What is pathophysiology of Colon cancer?

['Welisi hɔɔlʋʋ kʋnɛ']

Ɛbɛ payaɣ se cancer du côlon?

Kʊdɔŋ ŋgʊ kɩ-tɛ maɣzɩm taa wɛ ndɩ ndɩ nɛ ŋgʊ kɩ-tɛ ɖoŋ yɔ.

Calɩm taa hosi lɩʊ yaa calɩm hosi kʊdɔŋ kɛna kʊdɔŋ ŋgʊ kɩlɩna hosi sɔsɔsɩ yaa hosi nzɩ sɩ-taa calɩm cakɩ yɔ sɩ-taa.

Pɩpaɣzɩɣnɩ polipiki nakʋyʋ nɛ kɩkɔɔ kɩpɩsɩ kansɛɛrɩ kʋdɔŋ.

Kʊdɔŋ ŋgʊ kɩ-tɛ maɣzɩm wɛ ndɩ ndɩ, nɛ kɩ-taa kɔyɔ kʊdɔŋ ŋgʊ kɩlɩna calɩm taa yɔ, kʊdɔŋ ŋgʊ kɩlɩna calɩm taa yɔ nɛ kʊdɔŋ ŋgʊ kɩlɩna tomnaɣ taa yɔ.

Pɩpɩzɩɣ piyele nɛ calɩm tootoye nɖɩ ɖɩwɛ tomnaɣ taa yɔ ɖɩlɛɣzɩ nɛ ɖɩpaɣzɩ labʋ tʋmɩyɛ nɛ ɖɩɖɛɛnɩ ɛzɩdaa.

Pɩpɩzɩɣ nɛ pɩkɛnɩ wɛtʋ ndʋ tɩlɩɣnɩ ɛyʋ cɔlɔ yaa tomnaɣ yɔɔ wɛtʋ ndʋ tɩpɩzɩɣ nɛ tɩlɛɣzɩ ɛyʋ tomnaɣ yɔ.

Pɩtasɩ lɛ, ye ŋwɛnɩ kʋdɔŋ nakʋyʋ yɔ, kɩpɩzɩɣ kɩkpa-ŋ ɖoŋ.

Ye kʋdɔŋ nakʋyʋ ɛkpa ɛyʋ nɛ kɩwɛɛ nɛ kɩkpaɣ ɖoŋ yɔ, pɩpɩzɩɣ piyele nɛ tomnaɣ taa tomnasɩ nzɩ sɩpaɣlɩɣ nɛ sɩtayɩɣ yɔ, sɩpaɣzɩ labʋ kʋdɔŋ ŋgʋ payaɣ se cancer yɔ.

Pɩtasɩ lɛ, wɛtʋ ndʋ tɩ-taa ɛyʋ wɛɛ yɔ, tɩpɩzɩɣ tiyele nɛ ɛpaɣzɩ wɛnʋʋ kʋdɔŋ ŋgʋ.

Kpaɣ ɛzɩ nandʊ kɩsɛmtʊ nɛ nandʊ ndʊ tɩ-taa wɛ pʊtʊnaa sakɩyɛ yɔ, tɩpɩzɩɣ tɩhaɣ ɛyʊ kʊdɔŋ ŋgʊ.

Lɩmaɣza lɛɛna ɛzɩ kɩnamɩyɛ, taba nɛ tabakʋʋyaɣ ñɔʋ nɛ tomnaɣ yɔɔ hola aleɣya labʋ kadadayaɣ yɔ, apɩzɩɣ ɖɔɖɔ ayele nɛ pɩkpaɖɩ.

Kpaɣna ɖooo canaʊ ŋgʊ kɩpaɣzɩɣ nɛ pɩkɔɔ pɩtalɩ ɖooo canaʊ ŋgʊ kɩɖɛʊ nɛ kɩtalɩ tomnaɣ hɔɔlɩŋ lɛɛŋ taa.

Kansɛɛrɩ tomnaɣ pɩzɩɣ kakpa tomnaɣ hɔɔlɩŋ weyi ɩñɔtɩnɩ-kɛ yɔ, nɛ katɩŋnɩ ɖɔɖɔ calɩm taa nɛ kɔɖɛyɩ taa nɛ kɔkɔɔ kasɩɩ tomnaɣ hɔɔlɩŋ weyi ɩñɔtɩnɩ-kɛ yɔ.

Palakɩ-kʋ nɛ calɩm tootoye nɖɩ payaɣ se chimiothérapie yɔ nɛ mbʋ payaɣ se radiothérapie yɔ.

Kʋdɔŋ piye nɖɩ ɖɩ-tɛ paɣlɩka nɛ ɛzɩma pawazɩɣ-ɖɩ yɔ, pɩlɩɣnɩ ɛzɩma ɖɩ-tɛ paɣlɩka nɛ ɛzɩma ɖɩ-tɛ ɖoŋ ɖɔŋ yɔ pɩ-cɔlɔ.

Ye ɛyʋ ɛñakɩ pana se ɛtɩlɩ kʋdɔŋ piye nɖɩ nɛ ɛcɔŋnɩ ɖɩ-taa camɩyɛ yɔ, pɩsɩɣnɩ-ɩ nɛ ɛna se ɖɩpaɣzɩ-ɩ kpaʋ ɖoŋ yaa ɖɩtɩpaɣzɩ-ɩ kpaʋ ɖoŋ.

['Takayɩhatʋ ndʋ tɩtamsɩna \\ yɔ']

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.

['Tɔm ndʋ tɩ-yɔɔ ɖitisiɣ yɔ: ɖɔkɔtɔ']

['Ye ŋwobi intɛrnɛɛtɩ lone ɖɩnɛ ɖɩ-yɔɔ yɔ, ŋpɩzɩɣ nɛ ŋkpɛlɩkɩ tɔm sakɩyɛ ɖɩ-yɔɔ.']

['Pɩtɩpɔzɩ se patɩŋnɩ tɔm ndʋ pama takayaɣ kanɛ ka-taa yɔ tɩ-yɔɔ nɛ pañɩnɩ kʋdɔŋ nakʋyʋ yaa pawaa-kʋ.']

['Tɩlɩ camɩyɛ se ordinatɛɛrɩ yɔɔ tɔm ndʋ pɔpɔzʋʋ yɔ, tɩ-yɔɔ cosuu wɛ kaɖɛ, kɔzɩ kɔzɩ alɩwaatʋ ndʋ tɩ-taa pɔpɔzʋʋ tɔm natʋyʋ nɛ tɩ-taa tɔm pee tɩɖɔɔ yɔ.']

['Paa ɛzɩmtaa lɛ, pɔzɩ lɔŋ tasʋʋ fɛɖʋ weyi ɛsɩm ñɔ-yɔɔ tɔm sakɩyɛ yɔ nɛ ɛyɔɔdɩ-ŋ kʋdɔŋ ŋgʋ ŋwɛna yɔ kɩ-tɔm. Taayele nɛ lɔŋ tasʋʋ mbʋ fɛɖʋ ɛnʋ ɛha-ŋ yɔ, pɩɖɛɛ ñɔ-yɔɔ yaa ŋyele-pʋ ñɩnʋʋ mbʋ pʋyɔɔ yɔ ŋkalɩ tɔm natʋyʋ intɛrnɛɛtɩ lone ɖɩnɛ ɖɩ-yɔɔ. Ye ŋmaɣzɩɣ se pɩwɩɣ-ŋ yɔ, yaa ɛyaa 911 yaa ŋwolo ɖɔkɔtɔ ŋgʋ kɩñɔtɩnɩ-ŋ yɔ kɩ-taa kpaagbaa.']

['Takayɩhatʋ ndʋ tɩtamsɩna \\ Paɣtʋ \\ yɔ']

['Digital Millennium Copyright Act 1998 ñɩŋgʋ, 17 U.S.C. § 512 (DMCA) haɣ waɖɛ mba pɛwɛnɩ waɖɛ se pala tʋmɩyɛ intɛrnɛɛtɩ yɔɔ yɔ se pala mbʋ pɩkaɖɩɣnɩ waɖɛ nɖɩ pɛwɛna Etaazuunii ɛjaɖɛ taa yɔ.']

['Ye ŋmaɣzɩɣ se tɔm natʋyʋ yaa wonuu nakʋyʋ yɔɔ pama tɔm intɛrnɛɛtɩ lone ɖɩnɛ ɖɩ-yɔɔ yaa intɛrnɛɛtɩ lone ɖɩnɛ ɖɩ-yɔɔ nɛ pɩkaɖɩɣnɩ ña-paɣtʋ yɔ, ña-maɣmaɣ yaa weyi ɛsɩɣ-ŋ tʋmɩyɛ yɔ, ŋpɩzɩɣ nɛ ŋtiyini-ɖʋ takayaɣ nɛ ŋpɔzɩ se ɖɩlɩzɩ tɔm ndʋ yaa wonuu ŋgʋ yaa ɖitaayele nɛ nɔɔyʋ tɩlɩ-kʋ.']

['Pɩwɛɛ se pama takayaɣ nɛ petiyini ordinatɛɛrɩ yɔɔ.']

['DMCA paɣtʋ pɔzʋʋ se ye ŋnawa se nɔɔyʋ tɩma takayaɣ nakɛyɛ yɔ, ŋma tɔm tʋnɛ: (1) takayaɣ ŋga ŋnawa se nɔɔyʋ tɩma-kɛ yɔ kɔ-yɔɔ tɔm; (2) takayaɣ ŋga kɔ-yɔɔ pamawa se nɔɔyʋ tɩma takayaɣ nakɛyɛ yɔ kɔ-yɔɔ tɔm nɛ tɔm ndʋ tɩsɩɣnɩ-ɖʋ se ɖɩtɩlɩ ɖenɖe ŋnaɣ takayaɣ ŋga yɔ; (3) ña-hɩɖɛ, kaŋgalaafu mayaɣ nɛ intɛrnɛɛtɩ mayaɣ; (4) ŋyɔɔdɩ kpayɩ se ŋwɛnɩ tisuu se takayaɣ ŋga ŋnawa se nɔɔyʋ tɩma-kɛ yɔ, pɩtɩkɛ weyi ɛtɩnɩ takayaɣ ŋga yɔ ɛ-maɣmaɣ ɛlɩzɩnɩ-kɛ, yaa ɛ-tʋmlaɖʋ nɔɔyʋ lɩzɩnɩ-kɛ, yaa se paɣtʋ natʋyʋ ɛɛhaɣ nʋmɔʋ se palabɩnɩ-kɛ tʋmɩyɛ.']

['(5) Ye ŋlabɩ mbʋ yɔ, ŋpɩzɩɣ nɛ ŋcɛtɩnɩ ñɔ-tɔm yɔɔ nɛ ŋyɔɔdɩ se tɔm ndʋ pama takayaɣ ŋga ka-taa yɔ tɩkɛ toovenim nɛ ŋwɛnɩ waɖɛ se ŋlʋ nɛ ŋwa mba payʋsʋʋ se pɛwɛɛkɩ ña-takayaɣ yɔ.']

['Nɛ (6) ye nɔɔyʋ ɛtɩnɩ takayaɣ nakɛyɛ yɔɔ tɔm yɔ, pɩwɛɛ se ɛñɩɣ nesi takayaɣ ŋga kɔ-yɔɔ.']

['Ye patɩyɔɔdɩ tɔm ndʋ tɩ-tɩŋa yɔ, pɩpɩzɩɣ nɛ pɩkɔnɩ tɔm hʋʋ kaɖɛ.']

['Ɛyʋ weyi ŋkatɩɣ yɔ']

['Ye ŋwɛnɩ tɔm natʋyʋ yaa ŋñɩnɩɣ se ŋtasɩ tɔm natʋyʋ yɔ, ɖitendi-ŋ ma-ɖʋ takayaɣ.']

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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