Colorectal Cancer Pathophysiology: Oncogenes, Apoptosis, and Treatment
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This report delves into the pathophysiology of colorectal cancer, exploring the roles of oncogenes, apoptosis, cell cycles, and tumor suppressor genes in cancer development. It examines the characteristics of moderately differentiated adenocarcinoma grade three and its implications. The report f...

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Running Head: PATHOPHYSIOLOGY OF COLORECTAL CANCER
Pathophysiology of colorectal cancer
Student’s name:
3/13/2018
Running Head: PATHOPHYSIOLOGY OF COLORECTAL CANCER
Pathophysiology of colorectal cancer
Student’s name:
3/13/2018
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PATHOPHYSIOLOGY OF COLORECTAL CANCER
Table of contents
Contents
Table of contents............................................................................................................. 1
Succinctly discuss the pathophysiology of cancer.....................................................................2
Tumors in general............................................................................................................ 2
Role of oncogenes, apoptosis, ell cycle and tumor suppressor gene............................................2
The pathophysiology of colorectal cancer in relation to the results”...............................................3
Moderately differentiated Adenocarcinoma grade three”............................................................3
Discus one chemotherapeutic agents available for Betty.............................................................4
Pharmacokinetics.......................................................................................................... 4
Side effects and contraindications..................................................................................... 4
Drug interactions.......................................................................................................... 5
Bibliography............................................................................................................... 6
PATHOPHYSIOLOGY OF COLORECTAL CANCER
Table of contents
Contents
Table of contents............................................................................................................. 1
Succinctly discuss the pathophysiology of cancer.....................................................................2
Tumors in general............................................................................................................ 2
Role of oncogenes, apoptosis, ell cycle and tumor suppressor gene............................................2
The pathophysiology of colorectal cancer in relation to the results”...............................................3
Moderately differentiated Adenocarcinoma grade three”............................................................3
Discus one chemotherapeutic agents available for Betty.............................................................4
Pharmacokinetics.......................................................................................................... 4
Side effects and contraindications..................................................................................... 4
Drug interactions.......................................................................................................... 5
Bibliography............................................................................................................... 6

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PATHOPHYSIOLOGY OF COLORECTAL CANCER
Succinctly discuss the pathophysiology of cancer
Tumors in general
Pathophysiology refers to the changes that occur in an organ resulting into signs and
symptoms which alter daily activities of living. Cancer refers to the uncontrolled growth of cells
within an organ, which can result in metastasis or remain benign; which depends on the
aggressiveness of the cancer.
Role of oncogenes, apoptosis, ell cycle and tumor suppressor gene
Cancers are caused by oncogenes which are products of mutation and are expressed in
increased levels. Apoptosis is a mechanism which gets rid of altered cells during the cell cycle
and normal aged cells which have served their purposes, an alteration during this process which
likely results from oncogenes, then the cells destined for destruction survive the process, and
they are allowed to replicate and multiply causing disruption to the normal physiologic process
eventually causing cancer (Baar. M, 2017)
Another factor responsible for the development of cancer is the tumor suppressor gene;
a gene that protects the cell from cancer. It contributes to development of cancer if it fails or if it
is impaired; however if it is fully viable, then the cells are safe. Also an alteration in the cell
cycle, which is a process that results in cell division and duplication of DNA, can cause cancer in
PATHOPHYSIOLOGY OF COLORECTAL CANCER
Succinctly discuss the pathophysiology of cancer
Tumors in general
Pathophysiology refers to the changes that occur in an organ resulting into signs and
symptoms which alter daily activities of living. Cancer refers to the uncontrolled growth of cells
within an organ, which can result in metastasis or remain benign; which depends on the
aggressiveness of the cancer.
Role of oncogenes, apoptosis, ell cycle and tumor suppressor gene
Cancers are caused by oncogenes which are products of mutation and are expressed in
increased levels. Apoptosis is a mechanism which gets rid of altered cells during the cell cycle
and normal aged cells which have served their purposes, an alteration during this process which
likely results from oncogenes, then the cells destined for destruction survive the process, and
they are allowed to replicate and multiply causing disruption to the normal physiologic process
eventually causing cancer (Baar. M, 2017)
Another factor responsible for the development of cancer is the tumor suppressor gene;
a gene that protects the cell from cancer. It contributes to development of cancer if it fails or if it
is impaired; however if it is fully viable, then the cells are safe. Also an alteration in the cell
cycle, which is a process that results in cell division and duplication of DNA, can cause cancer in
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PATHOPHYSIOLOGY OF COLORECTAL CANCER
that the products of the cell cycle can be mutated and distorted leading to their accumulation or
the process of apoptosis can be altered (Wang X, 2015)
All of these four factors play a major role in the pathophysiology of cancer
The pathophysiology of colorectal cancer in relation to the results”
Moderately differentiated Adenocarcinoma grade three”
Moderately differentiated adenocarcinoma refers to colorectal cancer which results
from cells in the glands that line the colon and the rectum and metastasis slowly (Asare, 2016)
This type of cancer results from over growth of cells in the mucus producing glands lining the
colon, this overgrowth can be as a result of the following factors altered tumor suppressor gene,
overexpressed oncogenes, a faulted apoptosis process or alterations in the cell cycle, which
results in the production of altered cellular DNA leading to the accumulation of defaulted cells
(White, 2015).
One of these factors is enough to cause the uncontrolled cell proliferation, if other
factors predisposing to cancer are present or the four factors can work together augmenting each
other, despite the involvement of other predisposing factors such as lifestyle, and environmental
factors (Cerada, 2017)
The uncontrolled growth of cells in the glands that line the mucosa of the colon result
in the formation of a tumor in the colon, the growth results in the impaired movement of food
within the colon resulting into, impaired bowel movements, constipation, nausea, blood stained-
stool weight loss and back pains associated with the extensive growth of the tumor. A grade 3
moderately differentiated adenocarcinoma implies that the tumor is a high grade cancer, which is
PATHOPHYSIOLOGY OF COLORECTAL CANCER
that the products of the cell cycle can be mutated and distorted leading to their accumulation or
the process of apoptosis can be altered (Wang X, 2015)
All of these four factors play a major role in the pathophysiology of cancer
The pathophysiology of colorectal cancer in relation to the results”
Moderately differentiated Adenocarcinoma grade three”
Moderately differentiated adenocarcinoma refers to colorectal cancer which results
from cells in the glands that line the colon and the rectum and metastasis slowly (Asare, 2016)
This type of cancer results from over growth of cells in the mucus producing glands lining the
colon, this overgrowth can be as a result of the following factors altered tumor suppressor gene,
overexpressed oncogenes, a faulted apoptosis process or alterations in the cell cycle, which
results in the production of altered cellular DNA leading to the accumulation of defaulted cells
(White, 2015).
One of these factors is enough to cause the uncontrolled cell proliferation, if other
factors predisposing to cancer are present or the four factors can work together augmenting each
other, despite the involvement of other predisposing factors such as lifestyle, and environmental
factors (Cerada, 2017)
The uncontrolled growth of cells in the glands that line the mucosa of the colon result
in the formation of a tumor in the colon, the growth results in the impaired movement of food
within the colon resulting into, impaired bowel movements, constipation, nausea, blood stained-
stool weight loss and back pains associated with the extensive growth of the tumor. A grade 3
moderately differentiated adenocarcinoma implies that the tumor is a high grade cancer, which is
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PATHOPHYSIOLOGY OF COLORECTAL CANCER
growing and spreading very fast. Signs and symptoms will worsen as the cancer grows and
response to treatment is not very good; however in some cases the treatment may work (Cerada,
2017)
Discus one chemotherapeutic agents available for Betty
Betty’s diagnosis shows that her cancer is a high grade cancer, which implies that it
will spread and grow more quickly than anticipated; the diagnosis also shows that the probability
to respond to treatment compared to that of not responding to treatment is 1:1.
One of the chemotherapeutic agents used for the treatment of colorectal cancer is
Capecitabine, it is sold under the trade name Xeloda. Capecitabine is taken orally after/ within 30
minutes of taking a meal. The drug belongs to the class of fluoropyrimidines and once ingested
and it is in the system it is converted to 5-fluorouracil which is its active form. 5-Fu inhibits
synthesis of DNA through inhibition of the synthesis of thymidine monophosphate from a
thymidilate synthase inhibitor, which is the active from of the drug, 5-Fu (Z, 2014)
Pharmacokinetics
Capecitabine is metabolized by dihydropyrimidine dehydrogenase enzyme
Side effects and contraindications
This drug has the following side effects, elevated liver enzymes, fatigue, rash and
itching, low blood cell count abdominal pain and hand and foot syndrome. This drug is
contraindicated in pregnancy, hepatic impairment, and hypersensitivity to fluorouracil, DPD
deficiency, severe leukopenia, thrombocytopenia and neutropenia, hair loss, edema, dermatitis,
PATHOPHYSIOLOGY OF COLORECTAL CANCER
growing and spreading very fast. Signs and symptoms will worsen as the cancer grows and
response to treatment is not very good; however in some cases the treatment may work (Cerada,
2017)
Discus one chemotherapeutic agents available for Betty
Betty’s diagnosis shows that her cancer is a high grade cancer, which implies that it
will spread and grow more quickly than anticipated; the diagnosis also shows that the probability
to respond to treatment compared to that of not responding to treatment is 1:1.
One of the chemotherapeutic agents used for the treatment of colorectal cancer is
Capecitabine, it is sold under the trade name Xeloda. Capecitabine is taken orally after/ within 30
minutes of taking a meal. The drug belongs to the class of fluoropyrimidines and once ingested
and it is in the system it is converted to 5-fluorouracil which is its active form. 5-Fu inhibits
synthesis of DNA through inhibition of the synthesis of thymidine monophosphate from a
thymidilate synthase inhibitor, which is the active from of the drug, 5-Fu (Z, 2014)
Pharmacokinetics
Capecitabine is metabolized by dihydropyrimidine dehydrogenase enzyme
Side effects and contraindications
This drug has the following side effects, elevated liver enzymes, fatigue, rash and
itching, low blood cell count abdominal pain and hand and foot syndrome. This drug is
contraindicated in pregnancy, hepatic impairment, and hypersensitivity to fluorouracil, DPD
deficiency, severe leukopenia, thrombocytopenia and neutropenia, hair loss, edema, dermatitis,

5
PATHOPHYSIOLOGY OF COLORECTAL CANCER
stomatitis, myelosupression and indigestion. Patients receiving treatment with sorivudine or its
analogues are contraindicated from taking capecitabine (Twelves, 2009)
Drug interactions
Capecitabine has drug interactions with the following medications Phenytoin; it
increases its plasma concentration, calcium folinate enhances its therapeutic effects and worsens
diarrhea, warfarin and other coumarin-derived anticoagulants, and drugs with CYP2C9
substrates (Twelves, 2009)
PATHOPHYSIOLOGY OF COLORECTAL CANCER
stomatitis, myelosupression and indigestion. Patients receiving treatment with sorivudine or its
analogues are contraindicated from taking capecitabine (Twelves, 2009)
Drug interactions
Capecitabine has drug interactions with the following medications Phenytoin; it
increases its plasma concentration, calcium folinate enhances its therapeutic effects and worsens
diarrhea, warfarin and other coumarin-derived anticoagulants, and drugs with CYP2C9
substrates (Twelves, 2009)
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PATHOPHYSIOLOGY OF COLORECTAL CANCER
Bibliography
Asare, E. A. (2016). The imapact of stage,grade and mucinous histology on the
efficacy of systemic chemotherapy in adenocarcinomas of the appendix.
Baar. M, P. (2017). targeted apoptosis of senescent cells restore tissue homeostasis
in response to chemotoxicity and aging.
Cerada, I. m. (2017, january 19). A general overview and future perspective of
colorectal cancer. (W. C.-s. cho, Ed.) internal journal.
Twelves, B. a. (2009). capecitabine in colorectal cancer. future medicine(1475-
0708).
Wang X. (2015). protection against tumor growth beyond effect on cell cycle and
apoptosis.
White. (2015). role of autophagy in cancer. journal of clinical investigation.
Z, d. A.-D. (2014, january). pharmacokinetics and exposure-effect relationship of
capecitabine in elederly patients with breast and colorectal cancer. caner
chemotherapy and phamacology, 73(6), 1285-1293.
PATHOPHYSIOLOGY OF COLORECTAL CANCER
Bibliography
Asare, E. A. (2016). The imapact of stage,grade and mucinous histology on the
efficacy of systemic chemotherapy in adenocarcinomas of the appendix.
Baar. M, P. (2017). targeted apoptosis of senescent cells restore tissue homeostasis
in response to chemotoxicity and aging.
Cerada, I. m. (2017, january 19). A general overview and future perspective of
colorectal cancer. (W. C.-s. cho, Ed.) internal journal.
Twelves, B. a. (2009). capecitabine in colorectal cancer. future medicine(1475-
0708).
Wang X. (2015). protection against tumor growth beyond effect on cell cycle and
apoptosis.
White. (2015). role of autophagy in cancer. journal of clinical investigation.
Z, d. A.-D. (2014, january). pharmacokinetics and exposure-effect relationship of
capecitabine in elederly patients with breast and colorectal cancer. caner
chemotherapy and phamacology, 73(6), 1285-1293.
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