Download Carcinoma - Margaret O`Mara

Carcinoma
Maggie O’Mara
ANATOMY & PHYSIOLOGY SCI 2031
Professor Irit Cohen
February 9, 2011
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Table of Contents
Introduction: General Carcinoma
Specific Types: Aplastic Anemia
Colorectal Carcinoma
Lung Carcinoma
Melanoma
Meylodyplastic Syndrome
Prostate Carcinoma
Data:
Appendix A: Diagram of Normal and Caner Cell Structure (Figure 1.1)
Photo of Aplastic Anemia Cells (Figure 1.2)
Diagram of Colorectal Carcinoma (Figure 1.3)
Photo of Lung Cancer Cells (Figure 1.4)
Photo of Melanoma Cells (Figure 1.5)
Diagram Of Prostate Carcinoma (Figure1.6)
Appendix B: Family Pedigree Chart (Figure 2.1)
Age of Onset vs. Age of Death (Figure 2.2)
Occurrence in Type of Carcinoma (Figure 2.3)
Discussion: Description of Family Pedigree Chart 3
Conclusion: Final thoughts
Work Cited: List of Citations
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General Carcinoma
Historically Cancer was originally thought to be a result of completely unregulated
growth of cells, and logically corollary was that neoplastic cells divided at a more aggressive rat
than normal neoplastic cells. (Rubin) Cancer or Carcinoma is a group of cells, usually derived
from a single cell that has lost its ability to control mechanisms normally. Intern the cell has
unregulated growth. Theses cancerous cells known as malignant cells and can develop from any
tissue within any organ, in any organ system. As malignant cells grow and multiply they form a
mass of cancerous tissue know as a tumor. Tumors can be cancerous and non cancerous.
Malignant tumors invade and destroy normal adjacent tissue. The cells in this initial or primary
location can spread throughout the body; this is known as metastasizing (Merck).
Transformation is the complex process in which cancerous cells develop from healthy
cells (See Appendix A, Figure 1.1). Initiation is the first step in the process in which a change in
the cells genetic material primes the cell to become cancerous. This occurs in the
Deoxyribonucleic acid (DNA) and sometimes chromosome structure of the cell, the change can
occur spontaneously or can be brought on by an agent that causes cancer. Carcinoma causing
agents are called Carcinogens, and can include chemicals, tobacco, viruses, radiation, and
sunlight. Not all cells are equally susceptible to carcinogens; a genetic flaw or chronic irritation
in a cell may cause it to be more susceptible. The seconded and final step is known as Promotion.
Promoters are the agents that cause promotion; they can be substances in the environment or
even drugs such as barbiturates, which affect the central nervous system (CNS) (Barbiturate).
Promoters unlike carcinogens cannot cause carcinoma on their own rather promoters allow a cell
that has undergone initiation to become cancerous, thus non-initiated cells are not affect. Several
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factors or a combination of susceptible cells, and carcinogens are need for carcinoma to occur
(Merck).
Carcinoma can grow directly into surrounding tissue or spread to nearby or distant tissues
and organs. Carcinoma can spread through the lymphatic system or via the blood stream.
Cancers are divided into three types those of the Leukemias and Lymphomas, carcinomas, and
sarcomas. Leukemias and lymphomas are cancers of the blood and blood forming tissues. They
remain as separate cancerous cells rather than form a lump thus they harm the body by crowding
out normal blood cells in the bone marrow and blood stream. This causes normal functioning
cells to gradually be replaced by cancerous blood cells. Carcinomas are cancers of epithelial
cells; the cells that cover the body produce hormones and make up glands. This type occurs more
often in older people than younger people. Carcinomas include cancer of the skin lung, colon,
stomach, breast, prostate, and thyroid gland. Sarcomas are cancers of the meosdermal cells; the
cells that form muscles and connective tissue. Unlike carcinomas sarcomas occur more often in
younger people than in younger people. Examples of sarcomas include leiomyosarcoma; which
is cancer of smooth muscle found in the in the wall of digestive organs, and osteosarcoma; bone
cancer (Merck).
Chance of developing cancer can be increased by genetic and environmental factors.
Carcinogens are factors that act on deoxyribonucleic acid (DNA), causing dangerous changes or
it may work to increase the rate of cell division. This change in cell division may work to
increase the probability of DNA changes (Madison). Carcinogens can be found in the
environmental and industrial areas, life style choices, medicines, and medical treatments. Other
risk factors include genetics. Carcinoma can significantly affect some families more than others,
and put members at a high risk of developing certain cancers. A single gene or several genes
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interacting with one another can be to blame as genetic interaction alters cancer can develop.
Increased risk genetically may also be cause by an extra or abnormal chromosome (Merck).
The doctor in which you would be referred to for treatment is known was an Oncologist.
Oncologists are physicians who specialize in the diagnosis, treatment, and treatment of cancers.
If you are diagnosed with cancer you would then be referred to an Oncologist who specializes in
your type of cancer (What Is an Oncologist). Oncologist must be trained in all of the various
types of cancer, as well as the best treatment for each. However they may specialize in a specific
type of cancer. Oncologists are trained in what exactly to look for regarding the various
symptoms of cancer, as well as which tests to conduct to acquire and accurate diagnosis
(Crystal). Following a diagnosis they may then be able to advise the best treatment for each type
of cancer. Due to the amount of research conducted on the causes and treatments of cancer, new
information is discovered frequently. It is the job of Oncologists to be fully aware of all new
research and findings in the field of cancer (Crystal).
As see in Figure2.3 the types of cancer present in regards to this Family Pedigree Chart
(See Appendix B, Figure2.1) are; Aplastic Anemia, Colorectal, Lung, Melanoma,
Myelodysplastic Syndromes, Prostate, and Unknown (American Cancer Society).
Aplastic Anemia
Aplastic Anemia causes bone marrow to fail to make enough blood cells. The cells
present in bone marrow are made from blood-forming stem cells. In Aplastic Anemia the stem
cells are damaged and very few are present. Thus not enough blood cells are produced.
Typically Aplastic Anemia lowers the production of all three types of blood cells; red blood
cells, white blood cells, platelets, this is known as Pancytopenia. It is rare for just one cell line to
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be affected. This disorder is not an actually type of cancer but rather is associated with certain
types of cancer, usually Leukemia. Aplastic Anemia can be acquired; more common, or
inherited. Inheritance of Aplastic Anemia occurs when a gene mutates; or makes abnormal
copies, that are then passed on from parent to child.
There are two forms of Inherited Aplastic Anemia; Fanconi Anemia, and Dyskeratosis
Congenita (American Cancer Society).Fanconi Anemia is the more common of the two, and is
caused by the inheritance two mutated copies of one of the following genes FANCA, FANCB,
FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ, FANCL, FANCM,
and FANCN(American Cancer Society). Meaning one from each parent, if only one mutated
gene is present the individual will not develop the disorder but will be a carrier. Dyskeratosis
Congenita occurs when abnormal copies of the following genes are inherited; TERC, TERT, and
DKC1(American Cancer Society).
Warning signs that you may have Aplastic Anemia include; fatigue and shortness of
breath, which is caused by anemia, also people with anemia also tend to be pale. Problems with
infections that keep coming back or are severe may occur, as a result of not having enough white
blood cells to fight off infection. Finally abnormal bruising or bleeding may occur because of a
shortage of platelets (American Cancer Society). Diagnosis comes after positive results from one
or both of the following test; a Complete Blood Count, and a Bone Marrow Biopsy. When a
Complete Blood Count (CBC) is conducted on individual with Aplastic Anemia results will
show reduced counts of red blood cells, white blood cells, and platelets. A Bone Marrow Biopsy
looks at bone marrow which contains blood-forming cells, and is done by a Pathologist. In those
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who are affected by Aplastic Anemia the test will show reduced production of red blood cells,
white blood cells, and platelets (American Cancer Society). (See Appendix A, Figure 1.2).
There are treatments available for those who have been diagnosed with Aplastic Anemia.
You would be referred and Oncologist who specialized in this form of cancer. Two types of
tremens are offered. The first is Allogeneic stem cell transplant; is best suitable for young
patients as transplantation is successful more in children and young adults. Stem Cell transplant
occurs when a matching donor’s stem cells are a match. Matching is determined by a type of test
called HLA typing (American Cancer Society). The stem cells are then transplanted to the
recipient in need. Stem cell transplant is successful up to 80% to 90% of the time in patients with
Aplastic Anemia if cells from a matched related donor are used. Prior to transplantation you must
receive chemotherapy. Chemotherapy works by killing fast growing cells like cancer (Learn).
Unlike healthy cells, cancer cells reproduce continuously because they don't respond to the
normal signals that control cell growth. Chemotherapy works by disrupting cell division and
killing these actively dividing cancer cells. Chemotherapy works to treat cancer throughout the
body, unlike radiation therapy which destroys cancer cells in a specific area of the body i.e.,
tumors (Chemotherapy). Chemotherapy drugs most often used are cyclophosphamide and,
fludarabine (American Cancer Society).
The other treatment option is Immunosuppressive therapy. This form of treatment is more
suitable for older patients or those who are unable to find a matching donor. Immunosuppressive
therapy helps stop the immune system from killing bone marrow cells (American Cancer
Society).This treatment is more suitable for those with acquired A plastic Anemia rather than
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inherited as it is not caused by the immune system. The major drugs used are antithymocyte
globulin and cyclosporine (American Cancer Society)
Colorectal Carcinoma
Colorectal Cancer is caner of the colon and or rectum. Colorectal cancer develops slowly
over time. Before a cancer develops, a growth of tissue or tumor usually begins as a noncancerous polyp on the inner lining of the colon or rectum. Normally polyps are benign, noncancerous, however some may become cancerous but the transformation depend on the type of
polyp (American Cancer Society). There are two types of polyps Adenomatous Polyps and
Hyperplastic Polyps / Inflammatory Polyps. Adenomatous Polyps have to potential to become
cancerous; adenomas are called a pre-cancerous condition (American Cancer Society).
Hyperplastic Polyps or Inflammatory Polyps are not generally pre-cancerous. However some
doctors believe that these polyps increase the risk of developing adenomas and cancer,
particularly when these polyps grow in the ascending colon (American Cancer Society). Other
types of colon cancer include Adenocarcinomas, Carcinoid tumors, Gastrointestinal Stromal
tumors, and Lymphomas (American Cancer Society), (See Appendix A, Figure 1.3).
Early diagnosis is possible with regular screenings. These tests find polyps and cancer, or
just cancer. Test that can find both are Flexible Sigmoidoscopy, Colonoscopy, Double-Contrast
Barium Enema, and CT Colonography. Those tests that focus on the diagnosis of only cancer are
Fecal Occult Blood test, Fecal Immunochemical test and, Stool DNA tests. Treatment for colon
cancer varies by stage. At stage 0 due to the cancer not yet growing beyond the inner lining of
the colon, surgery to remove the tumors is all that is needed. In most cases this can be done by
polypectomy or local excision through a colonoscope (American Cancer Society).
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At stage I the cancer has grown through several layers of the colon, but has not yet spread
outside the colon wall its self. Surgery to remove the affect section of colon and nearby lymph
nodes is all that is needed (American Cancer Society). At stage II many of the cancers have
grown through the wall of the colon, and may have extended into nearby tissue. However the
cancer had not yet spread to nearby Lymph nodes. Removable of the affect section of colon via
surgery I needed, and your oncologist may all may also suggest chemotherapy based on
abnormality or aggressiveness of the caner (American Cancer Society). At stage III cancer has
spread beyond the colon wall and has spread to lymph nodes nearby, but has not yet spread to
surrounding organs. Surgery for removal of the affect section of colon paired with chemotherapy
is the usually treatment. Oncologists may suggest radiation in addition if cancer was thought it be
left behind after surgery. At stage IV cancer had spread beyond on the colon wall to distant
organs and tissue such as; liver, lungs, peritoneum, or ovaries (American Cancer Society). In this
stage surgery to remove the affected areas is unlikely to cure the patient. However in the event
that the metastases are mall and there are few of them surgery may be able to eliminate the
cancer, and allow you to live longer, and be cured. If the metastases cannot be removed via
surgery due to the larger size, or that there are more in them chemotherapy may be used first to
shrink the tumors and then. Allowing surgery to be an option after the initial chemotherapy and
chemotherapy would again be used following surgery. For more aggressive advanced cancer
your oncologist may suggest radiation therapy, as it may shrink the tumors. However radiation
therapy will not result in cure so other treatments may follow (American Cancer Society).
Colorectal cancer grows slow; as a result symptoms may not arise for some time.
Symptoms also depend on the type, location, and extend of the cancer. In some cases fatigue and
weakness may be a person’s only symptoms as a result of occult bleeding. If the cancer is a
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tumor located in the left, descending colon symptoms may be constipation or frequent bowl
movements, as well as abdominal pain ranging from cramping to sever (Merck). If the tumor
resides in the right ascending colon, a mass here takes longer to as the diameter of the colon is
larger than at the descending colon, thus a doctor may be able to feel the mass through the
abdominal wall by the time of diagnosis. In any event most colon cancers bleed thus stool may
be mixed with blood, however the blood is often hard to detect (Merck).
Those at risk for contracting the disease are people who have Ulcerative Colitis, and
Crohn’s Disease, as well as those with a family history of colorectal cancer, and polyps.
However those with the highest risk of colorectal cancer at those who have poor diets. High fat,
low fiber diets, and exposure to carcinogens in the air and water, can leave you more susceptible
to develop the disease (Merck).
Lung Carcinoma
Carcinoma of the Lungs is divided into three categories; Non-Small Cell, Small Cell and
Carcinoid Tumor. Of those diagnosed with Lung Cancer 85% to 90% are diagnosed with NonSmall Cell, While 10%-15% are diagnosed with Small Cell Lung cancer, and the fewer than 5%
are diagnosed with Carcinoid Tumor’s (American Cancer Society). This Family Pedigree Chat
(Figure 2.1) focuses on Non-Small Cell Lung Cancer. Non- Small Lung Cancer (NSCLC) is
subdivided into three types based on the size, shape and chemical makeup of cells when
observed under a micro scope. Due to similar prognosis and treatment they three different sub
types are grouped together (American Cancer Society). The following are the three major
subtypes of NSCLC; Squamous Cell Carcinoma, Adenocarcinoma, and Large cell Carcinoma.
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Squamous Cell Carcinoma equates for about 25% to 30% of NSCLC diagnoses.
Squamous Cell cancer begins in early versions of squamous cells. These cells are found in lining
of airways in the lungs and have a flat shape. Squamous is often linked with a history of
smoking, and often are found in the middle of the lungs near the bronchus (American Cancer
Society). Adenocarcinoma accounts for about 40% of NSCLC cases. This type of cancer is again
associated those who smoke of have smoked. Adenocarcinoma cancer begins in early versions of
cells that are normally responsible for secreting subsistence’s such as mucus. This type is more
likely to affect women than man, and is occurs in younger people more often than other types of
lungs (American Cancer Society). Adenocarcinoma is often found in the outer area of the lung.
It has a tendency to grow slower than the other two subtypes of Non-Small Cell Lung Cancer.
This subtype is often found earlier, before it has a chance to spread out side of the lungs, which
can lead to a better prognosis (American Cancer Society). Large cell Carcinoma equates to about
10% to 15% of NSCLC. It may appear in any area of the lungs, and has a tendency to grow more
quickly. These characteristic can make it more difficult to treat (American Cancer Society)
Carcinoma of the lungs is usually brought on by exposure to carcinogens. Cigarette
smoking is to blame for 90% of cases of lung cancer in men and 80% in women (Merck). Other
carcinogens that lead to cancer are those that are inhaled while are at work; which account for
10% of cases in men and 5% of cases in women Air pollution equate for about 1 % of cases
(Merck). Location, type, and spreading of lung cancer dictate the kind of symptoms a person
will experience. Some symptoms include; intense coughing, wheezing, sever bleeding, shortness
of breath, pneumonia, and chest pain. Kung cancer can spread and grow in to nerve in the neck,
and cause droopy eyelids, small pupils, sunken eyes, and reduced perception on one side of the
face (Horner’s Syndrome) (Merck).
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When diagnosing Lung cancer doctors will start with a chest x-ray due to occurs of some
symptoms. Shadows on an extra may be a result of cancer but are not a concrete diagnosis. Lager
tumors will show up on an x-ray while small ones may be missed. A Computed Tomography
(CT) may result in a more definitive answer, as it can show small nodules that will not appear on
an x-ray. CT scans can also reveal enlarged lymph nodes; however a biopsy of lymph nodes is
needed to determine if the inflammation is a result of cancer. Following a biopsy doctors will
conduct a microscopic examination of the lungs to confirm a diagnosis of cancer.
As in instances of other types of cancer the treat meant to lung cancer is similar. For
instances of lung cancer that has not yet spread beyond the lungs surgery may be an option, as
well as if the cancer is not small cell carcinoma. Radiation therapy may also be an option for
those who refuse surgery, or cannot receive surgery, and/ or whose cancer has spread beyond the
lungs to nearby structures. However radiation therapy, only reduces the size of the cancer and
slows the rate of growth treatment often times includes chemotherapy. Chemotherapy paired
with radiation therapy is often the best solution for this type of cancer. The effectiveness of
chemotherapy alone one this type of cancer can be limited due to the aggressiveness of the
carcinoma.
Melanoma
Skin cancer is one on the most common occurring types of carcinomas and can be
attributed to ultraviolet damage on the epidermis, thus affecting the integumentary system
(Cohen). There are types of skin cancer Squamous which involves more superficial layer of the
skin, Basal Cell Carcinoma which is the most common and affects deeper layers of the
Epidermis, and finally Melanoma, which occurs in the epidermis (Cohen). This Family Pedigree
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Chart (Figure 2.1) focuses on melanoma in reference to carcinoma of the integumentary system.
Melanoma usually begins from a mole but may appear anywhere on the body like between
figures and toes (Cohen). Melanoma occurs when melanocytes grow rapidly, and metastasize
through the lymphoid system (Martini) (See Appendix A, Figure 1.4). Melanocytes are the
pigmented cells responsible for giving skin its distinctive color. During times of sun exposure
melanocytes produce more melanin; which is the pigment that darkens the skin and increase the
risk of developing melanoma. (Merck). Cancerous melanocytes be preexisting in the form of
moles or develop from other normal preexisting cells.
The appearance of melanoma varies from flat, irregular, brown patches which contain
black spots, to raised brown patches with red, white black or blue spots. Other times its can
appear as a firm gray or black lump (Merck). Survival from a diagnosis of melanoma depends on
when the condition is detected, and treatment is received dud to the aggressiveness of the
disease. Precautionary steps can be taken to help reduce the risk of developing melanoma.
Avoiding exposure to ultraviolet radiation and using sun block during times of exposure can
lower your risk (Martini).
A diagnosis of Melanoma comes from an oncologist, or one that specializes in carcinoma
of the integumentary system. Warning signs of possible melanoma include; new moles, changes
in current moles i.e.; growth, darkening, inflammations, spotty color change, bleeding broken
skin itching and pain (Merck) Doctors will perform a biopsy for a definitive diagnosis.
Suspicious growths are removed entirely and examined to see if the mass is melanoma, if so
doctors will make sure all of the melanoma was removed.
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The less the melanoma has grown into the skin the great chance surgery will be
successful in removing the entire mass (Merck) Surgery can be 100% effective on even the
deepest masses if detected early enough. When surgically removing masse doctors cut at least a
½ inch border around the infected are to ensure the entire melanoma is removed. Melanomas that
have grown deeper that 1/32 inches into the skin are more likely to have metastasized through
the lymphatic system. And blood vessels thus surgery may not remove the entire melanoma
(Merck). Like other types of cancer chemotherapy can be a treatment for melanoma that has
metastasized beyond the hypodermis, but few are cured from this treatment (Merck) Survival is
based on early detection, course of treatment and strength of the immune system of the patient.
Yearly body scans and ultraviolet radiation protection are the best courses of action for
prevention and reduced risk of melanoma.
Myelodyplastic Syndrome
Myelodyplastic Syndrome describes the process in which a line of identical cells that
develops and occupies the bone marrow results in abnormal red blood cells, white blood cells,
and platelets that do not grow and mature normally(Figure 1.5)(Merck). The body thus destroys
these abnormal blood cells which leaves the patient with low blood counts due to the lack of
normal blood cells (American Cancer Society). Myelodyplastic Syndrome can progress into
aggressive carcinoma of bone marrow cells known as Acute Myeloid Leukemia, this
transformation occurs in about 1/3 of patients diagnose with Myelodyplastic Syndrome
(American Cancer Society). In relation to the Family Pedigree Chart (Figure 2.1) the member
diagnosed with Myelodyplastic Syndrome developed Acute Myeloid Leukemia.
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Acute Myeloid Leukemia is a life threatening disease in which the cells that normally
develop into nuetophills, basophills, eosinophils, and momcytes become cancerous and
aggressively replace normal cells in bone marrow (Merck). This type of leukemia is most
common among adults, though people of all ages can be diagnosed. Once the leukemia cells
accumulate in the bone marrow they then metastasize into the blood stream, thus are transported
to organs throughout the body and continuously grow and divide Small masses or chloromas cam
form in or under the skin, gums or eyes (Merck).
Symptoms occur as a result of bone morrows inability to produce enough normal blood
cells. Fever and excess sweating may occur as a result of infection from too few normal white
blood cells. Weakness, fatigue, and paleness indicating from anemia resulting from a lack of red
blood cells, can also be a sign of Acute Myeloid Leukemia (Merck). As a result of fewer plates
because of the disease easy bruising, bleeding of gums and nose may also occur. Headaches,
vomiting, and irritability can occur as a sign of leukemia cells that are in the brain.
Diagnosis will come from a general oncologist or one specializing in Acute Myeloid
Leukemia. A diagnose will come after a complete blood count is conducted. A biopsy of bone
marrow is also always preformed to confirm a diagnosis and to differentiate Acute Myeloid
Leukemia from other forms of leukemia (Merck). Acute Myeloid Leukemia treatment is aimed at
suppressing the bone marrow to destroy the leukemia cells. Treatment beings with
chemotherapy; using cytarabine by continuous infusion for 7 days followed by daunorubicin for
another 3 days (Merck). In the event that the patient does not respond to treatment, high doses of
chemotherapy may be given accompanied by stem cell transplant.
Those who receive a
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diagnosis of and do not receive treatment with a few weeks to months after diagnosis will die. Of
those who do receive treatment 20% to 40% will survive at least 5 years (Merck).
Prostate Carcinoma
The true cause of prostate carcinoma is unknown; however the disease is believed to be
cause by glad cells. Gland cells are responsible for making prostate fluid that is added to semen.
Adenocarcinoma is the type of cancer that occurs in the glands (American Cancer Society). The
carcinoma beings with a small bump in the gland, most prostate cancers metastasize very slowly
and never cause symptoms. However some metastasize rapidly, and spread outside the prostate
(Merck). Prostate carcinoma is thought to be caused by three pre-cancerous conditions; Prostatic
Intraepithelial Neoplasia (PIN), Atypical Small Acinar Proliferation (ASAP), and Proliferative
Inflammatory Atrophy (PIA). In all instances prostate cells look abnormal under a micro-scope,
the degree of abnormality, and number of cells present varies among each condition (American
Cancer Society).
African American and Hispanic men are at a greater risk of developing prostate
carcinoma and, while risk increases with age for all men. Prostate carcinoma is the most
common occurring cancer as well as the second most common cause of death among men in the
United Stated (Merck). Risk factor that increase chance of developing prostate carcinoma
includes; age, ethnicity, nationality, family history, genes, diet, obesity, exercise, smoking,
inflammation of prostate, infection, and vasectomy (American Cancer Society).
Symptoms of prostate cancer usually don’t present themselves until the carcinoma
reached an advanced stage. Symptoms that occur are similar to those of Benign Prostate
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Hyperplasia (BPH), which include; difficulty urinating, and frequent or urgent urination (Merck).
However in the event of prostate carcinoma symptoms arise after the cancer grows large enough
to compress the urethra, and partially blocks the flow of urine. Bloody urine or sudden inability
to urinate may also occur as a result of prostate cancer. In some cases symptoms occur after
metastasization of the carcinoma, those areas most affect by metastasis are bone; pelvis, ribs, or
vertebrae, and kidneys (Merck).
Based on occurrence of symptoms or results from a screening test, doctors may suspect
prostate carcinoma. The first step of diagnosis is a digital rectal examination, and measurement
of Prostate Specific Antigen (PSA) levels. In the event that cancer is suspect an ultrasound scan
is preformed (Merck). If those test further suggest cancer tissue sample will be obtained from
the prostate via a biopsy, and analyzed (Merck). In the event of cancer your doctor will refer you
to an oncologist, preferable one that specialized in carcinoma of the prostate.
Course of treatment is based on two factors; how malignant the cells are, and how far the
cancer has metastasized. Treatment options depend of the lifestyle of the patient as some
treatments can result in erectile dysfunction (Merck). One treatment involves waiting and
monitoring the cancer, this form of treatment is suitable for carcinoma that are unlike to spread
or spread slowly as well as older males who are more likely to die from other causes before those
of prostate carcinoma. Another course of treatment is Curative which is used to treat prostate
cancers that are more aggressive (Merck). Palliative therapy is also an option and is amid at
treating the symptoms caused by the cancer rather than the treatment of the caner itself. This
option is best suitable for men whose cancer is wide spread and other wise deemed incurable
(Merck).
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Unlike other forms of carcinoma chemotherapy is not usually used as a form of
treatment. However surgery and radiation therapy are still options as well as hormonal therapy.
Surgery is used in the removal of the prostate prostatectomy) in instances where the carcinoma
is confined to the prostates and has not metastasized (Merck). The goal of radiation therapy is to
eliminate the carcinoma while preserving the healthy tissue. This form of treatment is effective
for confined cancer and those that have metastasized. Hormonal therapy is used to slow the
progression of the cancer by blocking the effect of the hormone, as the relays on testosterone to
grow and metastasize (Merck). This course of treatment may be used to delay spread, or treat
wide spread carcinoma. Hormonal therapy works to treat the cancer as well as symptoms that are
caused by the cancer (Merck)
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Data: Appendix A
Figure 1.1
(Kenny)
The above figure show the affect Carcinoma has on the cells. The affected cells cytoplasm
becomes smaller, multiple nuclei and large nucleoli develop, and the chromatin becomes course;
verses the large cytoplasm, single nucleus and nucleolus, and fine chromatin of a normal cell.
Figure 1.2
(Aplastic Anemia)
This picture depicts the affects Aplastic Anemia has on the body. Shown on the (left) is normal
cell growth, and on the (right) is cell growth affect by Aplastic Anemia. You can see the lack of
blood cells in the image on the right.
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Figure 1.3
(Wellness)
Stage 0: Very early cancer on the innermost layer of the intestine, Stage I: Cancer is in
the inner layers of the colon, Stage II: Cancer has spread through the muscle wall of the colon,
Stage III: Cancer has spread to the lymph nodes Stage IV: Cancer that has spread to other organs.
Figure 1.4
(Dr. Weiss)
The above images are microscopic pictures cells that have been affected by the various
sub types of Non-Small Cell Lung Cancer (NSCLC). Beginning from top left to right is;
Adenocarcinoma, Squamous Cell Carcinoma, to bottom left which is Large Cell Tumor. The
bottom right image; Small Cell Lung Cancer is a type of skin cancer rather than a subtype of
Non-Small Cell Lung Cancer.
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Figure 1.4
(Science)
Melanoma cancer; Colored transmission electron micrograph (TEM) of a section
through human skin showing cancer cells (small black/green dots). These are melanocytes, the
cells that produce the brown pigment melanin in the skin. Cancer cells undergo continuous
division, growing chaotically and forming tumors that can impair the normal functioning of the
affected organ. Magnification unknown. (Science)
Figure 1.5
(Information)
This microscope image shows immature cells containing prominent nucleoli. The nuclei are
large, and/or irregular, resembling the nuclei of monocytes (Acute Myeloid Leukemia)
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Figure 1.6
(Prostate)
The above diagram, illustrates the inflammation caused by carcinoma of the prostate. Here you
can see how the growth causes pressure to the urethra which intern, causing many know
symptoms of prostate carcinoma.
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Data: Appendix B
Figure 2.2
Age of Onset vs. Age of Death
8
7
6
5
Age of Death (affected)
4
Age of Onset (affected)
3
2
1
0
20
40
60
80
100
(O’Mara)
Shown is the relationship between Age of onset, and age of death from Cancer. Concluded from
the graph the mean age of onset is 67.5, this data has been affect by the outlier age of 21. The
mean of death without the outlier is 69.5. Again this data is affected by the outlier age of 22.
Figure 2.3
Occurance in Type of Cancer
2.5
2
1.5
1
0.5
Frequancy
0
(O’Mara)
As shown in this chart the most frequent types of cancer reported are Unknown and
Melanoma. However one person who suffered for melanoma was diagnosed for having the
C a r c i n o m a | 25
disease though they did not died as a result of it. All of those persons who died from Unknown
types of Cancer, all were reported smokers.
Family Pedigree Chart Description
1st Generation
Name: John O’Mara
Relation: Paternal Great Grandfather,
Diagnosed: Not Affected
Died: N/A
Type: N/A
Name: Ruth O’Mara
Relation: Paternal Great Grandmother
Diagnosed: Died From Tuberculosis
Died: N/A
Type: N/A
Name: Frank Swint
Relation: Paternal Great Grandfather
Diagnosed: Age 73
Died: Age 77
Type: Aplastic Anemia
Name: Ruth Swint
Relation: Parental Great Grandmother
Diagnosed: Not Affected
C a r c i n o m a | 26
Died: Age 89, Natural Causes
Type: N/A
2nd
Generation
Name: Rosalie O’Mara
Relation: Paternal Great Aunt
Diagnosed: Age 70
Died: Age71
Type: Lung Cancer, Emphysema
* Smoker*
Name: Ruth O’Mara
Relation: Paternal Great Aunt
Diagnosed: Not Affected
Died: Still Living
Type: N/A
Name: William O’Mara
Relation: Paternal Great Uncle
Diagnosed: Age73
Died: Age74
Type: Colorectal, intestinal.
C a r c i n o m a | 27
Name: John Charles O’Mara
Relation: Paternal Grandfather
Diagnosed: Not Affected
Died: Age 77, Dementia
Type: N/A
Name: Mary Swint
Relation: Paternal Grandmother
Diagnosed: Age 67
Died: Age 69
Type: Myelodysplastic Syndrome
Name: Frank Swint
Relation: Paternal Great Uncle
Diagnosed: Age 80
Died: Age 85
Type: N/A Emphysema
*Smoker*
Name: Betty Swint
Relation: Paternal Great Aunt
Diagnosed: Age 78
C a r c i n o m a | 28
Died: Age 79
Type: N/A
*Smoker*
Name: Roberta Ferguson
Relation: Paternal Great Aunt
Diagnosed: Not Affected
Died: N/A
Type: N/A
Name: John Ferguson
Relation: Paternal Great Uncle
Diagnosed: Not Affected
Died: still living
Type: N/A
Name: Frances Burnham
Relation: Paternal Great Aunt
Diagnosed: Not Affected
Died: Age 84
Type: N/A
Name: Charlie Burnham
Relation: Paternal Great Uncle
Diagnosed: Not Affected
Died: Age 88
C a r c i n o m a | 29
Type: N/A
Name: George Swint
Relation: Paternal Great Uncle
Diagnosed: Age78
Died: Age79
Type: Prostate Cancer
*Smoker*
Name: Gene Swint
Relation: Paternal Great Aunt
Diagnosed: Not Affected
Died: Age 83
Type: N/A
3th Generation
Name: Daniel O’Mara
Relation: Parental Uncle
Diagnosed: Age 21
Died: Age22
Type: Melanoma
Name: Michael O’Mara
Relation: Parental Uncle
C a r c i n o m a | 30
Diagnosed: Not Affected
Died: Still Living
Type: N/A
Name: Teresa O’Mara
Relation: Parental Aunt
Diagnosed: Not Affected
Died: Still Living
Type: N/A
Name: Irene O’Mara
Relation: Parental Aunt
Diagnosed: Not Affected
Died: Still Living
Type: N/A
Name: John Patrick O’Mara
Relation: Paternal Father
Diagnosed: Not Affected
Died: Still Living
Type: N/A
Name: Patricia O’Mara
Relation: Paternal Mother
C a r c i n o m a | 31
Diagnosed: Not Affected
Died: Still Living
Type: N/A
4th Generation
Name: Erin O’Mara
Relation: Paternal Sister
Diagnosed: N/A
Died: Still Living
Type: N/A
Name: Margaret O’Mara
Diagnosed: Not Affected
Died: Still Living
Type: N/A
Name: Sean O’Mara
Relation: Paternal Brother
Diagnosed: Not Affected
Died: Still Living
Type: N/A
Franks Swint was my paternal great grandfather. He was diagnosed with Aplastic
Anemia at the age of 80, and as a result of his disease died 5 years later at the age of 85. Through
my research I discover that Aplastic Anemia is an inherited form of carcinoma that affects bone
C a r c i n o m a | 32
marrow. Frank inherited the abnormal gene that causes Aplasic Anemia from his parents. Frank
was not a smoker, however exposure to carcinogen would not have led to his diagnosis, though it
may had added to his predisposition for it. Aplastic Anemia is generally inherited from both
parents who pass on a mutated gene. This mean to my paternal great grandfather passed on the
gene to his children, who passed it along to their children. I now carrier of this form of cancer,
and in the event that I conceive children with a man who is aloes a carrier my children could be
diagnosed with the disease. It is unknown if Frank receive treatment for his condition, however it
can be inferred that he lead a rather healthy life style by looking at the age of onset, as it was
toward his later years that he was diagnosed. By looking at the age of death it can be concluded
that it may have been possible that he received some form of treatment because he lived for 5
years before dying as a result of Aplastic Anemia.
Rosalie O’Mara was my paternal great aunt. She was diagnosed with lung cancer at the
age of 70, her condition was also paired with emphysema It is unknown if she had any
predispositions to the disease related to family history. However she was reported to be a heavy
smoker throughout her life, as cigarettes are a known carcinogen that leads to lung cancer it is
likely that she was diagnosed with lung carcinoma as a result from smoking. Smoking would
also be mostly like to cause her emphysema. It is unknown if she received treatment following
her diagnosis, however based on the other occurring conditions, age of diagnosis, and death it
can be concluded that her condition was too advanced for successful treatment. After being
diagnosed at the age of 70 it can be inferred that her carcinoma was very aggressive and
advanced by the time of diagnosis being that she only lived a year with the condition before
dying as a result of her diagnosis.
C a r c i n o m a | 33
William O’Mara was my paternal uncle. Any predisposition for carcinoma that may
have affected his diagnosis are unknown, how every based on research it is likely that likely that
he may have had polyps that metastasized, and became cancerous. It was reported that William
all suffered from intestinal cancer. This is mostly likely a result the carcinoma metastasizing and
spreading into surrounding tissues. Being that not much was known about healthy diet and
exercise in the early 1900s at the time of William’s birth , these factor could have contribute to
his condition, as we know that high fat low fiber diets can increase risk of diagnosis. Aside from
these factors he was not a reposted smoker, and seemed to maintain a healthy weight. Thus based
on his as of diagnosis, and age of death it can be inferred that he was affect by a preexisting
condition such a polyps, that metastasized, and became aggressive. It is unknown if William
received treatment for his condition, however he was admitted to a nursing home at the time of
diagnosis, so it is likely that it was decided that the best course of action would be to let the
disease take its course. As a result of William’s condition he died at the age of 74.
Mary Swint was my paternal grandmother. Her diagnosis may have been due to
predisposition regarding family history as her father, my parental great grandfather, was
diagnosed with Aplastic anemia. Following her diagnosis of Myleodysplastic as a result she
developed Acute Myeloid Leukemia. Based on research it is known that Acute Myeloid
Leukemia is an aggressive carcinoma. Mary did received treatment for her condition, which is
support by her age of onset, and age of death, as she would not have been able to survive 2 years
without it. Based on her age, and condition Mary’s treatment involved chemotherapy and blood
transfusions, rather than a stem cell transplant. Mary received bluff transfusions to help her body
retain healthy blood cells to compete with the abnormal cells. Without stem cell transplant the
abnormal cells quickly metastasized and spread to surrounds organs and tissues. Mary died from
C a r c i n o m a | 34
organ system failure at a result of her diagnosis. Mary also suffered from carcinoma of the skin.
It is unknown which sub type however her diagnosis did not result in her death, but may have
been link to her diagnosis of Myelodysplastic Syndrome. Her carcinoma was surgically removed,
although it re occurred in different areas. Each time the affected area was surgically removed,
and again did not result in her death.
Frank Swint, was reported to have been diagnosed with cancer, and suffered from
emphysema, although it was unknown what type of carcinoma. Being a smoker for the majority
of his life, and diagnosed with emphysema, it can be suggested that he was diagnosed with
carcinoma of the lungs. His predispositions of this condition may have come from family history
as his father was diagnosed with Aplstic Anemia; however his long term exposure to the
carcinogen in cigarettes put him at a high risk of developing carcinoma. Not much is known
about his diet and life style, as these may have also put him at an increased risk as well. Based on
his Age on onset and Death it can be inferred that he did received treatment for his condition,
and he may have stopped smoking before his diagnosis which could have resulted in minute
repair of affect lung tissue. Despite the possible occurrence of treatment, Frank died as a result of
his condition at the age of 85, five years after his initial diagnosis. .
Betty Swint was my paternal great aunt, was reported to have been diagnosed with
cancer, although it was unknown what type of carcinoma. She was reported to be a heavy smoker
for the majority of his life. Based on her exposure to the carcinogens in cigarettes; which are
known to increase risk of cancer, it can be suggested that she was diagnosed with carcinoma of
the lungs. Betty was not a blood relative, but rather one by marriage thus any predispositions of
her condition coming from family history are unknown. Although not much is known about her
C a r c i n o m a | 35
diet and life style is known however her husband Frank Swit; my paternal great uncle was also a
heavy smoker, and it can be concluded that both we subjected to the inhalation of second hand
smoke. Based on Age on onset and Death it can be inferred that she did not received treatment
for her condition as she only lived a year following her diagnosis. Based on this information it
can be inferred that her carcinoma was aggressive and non responsive to treatment if it treatment
had occurred. She died at the age of 79 as a result of her condition.
George Swint was my paternal great uncle. He was diagnosed with prostate cancer at the
age of 78. Gorge may have acquired a predisposition for his carcinoma based on family history,
as his father was diagnosed with Aplastic Anemia. George was also a reported smoker for many
years as a result his exposure to known carcinogens in cigarettes could have in been a
contributing factor to his diagnosis. It is unknown but possible that his diet and lifestyle also put
him at risk of developing carcinoma. It is unknown if George received any treatment for his
condition. However based on research it is know that prostate carcinoma often goes undetected
until it reaches advanced stages. This may have been the case in George’s diagnosis. Also some
doctors suggest the “waiting” as a course of treatment. This could have been the course of
treatment that he took as suggested by his doctor based on George’s age. Based on the his age of
diagnosis, and death it can be concluded, that his carcinoma was very aggressive and unaffected
by treatment or treatment did not occur. As a result of his diagnosis of praste carcinoma George
died at the age of 79.
Daniel O’Mara was my paternal uncle, and was diagnosed with melanoma at the age of
21. Daniel may have been at a high risk for developing carcinoma as a result predispositions in
the area of family history and genetic. His mother; my paternal grandmother was diagnosed with
carcinoma of the skin, and Myelodysplastic Syndrome, and his grandfather; my paternal great
C a r c i n o m a | 36
grandfather was diagnosed Aplastic Anemia. It is unknown if he was expose to any chemical or
environmental carcinogens that would have further increased his risk of developing carcinoma. It
is know that Daniel had a mole removed from his upper back; as a result he was then diagnosed
with melanoma. Daniel did receive treatment for his diagnosis although it is unknown which
type of treatment was used following surgery. It can be concluded that the cancer metastasized
quickly and was very aggressive, and unsusceptible to treatment based on the age of diagnosis,
and death. At the age of 21 Daniel died as a result of his diagnosis of melanoma at the age of 20.
Conclusion
Carcinoma is a wide spread cellular disorder that affects all cells, tissues and organ
systems in the body. My family particularly has been affect ad diagnosed with 6 forms of cancer.
Due to the fact that carcinoma has been link to genetics, family history has posed s a
predisposition to member’s desisted members of the family and will continue to pose as a risk to
present and future members of my family. Of the carcinomas that affect my family one is proved
to inherit; Aplastic anemia is caused by the growth and spread of an abnormal gene. This means I
am now a carrier ad my paternal great grandfather passed iton to my paternal grandmother who
passed it on to my paternal father, who thus passed it on to me. I will remain carrier, and only
develop the disease of my mother is also a carrier, in which case my broth and sister will also
develop the disease.
Being that I am already at a high risk of developing cancer based on family history, I
must be on high alert and cautious. Preventative measures must be taken throughout my life as to
avoid developing, cancer as best as possible. As for Aplastic Anemia because of genetics I am a
C a r c i n o m a | 37
carrier, and may possible be diagnosed later in life. However that are ways to lower my risk of
development for the reaming tapes of cancer that affect my family.
In regards to colorectal cancer I can control my diet and excursive. Consuming a low fat
high fiber diet I can reduce my risk of developing this type of cancer. This means eating more
leafy green vegetables and lean proteins, moderate my consumption of fatty proteins, and deep
fried foods. Annual screens of my colon, can also act as a preventative measure although
screenings will not eliminate my risk, it can catch the carcinoma early which can help in the
treatment and cure of the diagnosis.
Carcinoma has been linked to the exposure to tobacco and cigarette smoke. I can greatly
reduce my risk of developing carcinoma of the lungs by refraining from smoking cigarette as
well avoid being in the surrounding of those who due. Recent studies have shown that second
hand smoke and also increase risk for developing carcinoma. As seen in my family history all of
those persons who smoked developed varying types of cancer. As a result those remaining
members who did smoke have recently quit for health reasons including carcinoma.
Melanoma affected two members of my family in 2 generations. This type of cancer is
usually aggressive and metastasizes quickly. To prevent myself from developing melanoma I
have taken many precautions. I first and foremost use sun screen when introduce to prolonged
exposure to the sun. Next I have had mole check and even had one removed as a precautionary
measure. I also refrain from fake tanning to reduce me risk of developing melanoma, and other
carcinomas of the skin.
I am not risk of developing prostate carcinoma as it only occurring in men. However I
still take general preventive measure to reduce my risk of developing carcinoma. Annual
C a r c i n o m a | 38
screening of high risk organs and tissue can help me protect myself by early detection so in the
even that I do develop carcinoma I have the best chance of survival based on early detection and
treatment. Based on the average age on onset throughout the 4 generation, the chance of
developing cancer doesn’t arise until late 60’s early 70’s however it can occur at anytime if
exposed to an abundance of carcinogens, thus I will take preventative measure throughout my
life to lower my risk of developing carcinoma.
C a r c i n o m a | 39
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