Pathophysiology de kansè nan kolon refere a sous mekanis ak pwosesis ki mennen nan devlopman ak pwogresyon de kansè nan kolon.
Kansè kolon, ke yo rele tou kansè kolorektal, se yon kalite kansè ki kòmanse nan kolon oswa rektòm, ki se pati nan gwo trip la.
Li kòmanse tankou yon kwasans ki rele yon polip, ki ka devlope nan kansè sou tan.
Patofizyoloji kansè kolon an enplike plizyè faktè, tankou mitasyon jenetik, enflamasyon, ak faktè anviwònman.
Mutasyon jenetik ka rive nan ADN nan selil kolon yo, ki mennen nan kwasans ak divizyon selil san kontwòl.
Mitasyon sa yo ka eritye oswa yo ka akeri, e yo ka afekte plizyè jèn ki patisipe nan kwasans, divizyon ak reparasyon selil yo.
Enflamasyon nan kolon an, ki ka koze pa kondisyon tankou maladi enflamatwa nan kolon, kapab ogmante risk kansè kolon an tou.
Enflamasyon kwonik ka mennen nan liberasyon pwodui chimik ki ankouraje kwasans selil ak divizyon, ki kapab mennen nan devlopman kansè.
Faktè anviwònman, tankou rejim alimantè, fason pou viv, ak ekspoze a sèten pwodui chimik, kapab kontribye tou nan devlopman kansè kolon.
Yon rejim ki gen anpil vyann wouj ak vyann trete, pa egzanp, te lye ak yon risk ogmante kansè kolon.
Gen lòt bagay ki ka fè moun nan vin gen plis pwoblèm tou, tankou lè l twò gwo, lè l fimen ak lè l pa fè anpil egzèsis.
Yon fwa kansè kolon devlope, li ka pwogrese nan plizyè etap, soti nan kansè bonè ki limite nan kolon pou plis etap avanse kote kansè a gaye nan lòt pati nan kò a.
Selil kansè yo ka anvayi tisi ak ògàn ki toupre yo, epi yo ka gaye tou nan sistèm lenfatik la oswa nan san an nan sit ki lwen, tankou fwa a oswa poumon yo.
Tretman pou kansè kolon tipikman enplike yon konbinezon operasyon, chimyoterapi, ak radyasyon terapi, selon etap ak kote kansè a.
Deteksyon bonè ak tretman yo se kle pou amelyore rezilta yo, paske kansè kolon souvan ka geri lè yo detekte li nan premye etap li yo.
Si nou fè tès regilye, tankou kolonoskopi, sa ka ede nou detekte kansè nan kolon nan premye etap li, lè li pi fasil pou trete.
Vidal-Vanaclocha F: The liver prometastatic reaction of cancer patients: implications for microenvironment-dependent colon cancer gene regulation. Cancer Microenviron. 2011, 4 (2): 163-80.
Yagi T, Kubota E, Koyama H, Tanaka T, Kataoka H, Imaeda K, Joh T: Glucagon promotes colon cancer cell growth via regulating AMPK and MAPK pathways. Oncotarget. 2018, 9 (12): 10650-10664.
Sharma SH, Thulasingam S, Nagarajan S: Terpenoids as anti-colon cancer agents - A comprehensive review on its mechanistic perspectives. Eur J Pharmacol. 2017, 795 (): 169-178.
Keshk WA, Zineldeen DH, Wasfy RE, El-Khadrawy OH: Fatty acid synthase/oxidized low-density lipoprotein as metabolic oncogenes linking obesity to colon cancer via NF-kappa B in Egyptians. Med Oncol. 2014, 31 (10): 192.
Dongfeng D, An C, Shujia P, Jikai Y, Tao Y, Rui D, Kai T, Yafeng C, Jianguo L, Xilin D: Explanation of colon cancer pathophysiology through analyzing the disrupted homeostasis of bile acids. Afr Health Sci. 2014, 14 (4): 925-8.
Tammali R, Ramana KV, Srivastava SK: Aldose reductase regulates TNF-alpha-induced PGE2 production in human colon cancer cells. Cancer Lett. 2007, 252 (2): 299-306.
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What is pathophysiology of colon cancer?
The pathophysiology of colon cancer refers to the underlying mechanisms and processes that lead to the development and progression of colon cancer.
Colon cancer, also known as colorectal cancer, is a type of cancer that begins in the colon or rectum, which are parts of the large intestine.
It typically starts as a growth called a polyp, which can develop into cancer over time.
The pathophysiology of colon cancer involves several factors, including genetic mutations, inflammation, and environmental factors.
Genetic mutations can occur in the DNA of colon cells, leading to uncontrolled cell growth and division.
These mutations can be inherited or acquired, and they can affect various genes involved in cell growth, division, and repair.
Inflammation in the colon, which can be caused by conditions such as inflammatory bowel disease, can also increase the risk of colon cancer.
Chronic inflammation can lead to the release of chemicals that promote cell growth and division, potentially leading to the development of cancer.
Environmental factors, such as diet, lifestyle, and exposure to certain chemicals, can also contribute to the development of colon cancer.
A diet high in red and processed meats, for example, has been linked to an increased risk of colon cancer.
Other factors, such as obesity, smoking, and lack of physical activity, can also increase the risk.
Once colon cancer develops, it can progress through several stages, from early-stage cancer that is confined to the colon to more advanced stages where the cancer has spread to other parts of the body.
The cancer cells can invade nearby tissues and organs, and may also spread through the lymphatic system or bloodstream to distant sites, such as the liver or lungs.
Treatment for colon cancer typically involves a combination of surgery, chemotherapy, and radiation therapy, depending on the stage and location of the cancer.
Early detection and treatment are key to improving outcomes, as colon cancer is often curable when caught in its early stages.
Regular screening, such as colonoscopy, can help detect colon cancer at its earliest stages, when it is most treatable.
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