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2d
A Study of Tucatinib and Trastuzumab in People With Rectal Cancer (clinicaltrials.gov)
P2, N=37, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026
Trial completion date • Trial primary completion date
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase)
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HER-2 positive • HER-2 overexpression • HER-2 amplification • RAS wild-type • HER-2 positive + HER-2 overexpression • HER-2 positive + RAS wild-type
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Herceptin (trastuzumab) • Tukysa (tucatinib)
3d
BCL-xL as a therapeutic target in cetuximab-refractory colorectal cancer. (PubMed, Cell Death Dis)
Multiplex immunofluorescence staining demonstrated that BCL-xL inhibition effectively triggered apoptosis in heterogeneous PDX tumor slice models, including models harboring oncogenic BRAF mutations. Our findings suggest that cetuximab-resistant CRC retains apoptotic competence, and that BCL-xL inhibition serves as a robust alternative therapeutic strategy that is largely independent of the tumor mutational profile.
Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • BCL2L1 (BCL2-like 1)
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BRAF mutation • KRAS wild-type • RAS wild-type
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Erbitux (cetuximab)
3d
Impact of KRAS Mutations and Co-Alterations on Outcomes in Stage III Non-Squamous Non-Small Cell Lung Cancer Treated with Chemoradiation and Immunotherapy. (PubMed, J Thorac Oncol)
KRAS mutant non-sq LA-NSCLC is associated with inferior outcomes, largely driven by increased distant and brain metastases. Tumors with concurrent CDKN2A and/or STK11 alterations had the poorest outcomes. These findings support the evaluation of KRAS inhibitors in this high-risk stage III population.
Journal • PD(L)-1 Biomarker • IO biomarker
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KRAS (KRAS proto-oncogene GTPase) • STK11 (Serine/threonine kinase 11) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A)
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KRAS mutation • STK11 mutation • KRAS wild-type • RAS wild-type
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Imfinzi (durvalumab)
3d
Exploratory Study of Disitamab Vedotin Combination Therapy in Advanced Gastrointestinal Tumors with HER2 Overexpression or Amplification (ChiCTR2500114011)
P2, N=90, Not yet recruiting, The First Affiliated Hospital of Henan University of Chinese Medicine; The First Affiliated Hospital of Henan University of Chinese Medicine
New P2 trial
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HER-2 (Human epidermal growth factor receptor 2)
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HER-2 overexpression • HER-2 amplification • RAS wild-type • HER-2 positive + RAS wild-type
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Erbitux (cetuximab) • Perjeta (pertuzumab) • Lenvima (lenvatinib) • Aidixi (disitamab vedotin)
3d
New P1/2 trial
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HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • MET (MET proto-oncogene, receptor tyrosine kinase) • MSI (Microsatellite instability) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK (Neurotrophic receptor tyrosine kinase)
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PD-L1 expression • KRAS mutation • EGFR mutation • MSI-H/dMMR • BRAF mutation • EGFR L858R • EGFR exon 19 deletion • EGFR T790M • ALK rearrangement • EGFR wild-type • MET exon 14 mutation • KRAS wild-type • RAS wild-type • ROS1 fusion • ROS1 rearrangement • MET mutation • NTRK fusion
3d
Atamparib in Patients With Advanced Solid Tumors ( PARP7 ) (ChiCTR2600117616)
P1/2, N=178, Not yet recruiting, Shanghai Eastern Hospital; Nerviano Medical Science Shanghai Ltd.
New P1/2 trial
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KRAS (KRAS proto-oncogene GTPase)
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KRAS wild-type • RAS wild-type
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atamparib (RBN-2397)
4d
Dual targeting of SLC25A51 and succinate dehydrogenase selectively depletes mitochondrial NAD+ to eradicate KRAS-driven AML. (PubMed, Cell Metab)
Conversely, KRAS-wild-type cells preserve NAD+ influx via sufficient baseline succinyl-SLC25A51, which stabilizes SLC25A51 and enables sufficient succinate accumulation to drive hypoxia inducible factor 1 subunit alpha (HIF1α)-mediated compensatory NAD+ production during treatment. Our work reveals a KRAS-specific metabolic vulnerability and proposes a dual-inhibition therapy for KRAS-driven AML.
Journal
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KRAS (KRAS proto-oncogene GTPase) • HIF1A (Hypoxia inducible factor 1, alpha subunit)
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KRAS mutation • KRAS wild-type • RAS wild-type
5d
New P1 trial
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PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • MET (MET proto-oncogene, receptor tyrosine kinase) • MSI (Microsatellite instability)
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PD-L1 expression • MSI-H/dMMR • BRAF mutation • BRAF V600 • KRAS wild-type • RAS wild-type
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Opdivo (nivolumab)
7d
Real-World Survival Outcomes Following Metastasectomy in RAS Wild-Type mCRC: Insights from a Multicentre National Cohort Study. (PubMed, J Clin Med)
Within surgically treated patients, baseline CA19-9 emerged as the most informative prognostic marker, while traditional clinicopathologic variables showed limited discriminatory value. These findings highlight the importance of careful patient selection and support further prospective studies integrating molecular and biomarker-based strategies to refine prognostication and optimize surgical decision-making in RAS-WT mCRC.
Journal • Real-world evidence
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KRAS (KRAS proto-oncogene GTPase) • NRAS (Neuroblastoma RAS viral oncogene homolog) • MSI (Microsatellite instability) • RAS (Rat Sarcoma Virus) • CA 19-9 (Cancer antigen 19-9)
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KRAS wild-type • RAS wild-type • NRAS wild-type
7d
Baseline and Dynamic Neutrophil-to-Lymphocyte Ratio as Prognostic Biomarkers in Metastatic Colorectal Cancer Patients Treated with Panitumumab. (PubMed, J Pers Med)
Ion Chiricuta" between 2015 and 2024 with first-line FOLFOX/FOLFIRI plus panitumumab...In multivariate analysis, only bNLR remained independently associated with PFS. These results suggest that both baseline and dynamic NLR may serve as low-cost prognostic biomarkers in mCRC patients treated with anti-EGFR therapy.
Journal
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KRAS (KRAS proto-oncogene GTPase)
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KRAS wild-type • RAS wild-type
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5-fluorouracil • Vectibix (panitumumab) • irinotecan • leucovorin calcium
8d
Two cases of metastatic colorectal cancer in which epidermal growth factor receptor gene amplification benefited from panitumumab monotherapy. (PubMed, Int Cancer Conf J)
After receiving capecitabine monotherapy as first-line therapy, S-1 plus irinotecan plus bevacizumab therapy as second-line, trifluridine/tipiracil (FTD/TPI) monotherapy as third-line, and regorafenib monotherapy as fourth-line therapy, the patient received panitumumab monotherapy as fifth-line therapy...After receiving mFOLFOX6 plus panitumumab therapy as first-line therapy, FOLFIRI plus bevacizumab as second-line, he underwent conversion surgery...As third-line therapy, he received pembrolizumab monotherapy...We encountered two patients with mCRC and EGFR gene amplification who responded to panitumumab monotherapy. EGFR gene amplification may be a potential biomarker for anti-EGFR antibodies, regardless of RAS status.
Journal • Tumor mutational burden • PD(L)-1 Biomarker
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TMB (Tumor Mutational Burden)
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TMB-H • EGFR amplification • RAS mutation • RAS wild-type
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Keytruda (pembrolizumab) • Avastin (bevacizumab) • 5-fluorouracil • Vectibix (panitumumab) • capecitabine • Stivarga (regorafenib) • oxaliplatin • irinotecan • Lonsurf (trifluridine/tipiracil) • leucovorin calcium • Teysuno (gimeracil/oteracil/tegafur)
12d
New P3 trial
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RAS mutation • RAS wild-type
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Lonsurf (trifluridine/tipiracil)