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Background: Colorectal cancer has a heterogeneous nature that is influenced by the tumour site. Many improvements have been made in identifying and characterizing the genetic alterations between colon and rectal cancers. However, there is not enough information about KRAS mutational differences between rectosigmoid and colon cancers arising elsewhere in the large bowel. The aim of this study was to determine the differences in the frequency of KRAS genetic alterations between rectosigmoid cancers and colon cancers.
Methods: Eighty-four patients diagnosed with colorectal cancer were included in this study. Genomic DNA was extracted from formalin-fixed paraffin-embedded tumour tissue sections. KRAS mutation analysis which was designed to detect the seven most common KRAS gene mutations (Gly12Ala, Gly12Asp, Gly12Arg, Gly12Cys, Gly12Ser, Gly12Val and Gly13Asp) was performed. Chi-square test was used to test the association between mutation status and other variables.
Results: This study represents the first KRAS mutational results from Turkish rectosigmoid cancer patients. The KRAS mutation frequency of rectosigmoid tumours is higher (34.3%, 12/35) than that of colon-localized tumours (30.6%, 15/49). However, there is no significant correlation between the KRAS mutation status and tumour location (rectosigmoid and colon).
Conclusions: KRAS mutation analysis has a predictive and prognostic value in identifying tumours that may be resistant to treatment. Our study shows that differences in the biological behaviour of rectosigmoid and colon cancers should be considered. This finding highlights the importance of personalized cancer management, which could be assisted by cancer genotyping tools.
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http://dx.doi.org/10.3978/j.issn.2078-6891.2014.038 | DOI Listing |
J Clin Invest
December 2024
Hillman Cancer Center, University of Pittsburgh Medical Center, Pittsburgh, United States of America.
KRAS is the most frequently mutated oncogene in lung adenocarcinoma, with G12C and G12V being the most predominant forms. Recent breakthroughs in KRASG12C inhibitors have transformed the clinical management of patients with G12C mutation and advanced our understanding of its function. However, little is known about the targeted disruption of KRASG12V, partly due to a lack of specific inhibitors.
View Article and Find Full Text PDFLung Cancer (Auckl)
December 2024
University of California Irvine School of Medicine, Department of Medicine, Orange, CA, 92868, USA.
Mutations in KRAS G12C are among the more common oncogenic driver mutations in non-small cell lung cancer (NSCLC). In December 2022, the US Food and Drug Administration (FDA) granted accelerated approval to adagrasib, a small molecule covalent inhibitor of KRAS G12C, for the treatment of patients with locally advanced or metastatic KRAS G12C mutant NSCLC who received at least one prior systemic therapy based on promising results from phase 1 and 2 trials wherein adagrasib demonstrated a median PFS of 6.5 months.
View Article and Find Full Text PDFDiscov Oncol
December 2024
Dr B R Ambedkar Center for Biomedical Research, University of Delhi, Delhi, 110007, India.
Cancer, a leading cause of death worldwide, is projected to increase by 76.6% in new cases and 89.7% in mortality by 2050 (WHO 2022).
View Article and Find Full Text PDFMol Cancer Ther
December 2024
Boehringer Ingelheim (Austria), Vienna, Austria.
KRASG12C selective inhibitors, such as sotorasib and adagrasib, have raised hopes of targeting other KRAS mutant alleles in cancer patients. We report that KRAS wild-type amplified tumor models are sensitive to treatment with the small molecule KRAS inhibitors BI-2493 and BI-2865. These pan-KRAS inhibitors directly target the "OFF" state of KRAS and result in potent anti-tumor activity in pre-clinical models of cancers driven by KRAS mutant proteins.
View Article and Find Full Text PDFArch Biochem Biophys
December 2024
Department of Pharmaceutical Sciences, School of Health Sciences and Technology, UPES Dehradun - 248007, Uttarakhand, India. Electronic address:
KRAS (Kirsten rat sarcoma viral oncogene homologue), the most common mutated protein in human cancers, is the leading cause of morbidity and mortality. Before Sotorasib (AMG-510) was approved for non-small cell lung cancer treatment in 2020, the oncogenic KRAS mutations were believed to be non-druggable. High-resolution X-ray crystal structures of GDP-bound KRAS mutants with and without inhibitor resolved.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!