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BIOMARKER:

KRAS mutation

i
Other names: KRAS, KRAS1, KRAS2, Kirsten rat sarcoma viral oncogene homolog
Entrez ID:
Related biomarkers:
Related tests:
15h
Comparison of Intratumoral and Peritumoral Deep Learning, Radiomics, and Fusion Models for Predicting KRAS Gene Mutations in Rectal Cancer Based on Endorectal Ultrasound Imaging. (PubMed, Ann Surg Oncol)
The feature-based fusion model DLRexpand10_FB can be employed to predict KRAS gene mutations based on pretreatment endorectal ultrasound images of rectal cancer. The integration of peritumoral regions enhanced the predictive performance of both the radiomics and deep learning models.
Journal
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation
21h
Papillary and ductal patterns of mesonephric-like adenocarcinomas are often overlooked: a retrospective revaluation of over 1000 endometrial carcinomas. (PubMed, Histopathology)
This study highlights the importance of a comprehensive diagnostic approach for accurately identifying endometrial MLA and for pathologists to be aware of papillary and ductal patterns in endometrial carcinoma assessment. Further exploration into the molecular landscape of MLA is essential for refining diagnostic criteria and developing targeted therapies.
Retrospective data • Journal
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KRAS (KRAS proto-oncogene GTPase) • NKX2-1 (NK2 Homeobox 1) • GATA3 (GATA binding protein 3)
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KRAS mutation
21h
Anionic polymer coating for enhanced delivery of Cas9 mRNA and sgRNA nanoplexes. (PubMed, Biomater Sci)
Post-transfection, the KRAS-ERK pathway was downregulated, resulting in significant increases in cell apoptosis and inhibition of cell migration. Taken together, this study reveals a new and promising formulation for CRISPR delivery as potential lung cancer treatment.
Journal
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12 • KRAS G12S
21h
The use of nutrigenomics and nutritional biomarkers with standard care of long-term recurrent metastatic rectal cancer: a case report. (PubMed, Front Oncol)
A multimodal approach to this patient's management appeared to contribute to his long-term survival of nearly 10 years from the initial diagnosis. Multidisciplinary management, including the use of additional biomarkers, may enhance survival rates in other similar cases with advanced disease resistant to differing therapies, and with potentially poor prognosis.
Journal • Metastases
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KRAS (KRAS proto-oncogene GTPase) • MTHFR (Methylenetetrahydrofolate Reductase)
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KRAS mutation
23h
Untangling sporadic brain arteriovenous malformations: towards targeting the KRAS/MAPK pathway. (PubMed, Front Surg)
Here, we review the history of brain AVMs, their treatments, and recent advances in uncovering the pathogenesis of sporadic brain AVMs. We specifically focus on the latest studies suggesting that pharmacologically targeting the KRAS/MEK pathway may be a potentially efficacious treatment for sporadic brain AVMs.
Review • Journal
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation
23h
Combination of farnesyl-transferase inhibition with KRAS G12D targeting breaks down therapeutic resistance in pancreatic cancer. (PubMed, Pathol Oncol Res)
Although we have shown that the 3D environment dramatically sensitizes cells to MRTX1133 treatment, the synergistic effect of this drug combination is present in both 2D and 3D in the PANC1 pancreatic adenocarcinoma model, which showed high resistance to MRTX1133 in 2D. The effects of the combination treatment show an association with the inhibition of farnesylated regulatory proteins, including HRAS and RHEB, along with the expression level of KRAS. Our study warrants further investigation for the potential applicability of KRAS G12D inhibitors in combination with farnesyl-transferase inhibitors for the treatment of KRAS mutant pancreatic adenocarcinoma.
Journal
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KRAS (KRAS proto-oncogene GTPase) • HRAS (Harvey rat sarcoma viral oncogene homolog) • RHEB (Ras Homolog, MTORC1 Binding)
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KRAS mutation • KRAS G12D • HRAS G12C • KRAS expression
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MRTX1133
1d
PIK3CA Mutations and Co-Mutations in Operated Non-Small Cell Lung Carcinoma. (PubMed, J Clin Med)
The top 10 mutations that most commonly accompanied PIK3CA variations were KRAS, NF1, TP53, EGFR, PTEN, BRAF, KIT, CDKN2A, SMARCA4, and ATM mutations, respectively. PIK3CA variations, along with other gene variations, may influence cancer progression and thus may play a crucial role in the determination of targeted treatment strategies.
Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • ATM (ATM serine/threonine kinase) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • NF1 (Neurofibromin 1) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4)
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TP53 mutation • KRAS mutation • BRAF mutation • PIK3CA mutation • ATM mutation • PIK3CA H1047R • PTEN mutation • PIK3CA E545K • CDKN2A mutation • SMARCA4 mutation • PIK3CA E545 • PIK3CA E542
1d
Redefining Therapeutic Approaches in Colorectal Cancer: Targeting Molecular Pathways and Overcoming Resistance. (PubMed, Int J Mol Sci)
Novel combination treatments are also discussed as strategies to improve outcomes and overcome resistance. Understanding these molecular mechanisms is critical to advancing personalized treatment approaches in CRC and improving patient prognosis.
Review • Journal • IO biomarker
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • NRAS (Neuroblastoma RAS viral oncogene homolog) • MSI (Microsatellite instability)
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TP53 mutation • KRAS mutation • BRAF mutation • NRAS mutation
1d
Plasticity and Tumor Microenvironment in Pancreatic Cancer: Genetic, Metabolic, and Immune Perspectives. (PubMed, Cancers (Basel))
Furthermore, we present the following two signaling pathways that we have identified: one based on the small G-protein ARF6 driven by KRAS/TP53 mutations, and the other based on the RNA-binding protein Arid5a mediated by inflammatory cytokines, which promote both metabolic reprogramming and immune evasion in pancreatic cancer. Finally, the striking diversity among pancreatic cancers in the relative importance of mutational burden and the tumor microenvironment, their clinical relevance, and the potential for novel therapeutic strategies will be discussed.
Review • Journal • Tumor mutational burden
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • ARID5A (AT-Rich Interaction Domain 5A)
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TP53 mutation • KRAS mutation
1d
Combined Therapeutic Strategies Based on the Inhibition of Non-Oncogene Addiction to Improve Tumor Response in EGFR- and KRAS-Mutant Non-Small-Cell Lung Cancer. (PubMed, Cancers (Basel))
The major translational relevance of this study is to exploit new targets for the development of innovative and improved therapeutic strategies with NOA drugs, over combinations including target genes within the oncogene pathway, to overcome resistance to TKI therapies in patients with NSCLC who are oncogene-addicted.
Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • EGFR mutation • EGFR mutation + KRAS mutation
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Tagrisso (osimertinib) • Koselugo (selumetinib) • gartisertib (M4344)
1d
First-line treatments for KRAS-mutant non-small cell lung cancer: current state and future perspectives. (PubMed, Cancer Biol Ther)
KRAS inhibitors and other emerging alternative treatments are also discussed, as combining these drugs with immunotherapy may serve as a promising first-line treatment for KRAS-mutated NSCLC in the future. We hope that this review will assist in first-line treatment choices and shed light on the development of novel agents for KRAS-mutated NSCLC.
Review • Journal • IO biomarker
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation
1d
Remote organ cancer induces kidney injury, inflammation, and fibrosis and adversely alters renal function. (PubMed, Am J Physiol Renal Physiol)
Our results confirm cancer-kidney crosstalk in specific cancer types. In the era of precision medicine, further research is essential to identify at-risk oncology populations, enabling early detection and management of renal complications.
Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • EGFR mutation • EGFR mutation + KRAS mutation
2d
Mixed pancreatic ductal adenocarcinoma and well-differentiated neuroendocrine tumor: A case report. (PubMed, World J Gastrointest Oncol)
Mixed NET/non-NET tumors with distinct histology and molecular profiles might be better classified as collision tumors rather than MiNENs.
Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
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TP53 mutation • KRAS mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
2d
Signet-ring cell carcinoma of the transverse colon in a 10-year-old girl: A case report. (PubMed, World J Gastrointest Oncol)
Primary colonic SRCC is a rare malignant tumor with atypical clinical symptoms, and timely identification and intervention are crucial for improving the prognosis.
Journal
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KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog)
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KRAS mutation • BRAF mutation • NRAS mutation • PIK3CA mutation
3d
Adagrasib in Combination With BI 1701963 in Patients With Cancer (KRYSTAL 14) (clinicaltrials.gov)
P1, N=7, Terminated, Mirati Therapeutics Inc. | Completed --> Terminated; The decision was made to terminate this study to further enrollment, as of 08 March 2022. The decision was made primarily due to a change in development strategy.
Trial termination • Combination therapy • Metastases
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12C • KRAS G12
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Krazati (adagrasib) • BI 1701963
3d
Study of MRTX1133 in Patients With Advanced Solid Tumors Harboring a KRAS G12D Mutation (clinicaltrials.gov)
P1/2, N=386, Active, not recruiting, Mirati Therapeutics Inc. | Recruiting --> Active, not recruiting
Enrollment closed • Metastases
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12D • KRAS G12
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MRTX1133
3d
Molecular pathology of gastrointestinal neoplasms (PubMed, Magy Onkol)
The responsiveness of gastrointestinal stromal tumors to imatinib requires validation via molecular testing. Patients diagnosed with pancreatic cancer may see enhanced survival rates by targeted therapy addressing microsatellite instability and BRCA mutations. In bile duct malignancies, especially intrahepatic cholangiocarcinoma of the small duct variant, the analysis of IDH1 mutations and FGFR2 fusions presents new treatment prospects.
Review • Journal • BRCA Biomarker
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • NRAS (Neuroblastoma RAS viral oncogene homolog) • MSI (Microsatellite instability) • FGFR2 (Fibroblast growth factor receptor 2) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • CLDN18 (Claudin 18) • BRCA (Breast cancer early onset)
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KRAS mutation • BRAF mutation • HER-2 amplification • NRAS mutation • IDH1 mutation • FGFR2 mutation • FGFR2 fusion • BRCA mutation • IDH1 mutation + FGFR2 fusion
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imatinib
4d
Association of Oncogene Driver Mutations with Recurrence and Survival in Stage I Nonsmall Cell Lung Cancer. (PubMed, Clin Lung Cancer)
Oncogene mutations such as KRAS G12V and EGFR may have implications for cancer surveillance strategies and inform future treatment trials of stage I NSCLC.
Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PTEN (Phosphatase and tensin homolog)
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TP53 mutation • KRAS mutation • EGFR mutation • PTEN mutation • KRAS G13D • MET mutation • KRAS G12 • KRAS G13
4d
Genetic profile in primary tumor tissue of advanced lung adenocarcinoma patients with adrenal metastasis. (PubMed, Cancer Genet)
EGFR mutations, especially rare variants (G724A, L747P, Q701 L, G719C, V769 L and S768I), exhibited significant enrichment in the non-AM group (P<0.001)...Meanwhile, patients with adrenal metastases harboring ALK or KRAS mutations have a poor prognosis and require more aggressive treatment. The TNF and TGF-β pathways might be associated with adrenal metastasis.
Journal • BRCA Biomarker • Metastases
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • RET (Ret Proto-Oncogene) • NOTCH1 (Notch 1) • KEAP1 (Kelch Like ECH Associated Protein 1) • LRP1B (LDL Receptor Related Protein 1B) • BRCA (Breast cancer early onset) • TGFB1 (Transforming Growth Factor Beta 1)
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KRAS mutation • ALK mutation • RET mutation • KEAP1 mutation • EGFR S768I • EGFR L747P • EGFR G719C
4d
Association of G12D mutation in the KRAS gene with HPV and EBV in gastrointestinal cancer tissues. (PubMed, J Int Med Res)
This study detected a significant correlation between the presence of viral agents and KRAS G12D mutations.
Journal
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12D • KRAS wild-type • RAS wild-type • KRAS G12
6d
Tumor sequencing before and after neoadjuvant chemoradiotherapy in locally advanced rectal cancer: Genetic tumor characterization and clinical outcome. (PubMed, Clin Transl Radiat Oncol)
Thus, NCRT does not seem to induce a relevant number of new driver mutations or mutational burden. Genetic profiling implies the potential to support tumor-informed approaches and outcome estimation in future.
Clinical data • Journal • Tumor mutational burden • Metastases
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • RYR1 (Ryanodine Receptor 1)
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TP53 mutation • KRAS mutation • ATM mutation • RYR1 mutation
6d
Correlations between 14-gene RNA-level assay and clinical and molecular features in resectable non-squamous non-small cell lung cancer: a cross-sectional study. (PubMed, Transl Lung Cancer Res)
Our results indicate that 14-gene RNA-level assay is correlated with specific genetic mutations, including TP53, KRAS, and LRP1B. These insights provide a stronger foundation for integrating molecular risk assessment with clinical and imaging data, offering more comprehensive information to guide more targeted and effective adjuvant therapy strategies in the future management of lung cancer.
Observational data • Journal • Tumor mutational burden
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • LRP1B (LDL Receptor Related Protein 1B)
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TP53 mutation • KRAS mutation
6d
Prognostic impact of targetable driver alterations in resected early-stage lung cancer. (PubMed, Transl Lung Cancer Res)
The lack of association between molecular alteration status and recurrence risk prevailed after multivariable adjustment for tumor stage and perioperative treatment (P=0.82 for KRAS G12C mutation and P=0.43 for any other molecular alteration). NSCLC patients with resected tumors that harbor molecular alterations have the same recurrence risk as patients with tumors without molecular alterations if treated with surgery plus chemotherapy when indicated.
Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase)
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BRAF V600E • KRAS mutation • EGFR mutation • KRAS G12C • BRAF V600 • ALK fusion • ALK mutation • KRAS G12
6d
Evaluation of the simultaneous effects of KRAS G12V and LCS6 alterations on the behavior of head and neck squamous cell carcinoma. (PubMed, Mutat Res)
The LCS6 region alteration of the KRAS may play a key role in further cancer progression, and more research is needed to fully understand the mechanisms by which the LCS6 alterations promote cancer progression.
Journal
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12
7d
Dynamic conformational equilibria in the active states of KRAS and NRAS. (PubMed, RSC Chem Biol)
We elucidated the mechanism of action of a potent KRAS G12D inhibitor, MRTX1133. Binding of this inhibitor to the switch-2 pocket causes a complete shift of KRAS G12D towards the "inactive" conformation and prevents binding of effector RAS-binding domain (RBD) at physiological concentrations, by signaling through an allosteric network.
Journal
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KRAS (KRAS proto-oncogene GTPase) • NRAS (Neuroblastoma RAS viral oncogene homolog)
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KRAS mutation • KRAS G12C • KRAS G12D • NRAS Q61 • NRAS G12D • NRAS G12 • KRAS G61 • NRAS G12V
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MRTX1133
7d
Enhancing efficacy of the MEK inhibitor trametinib with paclitaxel in KRAS-mutated colorectal cancer. (PubMed, Ther Adv Med Oncol)
Finally, the combination of trametinib with paclitaxel exhibited significant inhibition of tumor growth in several KRAS-mutant patient-derived xenograft mouse models. Our data provide evidence supporting clinical trials of trametinib with paclitaxel as a novel therapeutic option for patients with KRAS-mutated, metastatic CRC.
Journal
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation
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Mekinist (trametinib) • paclitaxel
7d
SHP2 Inhibitor BBP-398 in Combination With Nivolumab in Patients With Advanced Non-Small Cell Lung Cancer With a KRAS Mutation (clinicaltrials.gov)
P1, N=21, Terminated, Navire Pharma Inc., a BridgeBio company | N=45 --> 21 | Trial completion date: Jan 2025 --> Jul 2024 | Recruiting --> Terminated; Business reasons
Enrollment change • Trial completion date • Trial termination • Combination therapy • Metastases
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation
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Opdivo (nivolumab) • BMS-986466
7d
First-in-Human Study of the SHP2 Inhibitor BBP-398 in Patients With Advanced Solid Tumors (clinicaltrials.gov)
P1, N=72, Terminated, Navire Pharma Inc., a BridgeBio company | N=130 --> 72 | Trial completion date: Feb 2025 --> Jul 2024 | Active, not recruiting --> Terminated; Business decision
Enrollment change • Trial completion date • Trial termination • Metastases
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene)
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KRAS mutation • EGFR mutation • KRAS G12C • KRAS G12
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BMS-986466
7d
Argonaut: SHP2 Inhibitor BBP-398 in Combination With Sotorasib in Patients With Advanced Solid Tumors and a KRAS-G12C Mutation (clinicaltrials.gov)
P1, N=28, Terminated, Navire Pharma Inc., a BridgeBio company | N=85 --> 28 | Trial completion date: Jun 2025 --> Aug 2024 | Recruiting --> Terminated; Business Reasons
Enrollment change • Trial completion date • Trial termination • Combination therapy • Metastases
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12C • KRAS G12
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Lumakras (sotorasib) • BMS-986466
7d
SRC kinase drives multidrug resistance induced by KRAS-G12C inhibition. (PubMed, Sci Adv)
SRC inhibitors (DGY-06-116, dasatinib, and bosutinib) also exhibit synergistic effects with MRTX849 in eliminating various tumor cell lines carrying KRAS-G12C mutations. Thus, SRC inhibitors amplify the therapeutic utility of G12Ci.
Journal
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KRAS (KRAS proto-oncogene GTPase) • ABCC1 (ATP Binding Cassette Subfamily C Member 1)
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KRAS mutation • KRAS G12C • ABCC1 expression
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dasatinib • Bosulif (bosutinib) • Krazati (adagrasib)
8d
Sotorasib inhibits ubiquitination degradation of TXNIP and suppresses glucose metabolism in KRASG12C mutant bladder cancer. (PubMed, Am J Cancer Res)
Additionally, Sotorasib increased TXNIP expression by regulating the RAS/RAF/ERK axis. This study uncovers the mechanism by which Sotorasib inhibits glucose metabolism in KRASG12C mutant bladder cancer cells and suggests a potential therapeutic benefit for the treatment of KRASG12C mutant bladder cancer.
Journal
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KRAS (KRAS proto-oncogene GTPase) • LDHA (Lactate dehydrogenase A) • TXNIP (Thioredoxin Interacting Protein) • PKM (Pyruvate Kinase M1/2) • SLC2A1 (Solute Carrier Family 2 Member 1)
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KRAS mutation • KRAS G12C • KRAS G12D • KRAS G12
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Lumakras (sotorasib)
8d
MRTX1133 attenuates KRASG12D mutated-colorectal cancer progression through activating ferroptosis activity via METTL14/LINC02159/FOXC2 axis. (PubMed, Transl Oncol)
Our study provides novel insights into the therapeutic potential of MRTX1133 in treating KRASG12D-mutated CRC by identifying a METTL14/LINC02159/FOXC2 signalling axis that mediates drug response. Our findings highlight the importance of understanding the molecular mechanisms of lncRNAs in cancer to develop effective targeted therapies.
Journal
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KRAS (KRAS proto-oncogene GTPase) • METTL14 (Methyltransferase 14) • FOXC2 (Forkhead Box C2)
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KRAS mutation • KRAS G12D • KRAS G12
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MRTX1133
9d
Adagrasib in the Treatment of KRAS p.G12C Positive Advanced NSCLC: Design, Development and Place in Therapy. (PubMed, Drug Des Devel Ther)
Although once thought to be "undruggable", KRAS p.G12C inhibitors such as sotorasib and adagrasib have been developed. This paper focuses on adagrasib, the second KRAS p.G12C inhibitor to obtain regulatory approval by the FDA and describes the details on its study design, development and current place in therapy.
Review • Journal • Metastases
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12C • KRAS G12
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Lumakras (sotorasib) • Krazati (adagrasib)
9d
The role of silent mutations in KRAS-mutant tumors. (PubMed, Chin Med J (Engl))
Despite being in early stages, research on KRAS silent mutations holds promise for uncovering novel insights that could inform personalized cancer treatments. In conclusion, this review underscores the evolving landscape of KRAS silent mutations, advocating for further exploration to bridge fundamental biology with clinical applications in oncology.
Journal
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KRAS (KRAS proto-oncogene GTPase) • RAS (Rat Sarcoma Virus)
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KRAS mutation • RAS mutation
9d
Vinegar-induced Collection of Duodenal Pancreatic Juice Via Endoscopic Ultrasound (clinicaltrials.gov)
P=N/A, N=75, Recruiting, Peking Union Medical College Hospital | N=50 --> 75 | Trial completion date: Nov 2023 --> Dec 2025 | Trial primary completion date: Oct 2023 --> Jan 2025
Enrollment change • Trial completion date • Trial primary completion date • Tumor mutational burden
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation
9d
Phase 1/2 trial of XPO1 inhibitor selinexor plus docetaxel in previously treated, advanced KRAS mutant non-small cell lung cancer. (PubMed, Clin Cancer Res)
Selinexor plus docetaxel was relatively well tolerated in patients with advanced KRAS mutant NSCLC. The regimen has promising efficacy in TP53 wild type cases, where selinexor monotherapy may also have activity.
P1/2 data • Journal • IO biomarker • Metastases
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53)
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TP53 mutation • KRAS mutation • TP53 wild-type
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docetaxel • Xpovio (selinexor)
9d
Prevalence of HER3 Expression in Pancreatic Cancer Patients Treated With Systemic Chemotherapy. (PubMed, Cancer Med)
A high prevalence of HER3 expression was observed in pancreatic cancer patients after chemotherapy. Our findings indicate that HER3 is a potential therapeutic target for pancreatic cancer, deserving further clinical investigation.
Retrospective data • Journal
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3)
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TP53 mutation • KRAS mutation • ERBB3 expression • ERBB3 mutation • TP53 mutation + KRAS mutation • KRAS mutation + TP53 mutation
9d
Quantitative MRI Measurements Capture Pancreatic Cancer and Stroma Reactions to New KRAS Inhibitor. (PubMed, bioRxiv)
We tested this hypothesis in multiple preclinical PDAC models receiving MRTX1133, an investigational new drug specific for KRAS G12D mutation...Our data demonstrate the abilities of DWI, DCE and MTR derived imaging markers to detect the early (48h) cell death, pronounced stromal changes and development of resistance to KRASi. This study has high translational relevance by testing clinically ready MRI methods, an IND and a genetic engineered mouse model that recapitulates saline features of human PDAC.
Journal • Stroma
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KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12C • KRAS G12D • KRAS G12
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MRTX1133
10d
GO42144: A Study to Evaluate the Safety, Pharmacokinetics, and Activity of GDC-6036 Alone or in Combination in Participants With Advanced or Metastatic Solid Tumors With a KRAS G12C Mutation (clinicaltrials.gov)
P1, N=498, Recruiting, Genentech, Inc. | Trial completion date: Nov 2024 --> Mar 2026 | Trial primary completion date: Nov 2024 --> Mar 2025
Trial completion date • Trial primary completion date • Combination therapy • Metastases
|
KRAS (KRAS proto-oncogene GTPase)
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KRAS mutation • KRAS G12C • KRAS G12
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Avastin (bevacizumab) • Erbitux (cetuximab) • Tecentriq (atezolizumab) • erlotinib • divarasib (RG6330) • Itovebi (inavolisib) • migoprotafib (RLY-1971)
11d
Targeted Sequencing in Rosai-Dorfman Disease from Microdissected Specimens Reveals Higher Incidence of MAP2K1 Mutations (ASH 2024)
The incidence of MAP2K1 mutations was higher in the current study than in previous studies (Garces et al. 2017), though not statistically significant, at 29% (4/14) compared to 16% (8/49; p=0.15).These results highlight the value of stringent tissue microdissection for identifying targetable molecular alterations in RDD and suggest that such approaches may help uncover additional neoplastic drivers and/or mutations implicated in therapeutic resistance.
KRAS (KRAS proto-oncogene GTPase) • MAP2K1 (Mitogen-activated protein kinase kinase 1)
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KRAS mutation • KRAS G12D • KRAS G12 • MAP2K1 E203K • KRAS A146P • MAP2K1 G128D
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Oncomine Focus Assay
12d
KRAS Variants Are Associated With Survival Outcomes and Genomic Alterations in Biliary Tract Cancers. (PubMed, JCO Precis Oncol)
The adverse impact of KRAS mutations in BTC is driven by G12 alterations in patients with IHC regardless of resection status, which was not observed in GB or EHC. There are unique comutational partners in distinct BTC subsets. These differences have important clinical implications in the era of KRAS-targeted therapeutics.
Journal
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KRAS (KRAS proto-oncogene GTPase) • SF3B1 (Splicing Factor 3b Subunit 1)
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KRAS mutation • KRAS G12D • KRAS wild-type • SF3B1 mutation • KRAS G12
12d
Treatment of stage IV colorectal cancer: A retrospective cohort study assessing whether failure of first‑line treatment indicates failure of second‑line treatment. (PubMed, Mol Clin Oncol)
Although current first- and second-line therapies stratify for KRAS/NRAS/BRAF mutations, microsatellite instability, tumour location and co-morbidities, the therapeutic mainstay for the first- and second-line treatment of the majority of patients consists of 5-fluorouracil (5-FU)-based chemo-immunotherapy. By exchanging the chemotherapeutic combination partner from oxaliplatin to irinotecan or vice versa, plus the additive anti-epidermal growth factor receptor/anti-vascular endothelial growth factor antibody, the negative factor of non-response to first-line therapy could not be overcome by second-line treatment in this study population. These findings must be confirmed in larger studies, but indicate the need for novel treatment options, especially for patients not responding to first-line 5-FU-based chemo-immunotherapy.
Retrospective data • Journal • IO biomarker • Metastases
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • NRAS (Neuroblastoma RAS viral oncogene homolog) • MSI (Microsatellite instability)
|
KRAS mutation • BRAF mutation • NRAS mutation
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5-fluorouracil • oxaliplatin • irinotecan