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Abstract: In under developed nations, colorectal carcinogenesis (CRC) is a a significant health issue. It is the third most common outcome of cancer death. Despite a variety of therapy options, new medications are needed to lessen the severity of this condition. In the colon, Adenomatous polyps are the most common cause of CRC, occurring in 45 percent of cases, particularly in patients over 60 years old. Inflammatory polyps are acquiring popularity in CRC, as well as and inflammation appears to exert a function in the disease, according to mounting research. The Azoxymethane, Dimethyl hydrazine, APCmin/+ mouse model, and a combination of sulfated polysaccharide composed of dextran and sulfated and dimethylhydrazine are among the experimental models used to study CRC in animals. Numerous signal transduction pathways are engaged as CRC progresses. The p53, TGF-β, Delta-Notch,, Salvador-Warts-Hippo (SWH), and Kelch-like ECH assocd. protein 1pathways are among the key signal transduction pathways. To decide cell destiny, several signalling pathways work in tandem with death of cell modalitiessuch as autophagy, necroptosis, and apoptosis. In our lab, we've spent a lot of time looking into the Cell signalling and mechanisms of cell death in CRC. The pathogenesis of CRC, as well as the associated cell death and cell signalling pathways, are summarised in this study.

Ovarian cancer is characterized by the establishment of tolerance, the recurrence of disease, as well as a poor prognosis. Gene signatures in ovarian cancer cells enable cancer medicine research, therapy, prevention, & management problematic. Notwithstanding advances in tumor puncture surgery, novel combinations regimens, and abdominal radiation, which can provide outstanding reaction times, the bulk of gynecological tumor patients suffer from side effects & relapse. As a consequence, more therapy alternatives for individuals with ovarian cancer must always be studied to minimize side effects and improve progression-free and total response rates. The development of cancer medications is presently undergoing a renaissance in the quest for descriptive and prognostic ovarian cancer biomarkers. Nevertheless, abnormalities in the BRCA2 or BRCA1 genes, a variety of hereditary predispositions, unexplained onset and progression, molecular tumor diversity, and illness staging can all compromise the responsiveness and accuracy of such indicators. As a result, current ovarian cancer treatments must be supplemented with broad-spectrum & customized targeted therapeutic approaches. The objective of this review is to highlight recent contributions to the knowledge of the interrelations between selected ovarian tumor markers, various perception signs, and biochemical and molecular signaling processes, as well as one’s interpretation of much more targeted and effective treatment interventions.