Metastatic cancer genetic

metastatic cancer genetic

Oncogenetics - Mechanism of Cancer (tumor suppressor genes and oncogenes)

Article Introduction Colorectal cancer CRC is the third most common cancer in men and the second most common in women. Although screening, addressability and increased awareness metastatic cancer genetic augmented the number of cases in the non-metastatic setting, approximately one in four individuals with CRC will be diagnosed in stage IV.

Additionally, because this improvement in survival has also been associated with substantial health care financial burden, appropriate selection of patients for specific treatments is of utmost importance. Currently, there are several biomarkers that help clinicians in making the optimal treatment decision: KRAS, NRAS, BRAF mutations, human epidermal growth factor receptor 2 HER2 amplification and microsatellite instability MSI or mismatch repair MMRthey all play a significant role in the metastatic cancer genetic, facilitating selection of the right treatment for the right patient.

The aim of this review is to provide clinicians with an update on the particular features of these biomarkers.

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This paper shows the impact of such biomarkers analyzing the results of clinical trials and their outcomes from the perspective metastatic cancer genetic routine clinical practice. The exclusion criteria were: a articles not within the field of interest of this review: not discussing about clinical, pathological and molecular correlations, predictive factors, prognostic factors of the studied biomarkers; b editorials, letters to the editor, commentaries, conference proceedings; c case reports or small case series; d articles not in English; e studies not in humans.

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Figure 1 Flow chart of the search for the eligible studies. KRAS: an indispensable biomarker for anti-epidermal growth factor receptor treatment RAS is a family of proteins expressed in all cell organs belonging to a class of protein called GTPase, and its role is to transmit signals within cells.

These signals finally stimulate cell proliferation. RAS regulated signal pathways control processes like cell proliferation, cell differentiation, cell adhesion, apoptosis and cell migration.

When they are mutated, the cell will have an increased potential of invasion and metastasis. Moreover, these are frequently somatic mutations acquired during lifetime.

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Different KRAS mutations are mainly located in exon 3, codons 59—61, and in exon 4, codons and The distribution of KRAS mutation among clinical trials was Also, in one Middle Eastern study by Zekri et al.

It is unclear if such geographic and racial variations are due to genetic background or environmental and lifestyle differences. In a meta-analysis by Kafatos et alRAS mutations were distributed almost equally among men and women: Codon 12 mutations were more prevalent in women than in men These studies are limited by the lack of clinical and histological data, as well as by their retrospective observational methodology.

DOI: Single tumor cells circulating in the blood stream can be considered a major step in depicting dissemination of primary tumors, an event of clinical relevance for prognosis, staging or therapy monitoring of cancer. The third leading cause of cancer death in men is colorectal cancer and the hematogenous spreading of primary tumor cells is one of the main events in metastasis of this type of cancer. Hidden in the myriad of circulating blood cells, tumor cells need both a sensitive and affordable detection technique. In addition, we found distinct accumulation of porphyrin depending on cancer type cutaneous melanoma versus colorectal cancer.

It is a membrane-bound receptor tyrosine kinase and became a key target for monoclonal antibodies which bind on the extracellular domain of the receptor. The KRAS status is critical for the medical oncologists because it guides the treatment. This may be due to the more frequent activation of EGFR signalling in left-sided tumours compared to those on the right side.

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This phenomenon is probably due to the heterogeneity of tumours. It should also be noted that patients with tumours on the right colon exhibit more frequent BRAF mutations, which result in relative resistance to anti-EGFR treatment.

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Also, the presence of the KRAS mutation was found to be an independent risk factor for reduced survival. KRAS and NRAS mutant tumours exhibit similar metastasis patterns, namely their dissemination is frequently hepatic, pulmonary and peritoneal.

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De Roock et al.

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