Tag Archives: KRAS

Discrete Adaptive Responses to MEK Inhibitor in Subpopulations of Triple-Negative Breast Cancer

The authors defined the differential responses to trametinib in subpopulations of a clinically-relevant in vitro model of TNBC, and identified both adaptive and acquired elements that contribute to the emergence of drug resistance mediated by increased expression of CXCR7 and amplification of KRAS.
[Molecular Cancer Research]
Discrete Adaptive Responses to MEK Inhibitor in Subpopulations of Triple-Negative Breast Cancer | Molecular Cancer Research. (n.d.). Retrieved August 6, 2020, from https://mcr.aacrjournals.org/content/early/2020/08/04/1541-7786.MCR-19-1011 Cite
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Impaired AKT Signaling and Lung Tumorigenesis by PIERCE1 Ablation in KRAS-Mutant Non-Small Cell Lung Cancer

Investigators showed the tumor-promoting function of a cell cycle-related protein, PIERCE1, in KRAS-mutant non-small cell lung cancer. Mechanistically, PIERCE1 depletion inhibited cell growth and AKT phosphorylation at S473, which was particularly observed in KRAS-mutant lung cancers.
[Oncogene]
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Reduced Replication Origin Licensing Selectively Kills Kras-Mutant Colorectal Cancer Cells via Mitotic Catastrophe

Scientists showed vulnerability of KRAS-mutant cells towards suppression of minichromosome maintenance complex component 7 and suggested that inhibiting DNA replication licensing might be a viable strategy to target KRAS-mutant cancers.
[Cell Death & Disease]
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NRAS Mutant E132K Identified in Young-Onset Sporadic Colorectal Cancer and the Canonical Mutants G12D and Q61K Affect Distinct Oncogenic Phenotypes

The novel NRAS mutant E132K, identified in three tumor samples from Filipino young-onset, sporadic colorectal cancer patients, was investigated for its effects on different cancer hallmarks, alongside the NRAS canonical mutants G12D and Q61K which were yet poorly characterized in the context of colorectal cancer.
[Scientific Reports]
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High Expression of AMAP1, An ARF6 Effector, Is Associated with Elevated Levels of PD-L1 and Fibrosis of Pancreatic Cancer

With an aim to understand whether the ARF6-AMAP1 pathway was critically involved in the elevated levels of PD-L1 and fibrosis of pancreatic ductal carcinoma, investigators analyzed the relationship between AMAP1 and these malignant phenotypes.
[Cell Communication and Signaling]
Tsutaho, A., Hashimoto, A., Hashimoto, S., Hata, S., Kachi, S., Hirano, S., & Sabe, H. (2020). High expression of AMAP1, an ARF6 effector, is associated with elevated levels of PD-L1 and fibrosis of pancreatic cancer. Cell Communication and Signaling, 18(1), 101. https://doi.org/10.1186/s12964-020-00608-8 Cite
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Genome-Wide Association Meta-Analysis Identifies GP2 Gene Risk Variants for Pancreatic Cancer

Researchers identified three genome-wide significant loci, of which 16p12.3 have not been reported in the Western population. Functional analyses using cell lines provided supporting evidence of the effect of rs78193826 on KRAS activity.
[Nature Communications]
Lin, Y., Nakatochi, M., Hosono, Y., Ito, H., Kamatani, Y., Inoko, A., Sakamoto, H., Kinoshita, F., Kobayashi, Y., Ishii, H., Ozaka, M., Sasaki, T., Matsuyama, M., Sasahira, N., Morimoto, M., Kobayashi, S., Fukushima, T., Ueno, M., Ohkawa, S., … Matsuo, K. (2020). Genome-wide association meta-analysis identifies GP2 gene risk variants for pancreatic cancer. Nature Communications, 11(1), 3175. https://doi.org/10.1038/s41467-020-16711-w Cite
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Genome-Wide DNA Methylation Analysis of KRAS Mutant Cell Lines

Scientists analyzed the basal CpG methylation of 11 KRAS-mutant and dependent pancreatic cancer cell lines and observed strikingly similar methylation patterns. KRAS knockdown resulted in unique methylation changes with limited overlap between each cell line.
[Scientific Reports]
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Lineage Reversion Drives WNT Independence in Intestinal Cancer

Scientists showed that while WNT suppression blocked tumor growth in most organoid and in vivo colorectal cancer (CRC) models, the accumulation of CRC-associated genetic alterations enabled drug resistance and WNT-independent growth.
[Cancer Discovery]
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