Koloneko minbiziaren patofisiologiak koloneko minbiziaren garapena eta progresioa dakarten oinarrizko mekanismoak eta prozesuak aipatzen ditu.
Koloneko minbizia, koloneko minbizia bezala ere ezaguna, koloneko edo ondestean hasten den minbizia mota bat da, heste lodiaren zatiak direnak.
Normalean, polipo bat bezala hasten da, eta denborarekin minbizi bihur daiteke.
Koloneko minbiziaren patofisiologiak hainbat faktore ditu, besteak beste, mutazio genetikoak, hantura eta ingurumen-faktoreak.
Mutazio genetikoak gerta daitezke koloneko zelulen DNAn, zelulen hazkunde eta zatiketa kontrolatu gabeak eragiten dituztenak.
Mutazio hauek heredatu edo eskuratu daitezke, eta zelulen hazkundean, zatiketan eta konponketan parte hartzen duten hainbat gene eragin ditzakete.
Koloneko hantura, hesteetako hantura bezalako gaixotasunek eragin dezaketena, koloneko minbizia izateko arriskua ere handitu dezake.
Hantura kronikoak zelulen hazkundea eta zatiketa sustatzen dituzten substantzia kimikoak askatzen ditu, eta horrek minbiziaren garapena eragin dezake.
Ingurumen-faktoreek ere eragin dezakete koloneko minbizia, hala nola elikadurak, bizimoduak eta zenbait gai kimikoren eraginpean egotea.
Haragi gorri eta prozesatu asko jateak, adibidez, koloneko minbizia izateko arriskua handitzen du.
Beste faktore batzuek ere handitu dezakete arriskua, hala nola obesitateak, erretzeak eta jarduera fisiko faltak.
Behin koloneko minbizia garatzen denean, hainbat fasetan aurrera egin dezake, koloneko minbiziaren hasierako fasetik gorputzaren beste zati batzuetara zabaldu den fase aurreratuetaraino.
Minbizi-zelulek inguruko ehunak eta organoak inbaditu ditzakete, eta sistema linfatikoaren edo odol-fluxuaren bidez urruneko lekuetara, hala nola gibelera edo biriketara, hedatu daitezke.
Koloneko minbiziaren tratamenduan, normalean, kirurgia, kimioterapia eta erradiazio-terapia konbinatzen dira, minbiziaren fasearen eta kokapenaren arabera.
Detekzio goiztiarra eta tratamendua funtsezkoak dira emaitzak hobetzeko, koloneko minbizia askotan sendagarria baita bere hasierako fasean harrapatzen denean.
Kolonoskopia bezalako azterketa erregularrek koloneko minbizia bere lehen fasean detektatzen lagun dezakete, tratatu daitekeen unean.
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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