KRAS and TP53 mutations in colorectal carcinoma

Al‐Kuraya, Khawla S.

doi:10.4103/1319-3767.56087

Cited by 17 publications

(13 citation statements)

References 23 publications

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“…Recent studies of CRC have found that overexpression of SOX9 in vitro and in vivo was related to several pro-oncogenic properties, including the ability to promote proliferation, inhibit senescence, and collaborate with other oncogenes in neoplastic transformation [6, 49, 50, 73, 160]. The overexpression of SOX9 is related with recurrent distal truncating mutations as frameshift mutations and nonsense mutation in approximately 11% of CRCs; also, SOX9 mutation is strongly associated with coexistent mutant K-RAS and wild type TP53 [49, 50].…”

Section: Role Of Sox9 In Human Cancermentioning

confidence: 99%

SOX9 Stem-Cell Factor: Clinical and Functional Relevance in Cancer

Aguilar‐Medina

Avendaño-Félix

Lizárraga-Verdugo

et al. 2019

Journal of Oncology

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Transcriptional and epigenetic embryonic programs can be reactivated in cancer cells. As result, a specific subset of undifferentiated cells with stem-cells properties emerges and drives tumorigenesis. Recent findings have shown that ectoderm- and endoderm-derived tissues continue expressing stem-cells related transcription factors of the SOX-family of proteins such as SOX2 and SOX9 which have been implicated in the presence of cancer stem-like cells (CSCs) in tumors. Currently, there is enough evidence suggesting an oncogenic role for SOX9 in different types of human cancers. This review provides a summary of the current knowledge about the involvement of SOX9 in development and progression of cancer. Understanding the functional roles of SOX9 and clinical relevance is crucial for developing novel treatments targeting CSCs in cancer.

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Section: Role Of Sox9 In Human Cancermentioning

confidence: 99%

SOX9 Stem-Cell Factor: Clinical and Functional Relevance in Cancer

Aguilar‐Medina

Avendaño-Félix

Lizárraga-Verdugo

et al. 2019

Journal of Oncology

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“…Mutations in TP53 are believed to be a late event in colorectal carcinogenesis and are thought to have a possible role in the transition from adenoma to carcinoma. The KRAS oncogene plays an important role in tumor initiation of CRC; indeed, KRAS mutations have been reported in approximately 30% of colorectal adenomas and in 30% to 50% of CRC patients [9] .…”

Section: Introductionmentioning

confidence: 99%

Inducible Intestine-Specific Expression of kras Triggers Intestinal Tumorigenesis In Transgenic Zebrafish

Raghuram

Fong

et al. 2018

Neoplasia

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KRAS mutations are a major risk factor in colorectal cancers. In particular, a point mutation of KRAS of amino acid 12, such as KRASV12, renders it stable activity in oncogenesis. We found that krasV12 promotes intestinal carcinogenesis by generating a transgenic zebrafish line with inducible krasV12 expression in the intestine, Tg(ifabp:EGFP-krasV12). The transgenic fish generated exhibited significant increases in the rates of intestinal epithelial outgrowth, proliferation, and cross talk in the active Ras signaling pathway involving in epithelial-mesenchymal transition (EMT). These results provide in vivo evidence of Ras pathway activation via krasV12 overexpression. Long-term transgenic expression of krasV12 resulted in enteritis, epithelial hyperplasia, and tubular adenoma in adult fish. This was accompanied by increased levels of the signaling proteins p-Erk and p-Akt and by downregulation of the EMT marker E-cadherin. Furthermore, we also observed a synergistic effect of krasV12 expression and dextran sodium sulfate treatment to enhance intestinal tumor in zebrafish. Our results demonstrate that krasV12 overexpression induces intestinal tumorigenesis in zebrafish, which mimics intestinal tumor formation in humans. Thus, our transgenic zebrafish may provide a valuable in vivo platform that can be used to investigate tumor initiation and anticancer drugs for gastrointestinal cancers.

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“…Major genes involved in these alterations are TP53 (17p), Adenomatous polyposis coli protein (APC) (5q), and MADH2/MADH4/DCC (18q) [16,17]. The loss of chromosome is linked with instability at the chromosomal and molecular level.…”

Section: Genomic Instabilitymentioning

confidence: 99%

Microsatellite Instability in Colorectal Cancer

Parine¹,

Varsha²,

SaudAlanazi³

2016

Microsatellite Markers

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Cancer is a genetic disease. Cancer cells contain various mutations, which includes SNPs to chromosomal aberrations. Together, these changes are referred to as genome instability. Genetic instability is one of the common characteristics of colorectal cancer. In colorectal cancer three major types of genetic instability have been reported. They are chromosomal translocations, microsatellite instability (MSI), and chromosome instability (CIN). Microsatellite instability occurs due to variations in DNA mismatch repair genes, while chromosomal instability is distinguished by major chromosomal alterations occurring at cell division and usually involves -catenin and Adenomatous polyposis coli protein (APC) mutations. This chapter summarizes the major molecular mechanisms leading to genomic and microsatellite instability and tumorigenesis.

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KRAS and TP53 mutations in colorectal carcinoma

Cited by 17 publications

References 23 publications

SOX9 Stem-Cell Factor: Clinical and Functional Relevance in Cancer

SOX9 Stem-Cell Factor: Clinical and Functional Relevance in Cancer

Inducible Intestine-Specific Expression of kras Triggers Intestinal Tumorigenesis In Transgenic Zebrafish

Microsatellite Instability in Colorectal Cancer

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