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Cancer research papers

Nightly index of recent papers from PubMed, bioRxiv, and medRxiv. Filters are designed for both researcher precision and patient-friendly navigation.

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Starting focus

Cholangiocarcinoma

We’re indexing all cancers but highlighting cholangiocarcinoma while the evidence atlas expands.

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3 papersSorted by most recent
Peer-reviewedImpact 73

Topics

Treatment, Biology / Mechanism, Epidemiology

Modality

Targeted therapy, Imaging

Study type

Lab / Preclinical

Abstract

Although BRAF/MEK inhibitor (BRAFi/MEKi) therapy initially shows high efficacy in patients with BRAF V600 E/K cutaneous melanoma, resistance develops in over 75% of cases. We tested robustness of the umbrella trial strategy in this population by analyzing relationships between genomic status of a gene…

Authors

Vito W Rebecca, Min Xiao, Andrew Kossenkov, Tetiana Godok +23

AI-generated summary

Dasatinib resensitizes BRAF/MEK inhibitor efficacy in patient-derived xenografts from patients with progression on BRAF/MEK inhibitor treatment. reports: Although BRAF/MEK inhibitor (BRAFi/MEKi) therapy initially shows high efficacy in patients with BRAF V600 E/K cutaneous melanoma, resistance develops in over 75% of cases. We tested robustness of the umbrella trial strategy in this population by analyzing relationships between genomic status of a gene and associated downstream consequences at the protein level. The results revealed weak relationships among mutations, copy-number amplification, and protein expression and activation.

This summary may be inaccurate. Verify with the primary paper.

Primary source: PubMed.

BRAF/MEK Inhibition Induces Cell State Transitions Boosting Immune CheckpointSensitivity in BRAFV600E-mutant Glioma
cancer biology • 2025-04-01 • DOI: 10.1101/2023.02.03.526065 • Published in 10.1016/j.xcrm.2025.102183
PreprintImpact 55

Topics

Treatment, Outcomes / Survival

Modality

Immunotherapy, Targeted therapy, Cell therapy, Biomarker / Liquid biopsy, Imaging

Study type

Lab / Preclinical

Abstract

Resistance to BRAF plus MEK inhibition (BRAFi+MEKi) in BRAFV600E-mutant gliomas drives rebound, progression, and high mortality, yet it remains poorly understood. This study addresses the urgent need to develop treatments for BRAFi+MEKi-resistant glioma in novel mouse models and patient-derived materials. BRAFi+MEKi reveals glioma plasticity…

Authors

Xing, Y. L., Panovska, D., Park, J.-W., Grossauer, S. +23

AI-generated summary

BRAF/MEK Inhibition Induces Cell State Transitions Boosting Immune CheckpointSensitivity in BRAFV600E-mutant Glioma reports: Resistance to BRAF plus MEK inhibition (BRAFi+MEKi) in BRAFV600E-mutant gliomas drives rebound, progression, and high mortality, yet it remains poorly understood. This study addresses the urgent need to develop treatments for BRAFi+MEKi-resistant glioma in novel mouse models and patient-derived materials. BRAFi+MEKi reveals glioma plasticity by heightening cell state transitions along glial differentiation trajectories, giving rise to astrocyte- and immunomodulatory oligodendrocyte (OL)-like states. This is a preprint and not peer reviewed.

This summary may be inaccurate. Verify with the primary paper.

Primary source: bioRxiv (not peer reviewed).

Ethnicity-specific molecular alterations in MAPK and JAK/STAT pathways in early-onset colorectal cancer
genetic and genomic medicine • 2025-02-24 • DOI: 10.1101/2025.02.17.25322443 • Published in 10.3390/cancers17071093
PreprintImpact 53

Topics

Treatment, Biology / Mechanism, Outcomes / Survival, Prevention / Risk, Epidemiology

Modality

Targeted therapy, Imaging

Study type

Not listed

Abstract

Background/ObjectivesEarly-onset colorectal cancer (EOCRC), defined as colorectal cancer (CRC) diagnosed before the age of 50, has been increasing in incidence, particularly among Hispanic/Latino (H/L) populations. Despite this trend, the underlying molecular mechanisms driving EOCRC disparities remain poorly understood. The MAPK and JAK/STAT pathways play…

Authors

Monge, C., Waldrup, B., Carranza, F. G., Velazquez-Villarreal, E.

AI-generated summary

Ethnicity-specific molecular alterations in MAPK and JAK/STAT pathways in early-onset colorectal cancer reports: Background/ObjectivesEarly-onset colorectal cancer (EOCRC), defined as colorectal cancer (CRC) diagnosed before the age of 50, has been increasing in incidence, particularly among Hispanic/Latino (H/L) populations. Despite this trend, the underlying molecular mechanisms driving EOCRC disparities remain poorly understood. The MAPK and JAK/STAT pathways play critical roles in tumor progression, proliferation, and treatment response; however, their involvement in ethnicity-specific differences in EOCRC remains unclear. This is a preprint and not peer reviewed.

This summary may be inaccurate. Verify with the primary paper.

Primary source: medRxiv (not peer reviewed).