions inefficiently; therefore patients in
chemotherapy are more vulnerable to bacterial and viral illnesses. Red blood cells do not carry oxygen
optimally during chemotherapy, making patients breathless and “sickly.” Skin often becomes pale and
unhealthy looking. The digestive tract cells stop dividing, causing weight loss and digestive problems.
Finally, a less serious irritant for such patients is hair loss, since hair follicles are also prevented from
growing.
Accordingly, cancer surgery is inefficient, radiation therapy may cause as many problems as it solves,
and chemotherapy, despite its anticancer efficiency, is toxic and can make the patient very ill. The
problems for a cancer sufferer seem to have only just begun with their diagnosis since many of the
cures seem, in the short term, as potentially harmful as the disease. Chemotherapy has developed
such an unwholesome reputation that some patients refuse treatment, preferring death to the
“indignities” of chemotherapy’s effects. Oncologists are presently experimenting with a whole series of
promising new treatments that may be less harmful to patients while being more efficacious.
Antisense therapy is one method in the new arsenal of treatments emerging from advances in
biotechnology. Oncogenes, like other genes, are read (transcribed) by the machinery of the cell so that
cellular messages called messenger ribonucleic acid (mRNA) are made. The mRNA is then itself read
(translated) by the ribosomes of the cell to make proteins. Proteins are the major component of every
enzyme and structural part of a cell. The problem with oncogenes is that they have been turned on and
cannot be turned off, so the cancer cells continue growing. One type of antisense cancer therapy works
by injection into the cancer cells of a “backward” (complementary) copy of the mRNA molecule made
from the active oncogene. This “backward” copy interferes with the oncogene’s “forward” mRNA
message, causing it not to be made into an oncogenic protein. Consequently, this treatment stops the
cancer cells from growing, because the cells are no longer encouraged to grow by the oncogenic
protein. The advantages of this treatment are that it is very specific to cancer cells and has few side
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effects. The major disadvantages are that the physician must know precisely what oncogene is causing
the disease in order to design the antisense treatment and that the treatment must be individualized in
most cases, making a single “magic bullet” cure for all unavailable. University of Illinois oncologist
Herbert Engelhard reports that this method has been successfully used to keep glial tumor cells
(gliomas) of the brain from growing.
A related cancer treatment scheme is gene replacement therapy. In this method, an additional gene is
introduced into the tumor cell with a laboratory-designed virus. This gene moves into the nucleus of the
cell, becomes expressed as mRNA, and is translated into a protein. This protein is usually engineered
to replace a missing or nonfunctioning gene. For example, the introduced factor may restore a missing
tumor suppressor protein to the cancer cells, inducing them to become “normal” again.
A third biotechnologic approach to cancer treatment is gene-directed enzyme prodrug (“suicide gene”)
therapy. In this method, the cancer cells are treated with viral DNA containing a special suicide gene.
When an inactive antibiotic drug is later given to the cancer patient, the drug is converted into a toxic
form by the gene. This kills only the tumor cells making the enzyme. Other cells without the suicide
gene are unaffected. The chief advantages of this treatment are high cancer-cell specificity, few side
effects, and effectiveness with a wide variety of tumor types.
Yet another approach, oncolytic virus therapy, holds a great deal of promise. Genetically engineered
viruses are made “safe” by deleting essential genes but are left with the ability to replicate. They are
also given the ability to target and bind only cancer cells. Cancer cells are treated with these viruses.
Viral replication occurs within the cells. Many viruses are made within the cancer cell; it bursts open
(lyses) and dies. More viruses are then released that have the ability to infect and destroy adjacent
cancer cells. The herpes simplex virus 1 (HSV1) has become a popular virus for oncolytic therapy. The
“wild” HSV1 is usually quite virulent and induces illness in humans, but researchers have produced a
genetically modified virus with low binding capacity to normal cells but high affinity for tumor cells.
Another new therapeutic method is photodynamic therapy (PDT). Cancer cells are treated with certain
photosensitive dyes. In the presence of light, the dyes react to make molecular oxygen radicals. These
radicals are poisonous and specifically kill any cancer cells treated with the dye. Immunotherapy
treatments, which use various aspects of the immune system to attack cancer cells, are also the subject
of widespread research
Finally, a series of new types of anticancer drug treatments are being developed that do not simply kill
cancer cells but prevent them from proliferating and growing. These new drugs are called cytostatic
therapies and have a variety of functions. Some inhibit the formation of new blood vessels
(angiogenesis) essential to tumor tissue growth. Other drugs inhibit the proteases used by certain
tumors to dissolve the proteins that hold the normal tissues together. Without these proteases, tumor
cells could not invade tissues, gain access to blood vessels, and colonize distant sites. Still other
treatments inhibit growth by interfering with the signals that tell cancer cells to keep proliferating.
Perspective and Prospects
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In the mid-1990s, evidence of a potential new basis for cancer emerged. The hypothesis suggested that
overproduction of the enzyme telomerase, which synthesizes the telomeres at the ends of
chromosomes, may cause uncontrolled growth in cells.
In normal human cells, the telomeres, long DNA repeats of TTAGGG, are slowly shortened and erode
away as the cells age. The lengthening enzyme telomerase is not active in normal cells, so the ends of
the chromosomes shorten more and more over a lifetime; in fact, these chromosomal changes have
been postulated as one possible cause of cellular aging. When the telomeres become short enough,
cell senescence is induced as the cells stop dividing. Tumor cells have active telomerase and do not
lose their chromosomal ends. One source of immortality in cancer cells may be their long telomeres.
It is not clear whether lengthening of telomeres is an oncogenic event causing cells to become
cancerous or whether these events are simply crucial in tumor formation. The importance of the
telomerase activity in inducing cancer is quite controversial. Mice who have had telomerase genes
turned off permanently show no ill effects and age normally. Although researchers have shown that
oncogenes become operative if the telomerase is active in cell culture, it is unclear what role
telomerase plays in actual biological systems. Researchers have suggested that perhaps the loss of
that enzyme activity could be a protective mechanism against cancer. However, that is unlikely, since a
phenomenon that usually occurs at the end of an organism’s lifetime, and after reproduction, such as
cancer, would not be evolutionarily selected against.
Telomerase offers another possible avenue of treatment for cancer as a therapeutic agent. It may turn
out that treatments that shut off the telomerase activity in cancer cells will slow or stop their growth.
Pharmacological treatments may induce cancer cells to become normal cells once again. Once the
mechanism of telomerase activity is understood, medical treatments may even induce cancer cells to
destabilize and die.
Earlier detection and treatment have significantly improved the prognosis for people diagnosed with
cancer. Nevertheless, there are millions of cancer cases diagnosed each year, many of them fatal. In
2012, there were an estimated 14 million cancer cases worldwide, and 8 million deaths from cancer.
The American Cancer Society estimated more than half a million cancer deaths in the United States in
2016. Improved diagnosis and treatment have resulted in decreased mortality from the most common
forms of cancer (lung, breast, prostate, and colorectal). However, distribution and mortality of such
cancers among ethnic or racial lines continues to show significant differences.
Bibliography
American Cancer Society. Cancer Facts and Figures, 2016. Atlanta: Amer. Cancer Soc., 2016. PDF file.
Anderson, Greg. Cancer: Fifty Essential Things to Do. New York: Plume, 2013. Print.
Bognar, David, et al. Cancer: Increasing Your Odds for Survival—A Resource Guide for Integrating
Mainstream, Alternative, and Complementary Therapies. Alameda: Hunter House, 1998. Print.
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Cairns, John. Matters of Life and Death: Perspectives on Public Health, Molecular Biology, Cancer, and
the Prospects for the Human Race. Princeton: Princeton UP, 1998. Print.
"Cancer." MedlinePlus. US Nat'l Lib. of Medicine, 22 Sept. 2015. Web. 3 May 2016.
"Cancer." World Health Organization. WHO, 2016. Web. 3 May 2016.
Amer. Cancer Society. Cancer Facts and Figures, 2016. Atlanta: Amer. Cancer Society, 2016. PDF file.
Cornwall, Claudia Maria. Catching Cancer: The Quest for Its Viral and Bacterial Causes. Lanham:
Rowman, 2013. Print.
Dollinger, Malin, et al. Everyone’s Guide to Cancer Therapy. Rev. 5th ed. Kansas City: Andrews
McMeel, 2008. Print.
Greaves, M. F. Cancer: The Evolutionary Legacy. New York: Oxford UP, 2002. Print.
Kutikhin, Anton G., Arseniy E. Yuzhalin, and Elena B. Brusina. Infectious Agents and Cancer. New
York: Springer, 2013. Digital file.
McKinnell, Robert Gilmore, ed. The Biological Basis of Cancer. 2nd ed. New York: Cambridge UP,
2006. Print.
Weinberg, Robert. The Biology of Cancer. 2nd ed. New York: Garland Science, 2014. Print.
"What Is Cancer?" National Cancer Institute. Natl. Institutes of Health, 9 Feb. 2015. Web. 3 May. 2016.
Derived from: "Cancer." Magill's Medical Guide (Online Edition). Salem Press. 2013.
Copyright of Magill’s Medical Guide (Online Edition) is the property of Salem Press. The copyright in
an individual article may be maintained by the author in certain cases. Content may not be copied or
emailed to multiple sites or posted to a listserv without the copyright holder's express written
permission. However, users may print, download, or email articles for individual use.
Source: Magill’s Medical Guide (Online Edition), January, 2017, 5p
Item: 86193961
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Record: 1
Title: Cancer
Source: Funk & Wagnalls New World Encyclopedia, 2016, 1p.
Publication Information: World Book, Inc., Chicago
Subject Terms: CANCER
Document Type: Reference Entry
Accession Number: CA025900
Database: Funk & Wagnalls New World Encyclopedia
Cancer
Cancer, new growth of tissue resulting from a continuing proliferation of cells characterized by
abnormalities in the genes that control cell multiplication. These abnormal cells may arise from any type
of cell and in any body tissue, and have the ability to invade and destroy other tissues. The various
types of cancer may be classified according to the tissue and type of cell of origin into several hundred
groups, constituting three major subtypes:
•Sarcomas arise from connective and supportive tissue, such as bone, cartilage, nerve, blood vessel,
muscle, and fat.
•Carcinomas, which include the most frequently occurring forms of human cancer, arise from epithelial
tissue, such as the skin and the lining of the body cavities and organs, and the glandular tissue of the
breast and prostate. Carcinomas with a structure resembling skin are termed squamous cell
carcinomas. Those that resemble glandular tissue are called adenocarcinomas.
•Leukemias and lymphomas include the cancers that involve blood-forming tissue and are typified by
the enlargement of the lymph nodes, the invasion of the spleen and bone marrow, and the
overproduction of immature white cells.
NATURE OF THE DISEASE
A cancerous growth, or neoplasm, is clonal; that is, all its cells are descendants of a single cell. These
cells have escaped the control of the normal forces regulating cellular growth. Resembling embryonic
cells, they are unable to differentiate or mature into an adult, functioning state. As these cells multiply,
they may form a mass, called a Tumor, which enlarges and continues to grow without regard to the
function of the tissue of origin.
Tumors
Almost all cancers form tumors, but not all tumors are cancerous, or malignant; the greatest number are
benign. Benign tumors are characterized by entirely localized growth and are usually separated from
neighboring tissue by a surrounding capsule. Benign tumors generally grow slowly, and in structure
closely resemble the tissue of origin. In some instances they may endanger the patient by obstructing,
compressing, or displacing neighboring structures, as in the brain. A few benign tumors, such as polyps
of the colon, may be precancerous.
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Invasion and Spreading
The most significant attribute of malignant tumors is their ability to spread beyond the site of origin.
Cancer may invade neighboring tissues by direct extension or infiltration or may disseminate to distant
sites, forming secondary growths known as metastases. The routes and sites of metastases vary with
different primary cancers: (1) When a cancer extends through the surface of the organ of origin into a
cavity, cells may break away from the surface and implant on the surface of adjacent organs. (2) Tumor
cells may migrate into the lymphatic channels and be carried to the draining lymph nodes, or they may
penetrate the blood vessels. Once in the bloodstream the tumor cells are carried to the point at which
the vessels become too small for the large tumor cells to pass. Cells from tumors of the gastrointestinal
tract will be stopped in the liver. Later they may go on to the lungs. Cells from all other tumors will go to
the lungs before being carried to other organs. The lungs and liver are therefore common sites of
metastases. (3) Many cancers tend to shed cells into the bloodstream early in their course. Most such
cells die in the bloodstream, but some lodge against the surface and penetrate the wall into the tissue.
A few may find themselves in a favorable tissue in which they are able to survive and grow into a tumor,
a metastasis. Others may divide only a few times, forming a small nest of cells that then remain
dormant as a micrometastasis. They may remain dormant for many years, only to begin to grow again
as recurrent cancer for reasons unknown.
Cancer cells, even when widely disseminated, may retain the physical and biological characteristics of
their tissue of origin. Thus the pathologist can often determine the site of origin of metastatic tumors by
microscopic examination of the cancerous tissue. Identification of tumors of endocrine glands is
simplified because they may produce excessive amounts of the hormone elaborated by the parent
tissue. Such tumors may also respond to administration of the hormones that normally control that
tissue.
In general, the less closely a cancer resembles its tissue of origin, the more malignant and rapidly
invasive it tends to be, but the rate of growth of a cancer depends not only on cellular type and degree
of undifferentiation, but also on various host factors. A characteristic of malignancy is tumor cell
heterogeneity. Because of the abnormalities of proliferation in tumor cells, they are more susceptible to
mutation. With time a tumor tends to become less differentiated and to grow more rapidly. It may also
develop increased resistance to chemotherapy or irradiation.
CAUSES OF CANCER
A number of factors produce cancer in a proportion of exposed individuals. Among these factors are
heredity, viruses and other pathogens, radiation, chemicals, and alterations in the Immune System. For
a long time these various factors seemed to work in different ways, but now researchers are studying
how they interact in a multifactorial, sequential process resulting in malignancy. Basically, cancer is a
genetic process. Gene abnormalities may be inherited, but often they are induced in a body cell by a
virus or by damage from an outside source. Probably a series of mutations eventually leads to a single
cell that is malignant and proliferates as a clone.
Heredity
Several types of cancer run in families. Breast cancer is one example. Cancer of the colon is more
common in families with familial polyposis of the colon. A type of retinoblastoma has been
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demonstrated to occur only when a specific gene is deleted. In some hereditary disorders the
Chromosomes exhibit a high frequency of breakage; such diseases carry a high risk of cancer.
Infectious organisms
Viruses are the cause of many cancers in animals. In humans the Epstein-Barr virus is associated with
Burkitt’s lymphoma and lymphoepitheliomas, the hepatitis virus with hepatocarcinoma, and a
papillomavirus with carcinoma of the cervix. These viruses associated with human tumors are DNA
viruses. The HTLV virus that produces a T-cell leukemia is an RNA virus, or Retrovirus, as are most of
the viruses associated with animal tumors. In the presence of an enzyme called reverse transcriptase,
they induce the infected cell to make DNA copies of the virus’s genes, which can be incorporated into
the cell’s genome (the full complement of its DNA). An example of a bacterium linked with cancer is
Helicobacter pylori, which causes stomach ulcers; it has been associated with gastric cancer.
Regarding parasitic organisms, there is evidence suggesting an association between the parasite
Schistosoma haematobium, a cause of schistosomiasis, and bladder cancer, and between the
Clonorchis sinensis, known as the oriental or Chinese liver Fluke, and cancer of the gall bladder and
hepatobiliary ducts.
Radiation
Ionizing radiation, whether from Cosmic Rays or from terrestrial sources, is a potent cause of a variety
of types of cancer. Radiation induces changes in DNA, including chromosome breaks and
transpositions, in which the broken-off ends of two chromosomes are exchanged. It acts as an initiator
of carcinogenesis, inducing a change that progresses to cancer after a latent period of years. This delay
provides opportunity for exposure to other factors. Exposure to nonionizing radiation, notably ultraviolet
wavelengths in sunlight, is associated with certain types of skin cancer.
Chemicals
The process by which chemical agents cause cancer has been extensively studied. Some chemicals
act as initiators. Only a single exposure is required, but cancer does not follow until after a long latent
period and after exposure to another agent that acts as a promoter. Initiators produce irreversible
changes in DNA. Promoters do not change DNA, but they do increase synthesis of DNA and stimulate
expression of genes. They have no effect if given before the initiator, only if given after the initiator and
given repeatedly over a period of time. Tobacco smoke contains many chemical initiators and
promoters. The promoter action of cigarettes is very important, and if smoking is stopped, the risk of
lung cancer falls rapidly. Alcohol is an important promoter; chronic abuse greatly increases the risk of
cancers known to be induced by other agents, such as lung cancer in smokers. Carcinogenic chemicals
also produce chromosome breaks and translocations. See alsoCarcinogen.
Immune System
The immune system appears to be able to recognize malignant cells and stimulate the production of
cells able to destroy them. An important factor in the development of cancer may be a disease or other
damaging event leading to a state of immune deficiency. Such states are a consequence of AIDS (see
Acquired Immune Deficiency Syndrome), inherited immune deficiency diseases, and the administration
of immunosuppressive drugs.
Environmental Factors
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Pathogens, chemicals, and radiation may be grouped together with diet and smoking under the heading
of environmental factors, which are estimated to account for about three-quarters of all U.S. cancer
deaths. The best established cause is tobacco smoke, actively or passively inhaled, which is
responsible for about 30 percent of all deaths from cancer in the U.S. Dietary factors may account for
about a third of all deaths, but the causative relationship is not as clear, and the responsible
constituents of the diet are not clearly defined. Alcoholic beverages appear to increase the risk of
cancers of the mouth, esophagus, larynx, and breast. Obesity is a risk factor for a number of cancers,
especially cancers of the breast, colon, uterus, gallbladder, endometrium, and prostate. Evidence links
high-fat diets with an increased risk of cancers of the colon and rectum, prostate, and endometrium.
Dietary fat and obesity, like alcohol, appear to act as promoters. Among other notable findings,
consumption of meat, particularly red meat, has been linked with an increased risk of several cancers at
several sites, among them the colon and prostate, and low dietary fiber is associated with high
incidence of colon cancer.
Oncogenes and Suppressor Genes
These seemingly disparate mechanisms for triggering uncontrolled proliferation of cells all involve the
genes governing cell multiplication that are found in every cell. There are two types of such genes,
oncogenes, which promote cell growth and division, and tumor-suppressor genes, which inhibit such
cell multiplication. In cancer, typically, one or more oncogenes are activated and one or more tumorsuppressor genes are switched off. This may happen because of an inherited genetic defect, but most
often the genetic damage results from an environmental factor, such as a cancer-causing virus or
exposure to radiation or carcinogenic chemicals. Cancer’s uncontrolled cell growth also appears to
commonly involve the telomeres, the end sections of chromosomes. The telomere seems to place a
limit on the number of times a cell can multiply. It ordinarily becomes shorter each time the cell divides;
when the telomere becomes too short, the cell dies. Cancer cells, however, typically produce an
enzyme called telomerase, which keeps the telomere from shortening, thereby making the cell
“immortal.”
OCCURRENCE
Around the world, cancer kills more than 7 million people a year; cancer incidence has generally been
increasing, due partly to poor heath habits, and screening and treatment for cancer is often inadequate.
In the U.S., in 2006, according to the American Cancer Society (ACS), some 1.4 million new cases of
cancer were expected to be diagnosed, not counting basal and squamous cell skin cancers, which were
estimated to total more than 1 million new cases. Cancer is the second leading cause of death in the
U.S. (after heart disease), accounting for more than 550,000 deaths annually. Although cancer rarely
occurs in children, and advances in treatment have greatly improved survival rates for childhood
cancer, it is still the leading cause of death from disease in U.S. children between the ages of 1 and 14.
The incidence of cancer varies enormously among different geographic areas. Near the end of the 20th
century, according to the World Health Organization, the age-adjusted death rate from all cancers
(excluding skin) in males was 272.28 per 100,000 in Hungary (the highest) as compared to 40.99 in
Congo-Brazzaville (the lowest). For women it was 147.39 in Hungary and 44.49 in Tunisia. The
corresponding figures for the U.S. were 161.80 per 100,000 men and 116.43 per 100,000 women. For
particular cancers the difference between countries may be as high as 40-fold. Evidence from studies of
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populations that have migrated from one geographic area to another suggests that these variations are
due to differences in lifestyle rather than the differences in ethnic origin. This finding is consistent with
other evidence indicating that most cancers are predominantly related to environmental causes rather
than to heredity, although the two certainly interact.
In the U.S., overall cancer incidence rates climbed until 1992 and then started declining, falling an
average of 1.1 percent per year from 1992 to 1998. Over a longer term, from 1992 to 2002, incidence
rates for the top 15 sites have fallen an average of 0.6 percent a year. The trends for particular cancers
may often differ significantly from the overall picture. The incidence of reported female breast cancer,
for example, actually grew by an average of 1.2 percent a year between 1992 and 1998, continuing a
long-term rising pattern; breast cancer cases increased by more than 40 percent from 1973 to 1998
overall. Cases of breast cancer have continued to increase since then, though at a lower rate. The
reported rise is believed to largely reflect increased screening for breast cancer, particularly with
mammograms, although other factors, such as rising obesity and postmenopausal hormone use, may
also have played a role.
DETECTION AND DIAGNOSIS
The earlier a cancer is diagnosed and treated, the greater is the chance of cure, or at least
improvement in the quality and length of life. The regular screening of apparently healthy people has
been given a high priority because it permits diagnosis before development of symptoms, a stage when
the cancer is most curable. Excellent or reasonably good screening is available for such major killers as
cancers of the breast, colon and rectum, uterus, and prostate.
Individuals’ self-examination of their skin and, in the case of women, breasts has also been shown to
yield earlier tumor detection. Indeed doctors long urged patients to be alert to possible early signs of
disease. The following seven danger signals have often been cited as potential indications of cancer:
•Change in bowel or bladder habits
•A sore that does not heal
•Unusual bleeding or discharge
•Thickening or lump in breast or elsewhere
•Indigestion or difficulty in swallowing
•Obvious change in a wart or mole
•Nagging cough or hoarseness
It should be kept in mind, however, that these and other potential warning symptoms, such as an
unexplained change in weight, are often not due to cancer. They may also result from other conditions,
such as an infection or a benign tumor.
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Diagnostic study for cancer begins with a thorough history and physical examination, including
inspection and palpation of all accessible sites, especially the skin, neck, breasts, abdomen, testicles,
and lymph-node-bearing areas. It specifically includes examination of bodily orifices, particularly rectal
examination for cancers of the rectum or prostate and pelvic examination for cancers of the cervix or
body of the uterus. A variety of diagnostic tests may be done depending on the situation, including use
of devices to view less accessible parts of the anatomy, such as colonoscopy, or various imaging tests
making use of X rays, sound waves, radioactive particles, or magnetic fields to analyze body tissue.
Biopsy
The biopsy remains the only definitive method for the diagnosis of a cancer. It involves examination of a
section of tissue removed from the tumor itself or from a metastasis. Modern technology has greatly
reduced the need for open surgical biopsy. Guided by palpation or computerized axial tomography (CAT
or CT) scan, a tumor in almost any part of the body can be biopsied through a thin, flexible needle.
Alternatively, a flexible lighted tube known as an endoscope, perhaps equipped with a viewing camera,
may be used. Such techniques permit diagnosis before surgery and therefore a better choice of
therapeutic approach and better planning of surgery, should it be necessary.
Staging
Once a tissue diagnosis of cancer has been made, the extent, or stage, of the disease must be
evaluated because prognosis and appropriate treatment vary with the stage of the disease. For each
type of tumor, the stage (I, II, III, or IV) is defined in terms of findings with progressively more severe
prognostic implications: small local tumor, more extensive local tumor, regional lymph node
involvement, and distant metastases. The clinical stage, defined by information obtained prior to
surgical exploration, is used to decide appropriate initial treatment. The surgical stage, which may be
different from the clinical, incorporates the findings of the surgical exploration, and is used as a basis for
subsequent treatment and for prognosis. It is also used for any analyses of effects of different
treatments.
TREATMENT
Cancer may be treated by such means as surgery, radiation, chemotherapy, and immunotherapy. The
concerns of cancer treatment extend beyond the objectives of curing the patient, or increasing the
patient’s survival time. Even if cured, a cancer patient may be left with serious handicaps. Every effort
must be made to achieve the maximum possible quality of life through rehabilitative techniques,
including reconstructive surgery. For the patient who is not cured, palliative therapy may achieve
comfort and good function for months or years. Pain is a severe problem and can be relieved much
more effectively than it could in the past.
Surgery
The principal approach to curing cancer is to remove all of the malignant cells by a surgical operation.
In the past this meant the removal of all of the involved tissue and as much potentially involved tissue
as possible, including adjacent tissues and lymph nodes. For some tumors, notably cancer of the
breast, this radical degree of surgery (see Mastectomy) is not always necessary. Refinements in
surgical techniques, improved knowledge of physiology, advances in anesthesiology, ready availability
of blood products, and potent antibiotics have permitted less extensive surgery with more rapid
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recovery and less resulting disability. Many cancers, though, are at too advanced a stage at the time of
diagnosis to permit cure by surgery. If local extension involves neighboring tissues that cannot be
sacrificed or if distant metastases are already present, surgery will not be curative. Even when it is clear
that surgical cure is not possible, however, palliative surgery may be helpful to relieve symptoms, as of
obstruction, or to reduce the size of the tumor in an effort to improve response to subsequent radiation
or chemotherapy.
Radiation Therapy
Ionizing radiation, which may be either electromagnetic or particulate, is destructive to tissue.
Electromagnetic radiation includes gamma rays, emitted by radioactive decay, and X rays, produced
when a beam of electrons strikes a heavy-metal target. Particulate radiation includes beams of
electrons, protons, neutrons, alpha particles (helium nuclei), and negative pi mesons (pions).
Tumors vary greatly in their sensitivity to radiation. A “sensitive” tumor is one that is more susceptible
than surrounding normal tissues. When such a tumor is readily accessible—a superficial tumor, for
example, or one in an organ like the uterus, into which a radiation source can be introduced—it may be
curable by radiation therapy. Because of its relatively sparing effect on normal tissues, radiation is
useful when a tumor is located where it cannot be removed because surgery would damage vital
adjacent tissue or because a tumor has begun to infiltrate adjacent structures that cannot be sacrificed.
Radiation therapy is also extremely useful for palliation, especially of metastatic tumors.
Radiation can also be useful as an adjunct to surgery. Preoperative radiation may rapidly sterilize the
tumor cells and prevent seeding at surgery. It may also shrink the tumor and make surgery easier or
shrink an inoperable tumor so that it becomes operable. In other tumors postoperative radiation is used.
Chemotherapy
Chemotherapy involves the use of drugs in the treatment of cancer. Since a drug is distributed
throughout the body by the bloodstream, chemotherapy is useful for tumors that have spread beyond
the area accessible by surgery or radiotherapy. A number of different types of anticancer drugs are
used, but nearly all work by interfering with DNA synthesis or function. Rapidly dividing cells are
therefore more sensitive to chemotherapy. Cancers have a larger proportion of dividing cells than do
normal tissues, in which stem, or replenishing, cells are dormant and therefore resistant to drug effect.
The most rapidly proliferating normal tissues are the bone marrow and the lining cells of the
gastrointestinal tract. These are the most sensitive normal areas of chemotherapeutic effect and
constitute the sites of toxicity that will limit the tolerable dose of most drugs. To be effectively treated, a
tumor must have a sensitivity greater than that of the most sensitive normal tissue. Some tumors may
be many times more sensitive, but many are only slightly more sensitive. Fortunately the normal bone
marrow cells can divide faster than malignant cells and thus recover more rapidly. This permits a repeat
cycle of the drug before the tumor has regrown very much. Repeated cycles can steadily deplete a
tumor before resistance occurs. Some tumors are so sensitive to chemotherapy that a
chemotherapeutic cure is possible in a high percentage: examples are choriocarcinoma in the female;
acute Leukemia, especially in children; Hodgkin’s disease and diffuse large-cell lymphoma; testicular
carcinoma; ovarian carcinoma; small-cell carcinoma of the lung; and several of the cancers of children.
These cancers are often already disseminated at the time of diagnosis and cannot be treated by other
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means. Still other advanced cancers respond well to chemotherapy and can be controlled for a long
time, so chemotherapy is commonly used for palliation.
Two major problems limiting the usefulness of chemotherapy are toxicity and resistance. Techniques
that avoid or control toxicity and reduce the risk of resistance have steadily improved. It is important to
begin treatment as early as possible, to use the optimal dose of the drug, and to repeat cycles as
quickly as possible consistent with reasonable recovery from toxicity.
The use of multiple drugs is effective. Combination chemotherapy employs several drugs (often three to
six at a time), each of which is effective as a single agent. The drugs used have different mechanisms
of action, making cross-resistance less likely, and different types of toxicity, so that each may be given
at optimal dose without causing fatal additive toxicity.
Chemotherapy may be used together with surgery or radiation as combined modality therapy. It is often
used as an adjuvant, or helper, when surgery is the primary therapy. As such it is usually given after
surgery. This type of therapy has greatly increased the cure rate of breast cancer. The major purpose of
chemotherapy as an adjuvant is to kill off micrometastases that may have been established before
surgery. Recently, chemotherapy has been used before surgery as a neoadjuvant. This therapy has the
same effect as adjuvant chemotherapy but may also shrink a tumor, making it more easily removable.
Hormone Therapy
Many cancers arising from tissues that are hormone-dependent, such as the breast, the prostate, the
endometrium, and the thyroid, are responsive to hormone manipulation. This may consist of the
removal of the source of the stimulating hormone or the administration of various hormones and
antihormones.
Immunotherapy
Immunotherapy, also known as biotherapy or biological response modifier (BRM) therapy, is aimed at
bolstering the defenses offered by the body’s immune system against disease. It is also used to
enhance the effectiveness of other forms of cancer treatment or to relieve side effects. One approach
involves biological agents that stimulate certain cells, which can then attack the malignant cells.
Cytokines, non antibody proteins that are produced by the immune system and can affect the immune
response, may be used as such agents. An important group of such substances is the interleukins; for
example, interleukin-2 may be used to stimulate the patient’s lymphokine-activated killer lymphocytes
(LAK cells). Research has been very active concerning tumor-specific antigens against which
antibodies could be raised. These antitumor antibodies would be used to treat cancer either directly or
by coupling to a chemotherapeutic agent. The antibody could identify the malignant cell and adhere to
it, thus delivering the drug directly to the target. The drug trastuzumab, approved by the U.S. Food and
Drug Administration (FDA) in 1998 for use against breast cancer in women, harnesses monoclonal, or
factory produced, antibodies to target cancer cells that overproduce a growth factor protein believed to
be involved in a third of all breast cancers. It blocks the protein from promoting excessive cell growth.
Imatinib mesylate, approved by the FDA in 2001 for use against chronic myeloid, or myelogenous,
leukemia (CML), was the first true example of a molecularly targeted anticancer drug; focusing on a
molecule that causes the cancer, it blocks the action of a defective signaling protein responsible for the
uncontrolled proliferation of white blood cells characteristic of CML.
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Antiangiogenesis Therapy
Angiogenesis is the process through which new blood vessels are formed in the body; a cancer tumor,
for example, requires the development of new blood vessels so it can obtain nutrients needed for
growth. Researchers are investigating the possible use of drugs to “starve” a tumor by interfering with
the formation of these vessels. Initial experiments with such antiangiogenic drugs suggested that they
can sometimes eradicate cancers or at least shrink the tumors to non-life-threatening size. The drugs
generally appear to have mild side effects, in contrast to traditional chemotherapy drugs, which may kill
normal cells as well as cancerous ones. (Certain traditional chemotherapy drugs also have some
antiangiogenic effects, among them paclitaxel, doxorubicin, epirubicin, mitoxantrone, and
cyclophosphamide.) Antiangiogenesis drugs under study in the U.S. include angiostatin and endostatin,
which were reported in 1998 to have eliminated cancer in laboratory mice when used together. The
safety and effectiveness of such drugs in humans, however, remained to be established.
MORTALITY and CURABILITY
For many years the overall death rate from cancer in the U.S. rose more or less steadily, peaking in
1991. It remained level from 1991 to 1994 and then began to decline, at an average of 1.4 percent per
year between 1994 and 1998. According to American Cancer Society estimates for 2006, the cancer
that causes the most deaths in the U.S. for both sexes is lung cancer. This is followed by breast cancer
and then colorectal cancer among women; among men, prostate and colorectal cancer cause a similar
number of deaths. (Prostate cancer is relatively treatable, but the total number of cases is very high.).
Together, these cancers were expected to account for over half of all U.S. deaths from cancer in 2006.
Skin cancers, most of which are easily curable, cause roughly 10,000 deaths a year, most of them from
melanoma.
Since 1949 cancer mortality in the U.S. has been higher among men than among women. But the sex
ratios of different cancers vary considerably. Although the incidence of lung cancer among women
declined slightly between 1992 and 1998, the death rate rose 0.8 percent a year; this represented,
however, a slower increase than in the preceding three decades. Meanwhile, lung cancer death rates
for men fell 1.9 percent annually from 1992 to 1998, continuing a downward trend that began in 1990.
Many experts believed that the female lung cancer death rate was following a pattern already seen
among men—that is, mortality begins to decline as older smokers die while fewer young people start to
smoke. Women’s peak mortality rate thus comes later than men’s because they started smoking later
(see Smoking).
Cancer mortality is higher among blacks than whites for reasons that are not fully understood but are
under intensive study.
The treatment of cancer has improved remarkably since 1920, when fewer than 20 percent of U.S.
white patients with cancer survived more than five years. In 1960, 39 percent did so, and the figures
improved to 43 percent in 1970, 50 percent in 1980, and over 60 percent by the mid-1990s. In the
decade following 1990 some 13 million new cancer cases were diagnosed, and almost 5 million people
died of the disease. In general, patients who survive more than five years can be regarded as cured.
CANCER CONTROL
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The most important preventive measure in controlling cancer is the cessation of tobacco use, which is
the cause of 30 percent of all deaths from cancer. Since about one-third of U.S. cancer deaths can be
linked to nutritional factors, a large reduction might result from better diet. The ACS advocates a
balanced diet, coupled with regular physical activity, and a healthy body weight. In particular, it
recommends the following:•Eat mainly foods from plant sources, including at least five servings of fruits
and vegetables daily, in addition to such other foods from plant sources as breads, cereals, grain
products, rice, pasta, or beans.•Limit consumption of high-fat foods, particularly from animal
sources.•Be at least moderately active for at least 30 minutes most days of the week, and stay within a
healthy weight range.•Limit consumption of alcoholic beverages.
To prevent cancer of the skin, which is generally linked with sunlight, exposure to the sun should be
minimized, and sunscreens routinely used. The environment can be improved by the elimination of
carcinogenic chemicals from the workplace and the home, by the elimination of exposure to asbestos
fiber dust, and by the reduction of excess radon accumulation in homes.
Effective screening is available for some types of cancer. The ACS recommends that people without
symptoms have a cancer-related checkup during regular health examinations. Also, regarding breast
cancer, the society recommends that women undergo a breast examination by a health-care
professional at least once every three years between the ages of 20 and 39 and yearly thereafter.
Women should be aware of what their breasts normally look and feel like, and should report any change
to their doctor. For women at average risk of breast cancer, a mammogram is recommended every year
beginning at age 40. (Mammography may not be appropriate, however, for women with certain health
limitations or a short life expectancy.)
To check for cancer of the cervix, the society suggests that women start undergoing screening three
years after they begin having vaginal intercourse, but no later than the age of 21; the screening should
be performed annually with the regular Pap test or every two years with the liquid-based Pap test (see
Gynecology). Beginning at age 30, women who have had three consecutive normal Pap test results
may undergo screening every two to three years, unless they have risk factors justifying more frequent
testing. Beginning at age 70, women who have had three or more normal Pap tests in a row and no
abnormal results in the past decade may choose to stop cervical cancer screening, unless they have
certain risk factors. Women who have had a total hysterectomy (including removal of the cervix) may
also choose to stop cervical cancer screening, unless the surgery was performed as a treatment for
cervical cancer. In 2006 the U.S. Food and Drug Administration approved a vaccine for use in females
aged 9 to 26 that can prevent some cases of cervical cancer and precancerous conditions caused by
the human papillomavirus.
Regarding endometrial cancer, the ACS advises that women be made aware of the risks and symptoms
of the disorder, and urges them to discuss any unexpected bleeding or spotting with their doctor.
Women who have or are at risk for hereditary nonpolyposis colon cancer should be offered, starting at
age 35, an endometrial biopsy annually. To detect cancer of the colon and rectum, people of average
risk should adhere to one of the following schedules, starting at age 50: a fecal occult blood test (FOBT)
every year; a flexible sigmoidoscopy every five years; an FOBT every year and flexible sigmoidoscopy
every five years; a double-contrast barium enema every five years; or a colonoscopy every ten years.
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The ACS recommends that a digital rectal exam be performed at the same time as the sigmoidoscopy,
colonoscopy, or double-contrast barium enema. To detect prostate cancer, a prostate-specific antigen
(PSA) blood test and a digital rectal exam should be offered annually, starting at age 50, to men with a
life expectancy of at least ten years, although those at high risk (such as African-Americans and men
who with a first-degree relative who was diagnosed with prostate cancer at a young age) should start
testing at 45.
Widespread adoption of preventive measures could markedly reduce the incidence and death rates of
many types of cancer. Such measures, together with full use of present technology for diagnosis and
treatment, may permit the achievement of the ACS goals, announced in 1999, of a 50 percent reduction
in cancer deaths and a 25 percent drop in cancer incidence rates in the U.S. by the year 2015.
For further information on this topic, see the Bibliography, sections Cell, Cell,–Genetics, Disease,–
Disease,.
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