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Colon1 is a part of digestive system and the rectum is located at the end of the digestive system. Together the colon and the rectum form a long tube often referred to as the large bowel but can also are known as the large intestine.
Cancer is defined as the normal cells in human body grows and divide into an arranged fashion. At last they will die and replaced by new cells. But in case of cancer, the cells don't grow in an arranged fashion and they won't die in an arranged fashion. Cancer cells have such ability to continue living for an indefinite period. Even when damaged also in a way that should cause cell death and cancer cells may not die.
Colon cancer - History and current statistics:
Colon cancer is also called as colon cancer or rectal cancer or colorectal cancer.
Colon cancer is a cancer that occurs in the cells of the colon. Colon cancer is quite common, being the third most common cancer in men and women in the U.S. About 110,000 people in the U.S. are diagnosed with colon cancer each year. This may equal to approximately 100 people every day and it is considered to be a major health problem.
Colon cancer that growths form the colon, bowel, anus and rectum. Colon cancer and rectum cancer are also sometimes known as colorectal cancer. They are known to attack other organs and tissue as well as spread to other parts of the body and form new cancerous cells.
Colon cancer symptoms were classified into two types:
Local colon cancer
Systemic colon cancer
Symptoms for Local Colon Cancer:
The symptoms for Local colon cancer are mainly effecting on regular basis daily habits and the colon as well. And some of the common local symptoms for colon cancer include:
Changes in bowel movements to either more frequent or less frequent than the normal.
ConstipationÂ - difficulty with bowel movements and diarrhoea
Bright red or dark red blood in stoolsÂ or black, dark coloured - called as "tarry" stools.
"pencil stools" - Stools that are thinner than normalÂ or feeling that you cannot empty your bowels completely.
Systemic Colon Cancer Symptoms
The symptoms for Systemic colon cancer include the following:
Unintentional weight loss.
Loss of appetite.
Nausea or vomiting.
Causes for colon cancer:
Colon cancer may have 8 major causes:
On average at age 50 one in four people has polyps
Alcohol may increases the colorectal cancer risk
Insulin dependence may leads to colon cancer development
Food containing high fat and cholesterol may cause colon cancer
Environment may play a big role and may cause colon cancer
Ethnicity, race, social status, family medical history, lack of exercise, Obesity, Personal medication history, polyps, smoking and gender
IBW(inflammatory bowel disease)
Ulcerative colitis and chrons disease may increase the risk of colon cancer.
According to recent studies regarding colon cancer saying that 25% of colon cancer cases are because of genetic mutations. The most common genetic causes for colon cancer include the mutations leading toÂ FAP (familial adenomatous polyposis) andÂ HNPCCÂ (hereditary non-polyposis colorectal cancer).
Colon Cancer - Genetics:
The most common reason for the colon cancer are the mutations occurring in genesof colon such mutations may leading to
FAP - familial adenomatous polyposis.
HNPCCÂ - hereditary non - polyposis colorectal cancer.
FAP - familial adenomatous polyposis:
Patho physilology for familial adenomatous polyposis:
The genetic defect in FAP is a germline mutation in the adenomatous polyposis coli (APC) gene. Syndromes once thought to be distinct from FAP are now recognized to be, in reality, part of the phenotypic spectrum of FAP.
Diag1.3 Germline mutation
Syndromes with a germline mutation in theÂ APCÂ gene include FAP,Â Gardner syndrome, some families with Turcot syndrome, and attenuated adenomatous polyposis coli (AAPC).Â Gardner syndromeÂ is characterized by colonic polyposis typical of FAP, along with osteomas (bony growth most commonly on the skull and the mandible), dental abnormalities, and soft tissue tumors
TheÂ APCÂ gene is a tumor suppressor gene that is located on band 5q21. Its function is not completely understood but has been shown to play a part in metaphase chromosome alignment.3Â Normal APC protein promotes apoptosis in colonic cells. Its most important function may be to sequester the growth stimulatory effects of b-catenin, a protein that transcriptionally activates growth-associated genes in conjunction with tissue-coding factors. Mutations of theÂ APCÂ gene result in a truncated/nonfunctional protein.
The resultant loss ofÂ APCÂ function prevents apoptosis and allows b-catenin to accumulate intracellularly and to stimulate cell growth with the consequent development of adenomas. As the clonal expansion of cells that lackAPCÂ function occurs, their rapid growth increases the possibility for other growth-advantageous genetic events to occur. This causes alterations in the expression of a variety of genes, thereby affecting the proliferation, differentiation, migration, and apoptosis of cells.
Ultimately, enough genetic events happen that allow the adenomatous polyps to become malignant in patients with FAP. This process is similar to that which occurs in sporadic adenomas. As a result,Â APCÂ is considered the gatekeeper of colonic neoplasia. Its mutation/inactivation is the initial step in the development ofÂ colorectal cancerin patients with FAP.
Stages in Colon cancer
HNPCCÂ - hereditary non - polyposis colorectal cancer:
Pathophysiology for HNPCCÂ :
HNPCCÂ may obtain due to faulty mismatch repair gene-that is, a defect in a gene that plays a role in repair of damaged DNA. Changes in genes that help to persist DNA constancy during replication are characteristic of patients with HNPCC Â Alterations and inactivation of the MMR system cause genomic instability as a result of inadequate repair of base pair mismatches resulting from polymerase-generated replication errors. Seven genes-hMLH1, hMSH2, hMSH3, hMSH6, hPMS1, hPMS2, and EXO1-[27,28]Â operate in the MMR DNA repair system. Mutations inÂ hMSH2Â andÂ hMLH1Â are the most common in HNPCC-related families. Genomic instability or, more specifically, microsatellite instability (MSI) occurs in most cancers and adenomas detected in patients with HNPCC (that fulfill the Amsterdam criteria). It is recognized by the frequent occurrence of insertions and deletion mutations in microsatellite repeats. MSI is identified using DNA extracted from fresh or paraffin-embedded, formalin-fixed tumor tissue and is recommended by some authors as the initial test to be performed on tumor tissue of affected members in families suspected of HNPCC (Fig. 2). In 1997, the National Cancer Institute Workshop on Hereditary Nonpolyposis Colorectal Cancer Syndrome suggested five markers for evaluation of MSI (Â Table 2Â ). Results are classified as MSI-high if two or more markers are positive. The American Gastroenterological AssociationÂ published a literature summary of MSI test results that found that the highest percentage of MSI-high test results were found in families that met the Amsterdam criteria I, followed by patients with colorectal cancer who were diagnosed before age 35 years. Identical results were found for MMR gene testing.