Colorectal cancer ( CRC ), also known as colon cancer and colon cancer , is the development of cancer of the colon or rectum (part of the colon). Cancer is the growth of abnormal cells that have the ability to attack or spread to other parts of the body. Signs and symptoms may include blood in the stool, changes in bowel movements, weight loss and feeling tired all the time.
Most colorectal cancers are caused by old age and lifestyle factors, with only a small number of cases due to underlying genetic disorders. Some risk factors include diet, obesity, smoking and lack of physical activity. Food factors that increase risk include red meat and processed meats and alcohol. Another risk factor is inflammatory bowel disease, which includes Crohn's disease and ulcerative colitis. Some of the congenital genetic disorders that can cause colorectal cancer include familial adenomatous polyposis and non hereditary colon cancer; However, this represents less than 5% of cases. It usually begins as a benign tumor, often in the form of polyps, which over time become cancerous.
Bowel cancer can be diagnosed by obtaining samples from the colon during sigmoidoscopy or colonoscopy. This is then followed by medical imaging to determine if the disease has spread. Effective screening to prevent and reduce deaths from colorectal cancer. Screening, with one of a number of methods, is recommended from age 50 to 75. During colonoscopy, small polyps can be removed if found. If a large polyp or tumor is found, a biopsy may be performed to check if it is cancer. Aspirin and other non-steroidal anti-inflammatory drugs reduce the risk. Their general use is not recommended for this purpose, however, due to side effects.
Treatments used for colorectal cancer may include some combination of surgery, radiation therapy, chemotherapy and targeted therapy. Cancers that are enclosed within the colon wall can be cured by surgery, while widespread cancer is usually incurable, with management directed at improving quality of life and symptoms. The five-year survival rate in the United States is about 65%. The likelihood of an individual to survive depends on how advanced the cancer is, whether all cancers can be removed surgically and the overall health of a person. Globally, colorectal cancer is the third most common type of cancer, accounting for about 10% of all cases. In 2012, there are 1.4 million new cases and 694,000 deaths from the disease. This is more common in developed countries, where more than 65% of cases are found. This is less common in women than in men.
Video Colorectal cancer
Signs and symptoms
The signs and symptoms of colorectal cancer depend on the location of the tumor in the intestine, and whether it has spread elsewhere in the body (metastasis). Classic warning signs include: worsening of constipation, blood in the stool, decreased stool broth (thickness), loss of appetite, weight loss, and nausea or vomiting in someone over 50 years. While rectal bleeding or anemia is a high-risk feature in those over the age of 50, other commonly described symptoms including weight loss and changes in bowel habits are usually only if associated with bleeding.
Maps Colorectal cancer
Cause
More than 75-95% of colorectal cancers occur in people with little or no genetic risk. Risk factors include older age, male gender, high fat intake, alcohol, red meat, processed meats, obesity, smoking, and lack of physical exercise. About 10% of cases are associated with insufficient activity. The risk of alcohol seems to increase by more than one glass per day. Drinking 5 glasses of water a day is associated with a reduced risk of colorectal cancer and adenomatous polyps. Streptococcus gallolyticus is associated with colorectal cancer. Some strains of Streptococcus bovis/Streptococcus equinus complex are consumed by millions of people every day and thus may be safe. 25 to 80% of people with Streptococcus bovis/gallolyticus bacteremia have simultaneous colorectal tumors. Seroprevalence Streptococcus bovis/gallolyticus is considered a practical marker candidate for early prediction of underlying bowel lesions in high-risk populations. It has been suggested that the presence of antibodies against Streptococcus bovis/gallolyticus antigen or its own antigen in the bloodstream may act as a marker for carcinogenesis in the colon.
Inflammatory bowel disease
People with inflammatory bowel disease (ulcerative colitis and Crohn's disease) are at an increased risk of colon cancer. The risk increases the longer a person develops the disease, and the worse the severity of the inflammation. In this high-risk group, both prevention with aspirin and colonoscopy is recommended. People with inflammatory bowel disease are responsible for less than 2% of colon cancer cases each year. In those with Crohn's disease, 2% suffer from colorectal cancer after 10 years, 8% after 20 years, and 18% after 30 years. In those with ulcerative colitis about 16% develop either cancer precursors or colon cancer for 30 years.
Genetics
Those with a family history in two or more first-tier families (such as a parent or sibling) have two to three times greater risk of illness and this group accounts for about 20% of all cases. A number of genetic syndromes are also associated with higher rates of colorectal cancer. The most common of these are colorectal cancer of hereditary nonpolyposis (HNPCC or Lynch syndrome) present in about 3% of people with colorectal cancer. Other syndromes strongly associated with colorectal cancer include Gardner's syndrome, and familial adenomatous polyposis (FAP). For people with this syndrome, cancer almost always occurs and forms 1% of cancer cases. Total proctocolectomy may be recommended for people with FAP as a precaution because of the high risk of malignancy. Colectomy, removal of the large intestine, may not be sufficient as a precautionary measure because of the high risk of rectal cancer if the rectum remains.
Most deaths from colon cancer are associated with metastatic disease. A gene that appears to contribute to the potential for metastatic disease, metastasis associated with colon cancer 1 ( MACC1 ), has been isolated. This is a transcription factor that affects the expression of hepatocyte growth factors. This gene is associated with proliferation, invasion and spread of colon cancer cells in cell culture, and tumor and metastasis growth in mice. MACC1 may be a potential target for cancer intervention, but this possibility needs to be confirmed by clinical studies.
Epigenetic factors, such as abnormal DNA methylation of tumor suppressor promoters, play a role in the development of colorectal cancer.
Pathogenesis
Colorectal cancer is a disease that originates from epithelial cells lining the colon or rectum of the gastrointestinal tract, most often as a result of mutations in the Wnt signaling pathway that increases the signaling activity. Mutations can be inherited or acquired, and are most likely to occur in crypt stem cells. The most mutated gene in all colorectal cancers is the APC genes, which produce the APC protein. APC protein prevents the accumulation of protein katenin. Without APC, -cathenine accumulates to high levels and transplants (moves) into the nucleus, binds to DNA, and activates the transcription of proto-oncogenes. These genes are usually important for stem cell renewal and differentiation, but when expressed improperly at high levels, they can cause cancer. While APC mutates in most colon cancers, some cancers have increased? -cathenine due to mutation on? -cathenine (CTNNB1) that inhibits its own damage, or has mutations in other genes with functions similar to APC such as AXIN1, AXIN2, TCF7L2, or NKD1.
Beyond defects in Wnt signaling pathways, other mutations must occur in order for the cell to become cancerous. The p53 protein, produced by the TP53 gene, usually monitors cell division and kills cells if they have Wnt path defects. Finally, the cell line obtains a mutation in the TP53 gene and alters the tissue from a benign epithelial tumor to invasive epithelial cell cancer. Sometimes a gene encoding p53 does not mutate, but another protective protein named BAX mutates instead.
Another protein responsible for programmed cell death that is generally disabled in colorectal cancer is TGF-? and DCC (Removed in Colorectal Cancer). TGF-? has a mutation of deactivating at least half the colorectal cancer. Sometimes TGF-? not disabled, but the downstream protein named SMAD is disabled. DCC generally has a chromosomal segment removed in colorectal cancer.
About 70% of all human genes are expressed in colorectal cancer, with more than 1% having an increased expression in colorectal cancer compared to other forms of cancer. Some genes are oncogenes: they are overexpressed in colorectal cancer. For example, the protein-coding genes KRAS, RAF, and PI3K, which normally stimulate cells to divide in response to growth factors, may acquire mutations that result in excessive activation of cell proliferation. The chronological sequence of mutations is sometimes important. If a previous APC mutation occurs, primary KRAS mutations often develop into cancer, not hyperplastic lesions or limits. PTEN, a tumor suppressor, usually inhibits PI3K, but sometimes it can become mutated and deactivated.
A comprehensive genome-scale analysis has revealed that colorectal carcinoma can be categorized into hypermutated and non-hypermutated tumor types. In addition to the oncogenic mutations and inactivations described for the above genes, non-hypermutated samples also contain advanced CTNNB1, FAM123B, SOX9, ATM, and ARID1A. Advancing through a series of different genetic events, hypermutated tumors feature mutated forms of ACVR2A, TGFBR2, MSH3, MSH6, SLC9A9, TCF7L2, and BRAF. The common theme among these genes, in both types of tumors, is their involvement in WNT and TGF-? signal pathway, which results in an increase in MYC activity, a central performer in colorectal cancer.
Field disabled
The term "cancer field" was first used in 1953 to describe an area or "field" of pre-contracted epithelium (by a largely unknown process at the time) to influence the development of cancer. Since then, the terms "cancer field", "field of carcinogenesis", "field flaw", and "field effect" have been used to describe pre-malignant or pre-neoplastic tissue where new cancer is likely to appear.
An important field deformity in development becomes colon cancer.
However, in most cancer studies, as shown by Rubin "Most research in cancer research has been done on well-defined tumors in vivo, or in the discrete neoplastic focus in vitro < there is evidence that more than 80% of somatic mutations found in human phorotype human colorectal tumor mutators occur prior to the onset of clonal expansion of the terminal.Similarly, Vogelstein et al showed that more than half of the somatic mutations identified in the tumors occurred in the pre-neoplastic phase (in defects field), during normal cell growth.Similarly, epigenetic changes present in the tumor may occur in pre-neoplastic field defects.
The expanded view of the field effect has been called the "field etiological effect", which includes not only molecular and pathological changes in pre-neoplastic cells but also the influence of exogenous environmental factors and molecular changes in local micro-environments on neoplastic evolution from tumor initiation to death..
Epigenetics
Epigenetic changes are more common in colon cancer than genetic alterations (mutations). As described by Vogelstein et al., The average cancer of the colon has only 1 or 2 mutations of oncogenes and 1 to 5 tumor suppressor mutations (together called "driver mutations"), with some 60 further "passenger" mutations. Oncogenes and tumor suppressor genes are well studied and described above under Pathogenesis.
However, by comparison, epigenetic changes in colon cancer are common and affect hundreds of genes. For example, there is a small RNA type called microRNA that has a length of about 22 nucleotides. These microRNAs (or miRNAs) do not encode proteins, but they can target protein-encoding genes and reduce their expression. This myRNA expression can be changed epigenetically. As an example, an epigenetic change consisting of CpG island methylation of the miR-137 DNA encoding sequence reduces its expression. This is a frequent epigenetic event in colorectal carcinogenesis, occurring in 81% of colonic cancers and 14% of the normally-appearing colonic mucosa adjacent to the cancer. The adjacent tissue associated with this cancer is called a field defect. The miR-137 damper may affect the expression of about 500 genes, targeting this miRNA.
Changes in the expression level of miR-137 resulted in changes in mRNA expression of the target gene by 2 to 20-fold and, more often, although smaller, changes in protein product expression of the gene. Other microRNAs, with a possible number of comparable target genes, are even more often epigenetically altered in colonic field defects and in colonic cancers that arise therefrom. These include miR-124a, miR-34b/c and miR-342 silenced by CpG island methylation of their DNA encoding sequences in primary tumors at 99%, 93% and 86% levels, respectively, and in the surrounding normal mucosal at 59%, 26% and 56%, respectively.
In addition to the epigenetic changes of miRNA expression, other common types of epigenetic changes in cancer change the level of gene expression including direct hypermethylation or hypomethylation of the cpG island protein-encoding genes and changes in histones and chromosomal architecture that affect gene expression. For example, 147 hypermethylation and 27 hipometilasi of protein coding genes are often associated with colorectal cancer. Of the hypermethylated genes, 10 are hypermethylated in 100% of colon cancers, and many others are hypermethylated in more than 50% of colon cancers. In addition, 11 hypermethylation and 96 miRNA hipometilasi also associated with colorectal cancer.
Recent evidence suggests that early epigenetic reduction of DNA repair expression enzyme tends to lead to the characteristics of genomic and epigenomic instability of cancer.
As summarized in the article Carcinogenesis and Neoplasm, for sporadic cancer in general, deficiencies in DNA repair are sometimes caused by mutations in DNA repair genes, but much more often because of epigenetic changes that reduce or eliminate expression of DNA repair gene..
Diagnosis
The diagnosis of colorectal cancer is performed by sampling suspicious colon areas for possible tumor progression, usually during colonoscopy or sigmoidoscopy, depending on the location of the lesion. This is confirmed by microscopic examination of tissue samples.
The degree of the disease is usually determined by a CT scan of the chest, abdomen and pelvis. Other potential imaging tests such as PET and MRI can be used in certain cases.
Staging colon cancer is done next and is based on radiology and pathology. For all other forms of cancer, tumor staging is based on a TNM system that considers how many early tumors have spread, if and where there is lymph node metastasis and if there is a metastasis in the more distant organs, usually the liver.
Characteristics of microscopic cells from tumors are reported from tissue analysis taken from biopsy or surgery. The pathology report contains descriptions of microscopic characteristics of tumor tissue, including tumor cells and how tumors invade healthy tissue and eventually if the tumor is completely removed. The most common form of colon cancer is adenocarcinoma. Others, less common types include lymphoma, adenosquamous and squamous cell carcinoma. Some subtypes are found to be more aggressive.
Macroscopy
Cancer on the right side of the large intestine (ascending colon and cecum) tends to be eco- phytic, ie, the tumor grows out from one location on the intestinal wall. It rarely causes faecal obstruction, and presents with symptoms such as anemia. Left side tumors tend to be circular, and may block the intestinal lumen, such as napkin rings, and produce thinner caliber stools.
Microscope
Adenocarcinoma is a malignant epithelial tumor, derived from the epithelial cells of the superficial glands that line the colon and rectum. It attacks the wall, infiltrates the muscularis mucosal layer, submucosa, and then the muscularis propria. The tumor cells describe irregular tubular structures, save pluristratification, double lumen, reduce stroma ("back to back" aspect). Occasionally, tumor cells are discohesive and secrete mucus, which attacks the interstitium that produces large mucus inundations. It occurs in adenocarcinoma musinosum , in which cells are poorly differentiated. If the mucus is still inside the tumor cell, it pushes the nucleus in the periphery, this occurs in the "ring cell". Depending on the gland architecture, cellular pleomorphism, and mucosecretion of the dominant pattern, adenocarcinoma may show three differentiation degrees: good, moderate, and less differentiated.
Immunochemistry
In cases where metastasis of colorectal cancer is suspected, immunohistochemistry is used to confirm the correct diagnosis. More specific proteins are expressed in colorectal cancer and can be used as diagnostic markers of cytokeratin 20, CDX2, SATB2 and CDH17. Most (50%) colorectal adenomas and (80-90%) colorectal cancer tumors are considered to be more expressed to the cyclooxygenase-2 enzyme (COX-2). This enzyme is not generally found in healthy colonic tissue, but is thought to trigger abnormal cell growth.
Makroskopi
Mikrograf (H & amp; E stain)
Staging
Staging is usually made in accordance with the TNM staging system of WHO, UICC and AJCC organizations. The Astler-Coller classification (1954) and the Dukes classification (1932) are now under-utilized.
The most common metastatic sites for colorectal cancer are liver, lung and peritoneum.
Beginner Tumor
Leaf tumors in colorectal cancer are loosely determined by the presence of individual cells and small groups of tumor cells in front of invasive carcinomas. It has been postulated to represent the mesenteral epithelial transition (EMT). Beginning tumors are independent independent markers of potentially poor results in colorectal carcinoma which allows to divide people into more meaningful risk categories than those defined by TNM staging, and also potentially guide treatment decisions, especially in T1 and T3 N0 (Stage Colorectal Carcinoma II, Dukes' B). Unfortunately, universal acceptability as a factor that can be reported has been withheld by the lack of uniformity of definition with respect to the qualitative and quantitative aspects of budding tumors.
Prevention
It is estimated that about half of cases of colorectal cancer are due to lifestyle factors, and about a quarter of all cases can be prevented. Improving supervision, physical activity, eating high fiber foods, and reducing smoking and alcohol consumption reduce the risk.
Lifestyle
Current dietary recommendations to prevent colorectal cancer include increasing consumption of whole grains, fruits and vegetables, and reducing intake of red meat and processed meats. Higher physical activity is also recommended. Physical exercise is associated with a moderate decrease in the colon but not the risk of anal cancer. High levels of physical activity reduce the risk of colon cancer by about 21%. Sitting regularly for long periods is associated with a higher mortality of colon cancer. The risk is not negated by regular exercise, even if it is lowered. The risk of colon cancer can be reduced by maintaining a normal weight. The evidence for the protective effect provided by fiber and fruits and vegetables, however, is poor.
Drugs
Aspirin and celecoxib appear to decrease the risk of colorectal cancer in those at high risk. Aspirin is recommended in those aged 50 to 60 years, has no increased risk of bleeding, and is at risk of developing cardiovascular disease to prevent colorectal cancer. Not recommended for those at average risk. There is temporary evidence for calcium supplementation, but that is not enough to make recommendations. Vitamin D intake and blood levels are associated with lower risk of colon cancer.
Screening
Because more than 80% of colorectal cancers arise from adenomatous polyps, screening for these cancers is effective not only for early detection but also for prevention. Diagnosis of colorectal cancer cases through screening tends to occur 2-3 years before diagnosis of cases with symptoms. Any polyp that is detected can be removed, usually by colonoscopy or sigmoidoscopy, and thus prevent it from turning into cancer. Screening has the potential to reduce colorectal cancer death by 60%.
The three major screening tests are colonoscopy, faecal occult blood test, flexible sigmoidoscopy. Of the three, only sigmoidoscopy can not filter the right side of the colon where 42% of malignancies are found. However, flexible sigmoidoscopy has the best evidence to reduce the risk of death from any cause.
Other options may include virtual colonoscopy and stool DNA screening testing. Virtual colonoscopy via CT scan appears as good as standard colonoscopy to detect cancers and large but expensive adenomas, associated with radiation exposure, and can not eliminate abnormal growths detected like standard colonoscopy.
Fecal occult blood testing (FOBT) of the stool is usually recommended every two years and can be either guaiac-based or immunochemical. If abnormal FOBT results are found, participants are usually referred for advanced colonoscopy examinations. Every year for every two years filtration of FOBT reduces colorectal cancer mortality by 16% and among those who participate in colorectal cancer death screening can be reduced to 23%, although it has not been proven to reduce all-cause mortality. Immunochemical tests are accurate and require no diet or drug changes prior to testing. Stool DNA screening tests look for biomarkers associated with colorectal cancer and precancerous lesions, including altered DNA and blood hemoglobin. Positive results should be followed by colonoscopy. If used, screening is recommended every 3 years, starting at age 50.
Recommendations
In the United States, screening is usually recommended between the ages of 50 and 75. The American Cancer Society recommends starting at age 45. For those between the ages of 76 and 85, the decision to screen must be individual. Several screening methods may be used, including stool-based tests every 3 years, sigmoidoscopy every 5 years and colonoscopy every 10 years. For those at high risk, playback usually starts around 40. It is unclear which method is better. Colonoscopy may find more cancers in the first part of the colon, but is associated with greater costs and more complications. For people at an average risk who have a high-quality colonoscopy with normal results, the American Gastroenterological Association does not recommend this type of screening within 10 years after colonoscopy. For people over 75 years old or those who have a life expectancy of less than 10 years, screening is not recommended. It takes about 10 years after screening for one in 1,000 people to benefit.
In Canada, among those aged 50 to 75 years at normal risk, a fecal immunochemical or FOBT test is recommended every two years or sigmoidoscopy every 10 years. Colonoscopy is less favored.
Some countries have national colorectal screening programs that offer FOBT screening for all adults in certain age groups, usually starting between the ages of 50 and 60. Examples of countries with organized viewers include the UK, Australia and the Netherlands.
Treatment
Treatment of colorectal cancer can be aimed to cure or palliative. Decisions that aims to adopt depend on a variety of factors, including one's health and preferences, as well as the tumor stage. When colorectal cancer is caught early, surgery can be curative. However, when detected at a later stage (for which metastasis is present), this is less likely and treatment is often directed at palliation, to relieve symptoms caused by tumors and keep people as comfortable as possible.
Surgery
If the cancer is found at a very early stage, this cancer can be removed during colonoscopy. For people with local cancer, the preferred treatment is surgical removal complete with sufficient margin, with efforts to achieve healing. This can be done with an open laparotomy or sometimes with laparoscopy. The colon can then be reconnected or someone may have a colostomy.
If there are only a few metastases in the liver or lungs, they can also be excreted. Sometimes chemotherapy is used before surgery to shrink the cancer before trying to get rid of it. The two most common sites of recurrence of colorectal cancer are liver and lung.
Chemotherapy
In both colon and rectal cancers, chemotherapy may be used in addition to surgery in certain cases. The decision to add chemotherapy in the management of colon and rectal cancers depends on the stage of the disease.
In Stage I colon cancer, no chemotherapy is offered, and surgery is the definitive treatment. The role of chemotherapy in Stage II colon cancer is debatable, and is usually not offered unless risk factors such as T4 tumor or inadequate sampling of lymph nodes are identified. It is also known that people who carry gene repair abnormalities do not match not benefit from chemotherapy. For stage III and stage IV stomach cancer, chemotherapy is an integral part of treatment.
If the cancer has spread to lymph nodes or distant organs, which is the case with stage III and stage IV colon cancer respectively, adding a fluorouracil chemotherapy agent, capecitabine or oxaliplatin increases life expectancy. If the lymph nodes do not contain cancer, the benefits of chemotherapy are still controversial. If the cancer is widely metastatic or inoperable, treatment is palliative. Usually in this setting, a number of different chemotherapy drugs can be used. Chemotherapy drugs for this condition may include capecitabine, fluorouracil, irinotecan, oxaliplatin and UFT. The drug capecitabine and fluorouracil may be interchangeable, with capecitabine being an oral drug while fluorouracil is an intravenous drug. Some of the special regimens used for CRC are FOLFOX, FOLFOXIRI, and FOLFIRI. Antiangiogenic drugs such as bevacizumab are often added in first-line therapy. Other class drugs used in second-line settings are epidermal growth factor receptor inhibitors, in which two FDA-approved are cetuximab and panitumumab.
The main difference in the low-level rectal cancer approach is the incorporation of radiation therapy. Often, these are used in conjunction with chemotherapy in neoadjuvant mode to allow for surgical resection, so ultimately as a colostomy is not necessary. However, it may not be possible in a low tumor, in this case, a permanent colostomy may be necessary. Stage IV rectal cancer is treated similarly to stage IV bowel cancer.
Radiation therapy
While a combination of radiation and chemotherapy may be useful for rectal cancer, its use in colon cancer is not routine because of intestinal sensitivity to radiation. Just as for chemotherapy, radiotherapy can be used in neoadjuvant and adjuvant settings for some stage of rectal cancer.
Immunotherapy
Immunotherapy with immune-inhibitory inhibitors has been found useful for this type of colorectal cancer with deficiency of mismatch and microsatellite instability. Most people who improve, however, are still deteriorating after months or years. Other types of colorectal cancer in 2017 are still being studied.
Palliative care
Palliative care is a medical treatment that focuses on the treatment of symptoms from serious illnesses, such as cancer, and improves quality of life. Palliative care is recommended for anyone who has colon cancer or has significant symptoms.
The involvement of palliative care may be beneficial for improving the quality of life for both people and their families, by improving symptoms, anxiety and preventing hospital admission.
In people with colorectal cancer who can not be cured, palliative care may consist of a procedure that relieves the symptoms or complications of the cancer but does not attempt to cure the underlying cancer, thereby improving the quality of life. Choice of surgery may include non-curative removal surgery of some cancer tissue, passing part of the intestine, or stent placement. These procedures can be considered to improve symptoms and reduce complications such as bleeding from tumors, abdominal pain and bowel obstruction. Non-operative symptomatic treatment methods include radiation therapy to reduce tumor size and pain medication.
Followup
The purpose of follow-up is to diagnose, in the earliest possible stage, any metastasis or tumor that develops later, but not from the original cancer (metachronous lesions).
The US National Comprehensive Cancer Network and the American Society of Clinical Oncology provide guidelines for colon cancer follow-up. Medical history and physical examination are recommended every 3 to 6 months for 2 years, then every 6 months for 5 years. Measurement of Carcinoembryonic blood antigen levels follows the same time, but is only recommended for people with T2 or larger lesions who are candidates for intervention. CT scan of the chest, abdomen, and pelvis can be considered annually for the first 3 years for people at high risk of recurrence (eg, those who have tumors with poor differentiation or venous or lymphatic invasion) and are curative candidates of surgery (with a view to cure). A colonoscopy may be performed after 1 year, unless it can not be performed during the initial staging due to blocking masses, in this case should be done after 3 to 6 months. If the villous polyp, polyp & gt; 1 centimeter or high degree dysplasia is found, can be repeated after 3 years, then every 5 years. For other disorders, colonoscopy may be repeated after 1 year.
Routine PET or ultrasound scans, chest x-rays, full blood count or liver function tests are not recommended. A systematic review of 2016 concluded that tighter surveillance and more rigorous follow-up did not provide additional survival benefits for non-metastatic colorectal cancer.
Exercise
Exercise can be recommended in the future as a secondary therapy for cancer patients. In epidemiological studies, exercise can decrease the specific mortality of colorectal cancer and all-cause mortality. Results for a certain amount of exercise are required to observe conflicting benefits. These differences may reflect differences in tumor biology and biomarker expression. Patients with tumors without CTNNB1 (? -catenin) expression, involved in the Wnt signaling pathway, require more than 18 hours of Metabolic equivalent (MET) per week, a measure of exercise, to observe a reduction in colorectal cancer mortality. The mechanism by which survival benefits can be involved in immune surveillance and inflammatory pathways. In clinical studies, a pro-inflammatory response was found in patients with stage II-III colorectal cancer who underwent 2 weeks of moderate exercise after completing their primary therapy. The oxidative balance may be another possible mechanism for the observed benefit. A significant reduction in 8-oxo-dG was found in urine patients who underwent 2 weeks of moderate exercise after primary therapy. Another possible mechanism may involve the metabolic hormone and steroid-sex hormones, although this pathway may be involved in other types of cancer
Another possible biomarker potential is p27. Survivors with tumors showing p27 and performing larger and equal to 18 hrs of MET per week were found to have reduced survival of colorectal-cancer deaths compared with those who were less than 18 hrs MET per week. Survivors without p27 expression are shown to have a worse outcome. Constitutive activation of the PI3K/AKT/mTOR pathway may explain the loss of p27 and excessive energy balance can increase p27 to stop cancer cells dividing.
Prognosis
In Europe the five-year survival rate for colorectal cancer is less than 60%. In developed countries about one-third of people affected by this disease die.
Survival is directly related to the detection and type of cancer involved, but is overall bad for symptomatic cancer, as they are usually advanced enough. The survival rate for early-stage detection is about five-fold from end-stage cancer. People with tumors that have not penetrated the mucosal muscularis (TNM stage Tis, N0, M0) have a 100% survival rate of 100%, while those with invasive T1 cancer (in the submucosal layer) or T2 (in muscle) layer) have an average rate five year survival is about 90%. Those with more invasive tumors but without nodal involvement (T3-4, N0, M0) had a mean survival rate of five years at about 70%. Patients with positive regional lymph nodes (each T, N1-3, M0) had an average five-year survival rate of about 40%, whereas those with distant metastases (T, N, M1) had a mean survival of five years rate of about 5%.
According to American Cancer Society statistics in 2006, more than 20% of people with colorectal cancer came to medical attention when the disease was advanced (stage IV), and up to 25% of this group would have potentially operable insectable liver metastases. In this selective group, those who underwent curative resection experienced a five-year survival outcome in a third of cases.
Less than 600 genes are associated with outcomes in colorectal cancer. These include poor genes, where high expression is associated with poor results, eg heat shock of 70 kDa protein 1 (HSPA1A), and favorable genes where high expression is associated with better survival, eg putative RNA-binding 3 (RBM3).
Epidemiology
Globally more than 1 million people suffer from colorectal cancer each year which causes about 715,000 deaths in 2010 to rise from 490,000 in 1990.
In 2012, it is the second most common cause of cancer in women (9.2% of diagnoses) and the third most common in men (10.0%) with it being the fourth most common cause of cancer deaths after lung, stomach, and liver cancer. This is more common in developed countries than in developing countries. Global events vary 10-fold with the highest rates in Australia, New Zealand, Europe and the US and the lowest rates in Africa and South-Central Asia.
United States
Colorectal cancer is the second leading cause of cancer and death for men and women in the United States combined. An estimated 141,210 cases were diagnosed in 2011.
Based on levels from 2007 to 2009, 4.96% of US men and women born today will be diagnosed with colorectal cancer during their lifetime. From 2005 to 2009, the median age at diagnosis for cancer of the colon and rectum in the US was 69 years. About 0.1% were diagnosed under the age of 20; 1.1% between 20 and 34; 4.0% between 35 and 44; 13.4% between 45 and 54; 20.4% between 55 and 64; 24.0% between 65 and 74; 25.0% between 75 and 84; and 12.0% 85 years. Prices are higher among men (54 per 100,000 c.f. 40 per 100,000 for women).
United Kingdom
In the UK about 41,000 people per year suffer from colon cancer so it becomes the fourth most common type.
Australia
One in 19 men and one in 28 women in Australia will develop colorectal cancer before age 75; one in 10 men and one in 15 women will develop it at the age of 85 years.
History
Rectal cancer has been diagnosed in an ancient Egyptian mummy who had lived in Dakhleh Oasis during the Ptolemaic period.
The Biblical King Joram of Judah was recorded in 2 Chronicles 21 to be cursed with an incurable intestinal disease, which caused his death, because of his evil deeds. Modern scholarship shows that the condition is most likely to be colon cancer.
Society and culture
In the United States, March is a month of colorectal cancer awareness.
Research
Early in-vitro evidence suggests lactic acid bacteria (eg, lactobacilli, streptococci or lactococci) may protect against the development and development of colorectal cancer through several mechanisms such as antioxidant activity, immunomodulation, promoting programmed cell death, antiproliferative effects, and epigenetic modification of cancer cells.
Large-scale genomic sequencing studies have been conducted to identify mutations in the genomes of colorectal cancer patients.
Clostridium novyi-NT bacteria, also being studied.
- Model of colorectal and intestinal cancer rats
- Cancer Genome Atlases
- The Colorectal Cancer Atlas that integrates genomic and proteomic data related to colorectal cancer tissue and cell lines has been developed.
References
External links
- Colorectal cancer in Curlie (based on DMOZ)
Source of the article : Wikipedia
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