What is pathophysiology of Colon cancer?

['Lalela lelikhasi']

Iyini i-pathophysiology yemdlavuza wemaphaphu?

I-Pathophysiology ye-colon cancer isho tindlela letisisekelo kanye netinchubo letiholela ekutfutfukeni nasekugucukeni kwe-colon cancer.

Umdlavuza wemaphaphu, lophindze watiwe ngekutsi ngumdlavuza wemlomo, luhlobo lwemdlavuza lolucalisa emgceni lomkhulu nobe umgogodla, lokutincenye temathumbu lamakhulu.

Kuvame kucala njengentfo lenkhulu lebitwa ngekutsi yi-polyp, lengase igucuke ibe ngumdlavuza ngekuhamba kwesikhatsi.

I-Pathophysiology ye-colon cancer ifaka tintfo letinyenti, kufaka ekhatsi kugucuka kwemizila yemvelo, kuvuvuka, kanye netintfo letiphatselene nemvelo.

Kugucuka kwemizila yemvelo kungenteka ku-DNA yemaseli emathumbu, lokuholela ekukhuleni kwemaseli lokungakacondzi kanye nekwehlukana.

Letingucuko tingaba yintfo loyitfola njengelifa nobe utitfole ngekuhamba kwesikhatsi, futsi tingatsintsa takhi temtimba letihlobene nekukhula kwetinhlayiya, kutihlukanisa kanye nekutakha kabusha.

Kuvuvuka kwemathumbu, lokungentiwa tifo letifana nesifo semathumbu, nako kungakhulisa ingoti yemdlavuza wemathumbu.

Kuvuvuka lokungapheli kungabangela kutsi kukhiciteke emakhemikhali lakhutsata kukhula nekwehlukana kwetinhlayiya, lokungabangela kutsi ube nemdlavuza.

Tintfo letiphatselene nemvelo, njengekudla, indlela yekuphila, kanye nekutsintfwa ngemakhemikhali, nako kungabangela kutsi ube nemdlavuza wemaphaphu.

Kudla lokunenyama lebovu kanye nenyama leyakhiwe, sibonelo, kuhlanganiswe nekukhula kwebungoti bekhensa yematfumbu.

Letinye tintfo letifaka ekhatsi kukhuluphala kakhulu, kubhema kanye nekungawuvivinyi umtimba nako kungenta kutsi ube sengotini yekungenwa ngulesifo.

Uma umdlavuza wemaphaphu sewukhule, ungachubeka ngetindlela letehlukene, kusukela esigabeni sekucala lapho khona umdlavuza usuke usemaphaphu kuphela kuya esigabeni lesisetulu lapho khona umdlavuza sewusabalele nakuletinye tincenye temtimba.

Tinhlayiya temdlavuza tingahlasela titfo temtimba letisedvute, futsi tingasakateka ngekuhamba kwengati tiye etindzaweni letikhashane, njengesibindzi noma emaphaphu.

Kwelashwa kwemdlavuza wemaphaphu kufaka ekhatsi kuhlindvwa, ikhemotherapy, kanye nekwelashwa ngemisebe, kushiyane ngesigaba kanye nendzawo yalomdlavuza.

Kutfola nekwelapha umdlavuza wesinye kusenesikhatsi kubalulekile kute utfole imiphumela lemihle, njengobe umdlavuza wesinye uvame kwelasheka uma utfolwe usesigabeni sekucala.

Kuhlolwa njalo, njengekuhlolwa kwesinye sigodzi semtimba, kungasita kutsi utfole kutsi unesifo semdlavuza wesinye sikhatsi sisengakacali, futsi singelapheka.

['Tintfo letibhalwe phansi']

PubMed/Medline https://www.nlm.nih.gov/databases/download/pubmed_medline.html

RefinedWeb https://arxiv.org/abs/2306.01116

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.

Chen JK, Yaffe MB: Atlas Drugged. Cell. 2019, 177 (4): 803-805.

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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