John V. Heymach
A5048380048- Lung Cancer Treatments and Mutations
- Cancer Immunotherapy and Biomarkers
- Cancer Genomics and Diagnostics
- Lung Cancer Research Studies
- RNA modifications and cancer
- Colorectal Cancer Treatments and Studies
- Lung Cancer Diagnosis and Treatment
- Radiomics and Machine Learning in Medical Imaging
- Pancreatic and Hepatic Oncology Research
- Cancer, Hypoxia, and Metabolism
- Ferroptosis and cancer prognosis
- Peptidase Inhibition and Analysis
- HER2/EGFR in Cancer Research
- Genetic factors in colorectal cancer
- Cancer-related Molecular Pathways
- Immunotherapy and Immune Responses
- Phagocytosis and Immune Regulation
- CAR-T cell therapy research
- Angiogenesis and VEGF in Cancer
- Cancer therapeutics and mechanisms
- Neuroendocrine Tumor Research Advances
- Hepatocellular Carcinoma Treatment and Prognosis
- Cancer Mechanisms and Therapy
- Cancer Cells and Metastasis
- Chronic Lymphocytic Leukemia Research
The University of Texas MD Anderson Cancer Center
2016-2025
Scripps MD Anderson Cancer Center
2018-2025
Moffitt Cancer Center
2025
RELX Group (United States)
2024
Faculty of 1000 (United States)
2024
University of Tampa
2024
Brigham and Women's Hospital
2004-2023
Harvard University
2004-2023
Texas Medical Center
2023
Centre for Cancer Biology
2023
Abstract KRAS is the most common oncogenic driver in lung adenocarcinoma (LUAC). We previously reported that STK11/LKB1 (KL) or TP53 (KP) comutations define distinct subgroups of KRAS-mutant LUAC. Here, we examine efficacy PD-1 inhibitors these subgroups. Objective response rates to blockade differed significantly among KL (7.4%), KP (35.7%), and K-only (28.6%) (P < 0.001) Stand Up To Cancer (SU2C) cohort (174 patients) with LUAC patients treated nivolumab CheckMate-057 phase III...
Our previously published findings reported that local consolidative therapy (LCT) with radiotherapy or surgery improved progression-free survival (PFS) and delayed new disease in patients oligometastatic non-small-cell lung cancer (NSCLC) did not progress after front-line systemic therapy. Herein, we present the longer-term overall (OS) results accompanied by additional secondary end points.
Epithelial-mesenchymal transition (EMT) has been associated with metastatic spread and EGF receptor (EGFR) inhibitor resistance. We developed validated a robust 76-gene EMT signature using gene expression profiles from four platforms non-small cell lung carcinoma (NSCLC) lines patients treated in the Biomarker-Integrated Approaches of Targeted Therapy for Lung Cancer Elimination (BATTLE) study.We conducted an integrated expression, proteomic, drug response analysis tumors NSCLC. A was...
Cancers are composed of populations cells with distinct molecular and phenotypic features, a phenomenon termed intratumor heterogeneity (ITH). ITH in lung cancers has not been well studied. We applied multiregion whole-exome sequencing (WES) on 11 localized adenocarcinomas. All tumors showed clear evidence ITH. On average, 76% all mutations 20 out 21 known cancer gene were identified regions individual tumors, which suggested that single-region may be adequate to identify the majority With...
The Biomarker-integrated Approaches of Targeted Therapy for Lung Cancer Elimination (BATTLE) trial represents the first completed prospective, biopsy-mandated, biomarker-based, adaptively randomized study in 255 pretreated lung cancer patients. Following an initial equal randomization period, chemorefractory non-small cell (NSCLC) patients were to erlotinib, vandetanib, erlotinib plus bexarotene, or sorafenib, based on relevant molecular biomarkers analyzed fresh core needle biopsy...
The molecular underpinnings that drive the heterogeneity of KRAS-mutant lung adenocarcinoma are poorly characterized. We performed an integrative analysis genomic, transcriptomic, and proteomic data from early-stage chemorefractory identified three robust subsets dominated, respectively, by co-occurring genetic events in STK11/LKB1 (the KL subgroup), TP53 (KP), CDKN2A/B inactivation coupled with low expression NKX2-1 (TTF1) transcription factor (KC). further revealed biologically...
Abstract Despite recent advances in the use of immunotherapy, only a minority patients with small cell lung cancer (SCLC) respond to immune checkpoint blockade (ICB). Here, we show that targeting DNA damage response (DDR) proteins PARP and kinase 1 (CHK1) significantly increased protein surface expression PD-L1. or CHK1 inhibition remarkably potentiated antitumor effect PD-L1 augmented cytotoxic T-cell infiltration multiple immunocompetent SCLC vivo models. CD8+ depletion reversed effect,...
Abstract Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors gefitinib and erlotinib are effective treatments for a subset of non–small cell lung cancers. In particular, cancers with specific EGFR-activating mutations seem to be the most sensitive these agents. However, despite their initial response, such almost invariably develop resistance. 50% cancers, secondary EGFR mutation, T790M, has been identified that renders ineffective activity. Thus, there is clinical need novel...
A splice-site mutation that results in a loss of transcription exon 14 the oncogenic driver MET occurs 3 to 4% patients with non-small-cell lung cancer (NSCLC). We evaluated efficacy and safety tepotinib, highly selective inhibitor, this patient population. In open-label, phase 2 study, we administered tepotinib (at dose 500 mg) once daily advanced or metastatic NSCLC confirmed skipping mutation. The primary end point was objective response by independent review among who had undergone at...
A MESSAGE FROM ASCO’S PRESIDENT I am pleased to present Clinical Cancer Advances 2017, which highlights the most promising advances in patient-oriented cancer research over past year. The report gives us an opportunity reflect on what exciting time it is for and how swiftly our understanding of has improved. One year ago, White House announced national Moonshot program accelerate progress against cancer. This shared vision reinvigorated community, identified new areas scientific...
Abstract STK11/LKB1 is among the most commonly inactivated tumor suppressors in non–small cell lung cancer (NSCLC), especially tumors harboring KRAS mutations. Many oncogenes promote immune escape, undermining effectiveness of immunotherapies, but it unclear whether inactivation suppressor genes, such as STK11/LKB1, exerts similar effects. In this study, we investigated consequences loss on microenvironment a mouse model KRAS-driven NSCLC. Genetic ablation resulted accumulation neutrophils...
Abstract Small cell lung cancer (SCLC) is an aggressive malignancy distinct from non–small (NSCLC) in its metastatic potential and treatment response. Using integrative proteomic transcriptomic analysis, we investigated molecular differences contributing to the clinical behavior of SCLCs NSCLCs. showed lower levels several receptor tyrosine kinases decreased activation phosphoinositide 3-kinase (PI3K) Ras/mitogen-activated protein (MAP)/extracellular signal–regulated kinase (ERK) (MEK)...
Mutations in the v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) play a critical role cancer cell growth and resistance to therapy. Most mutations occur at codons 12 13. In colorectal cancer, presence of any mutant KRas amino acid substitution is negative predictor patient response targeted However, non–small lung (NSCLC), evidence that KRAS mutation predictive factor conflicting. We used data from molecularly clinical trial for 215 patients with tissues available out 268...
Purpose We investigated the efficacy of fluorouracil (FU), leucovorin, irinotecan, and bevacizumab (FOLFIRI + B) in a phase II trial patients previously untreated for metastatic colorectal cancer (mCRC), changes during treatment plasma cytokines angiogenic factors (CAFs) as potential markers response therapeutic resistance. Patients Methods conducted II, two-institution FOLFIRI B. Each 14-day cycle consisted (5 mg/kg), irinotecan (180 mg/m 2 ), bolus FU (400 leucovorin ) followed by 46-hour...
EGFR is frequently mutated and amplified in lung adenocarcinomas sensitive to inhibitors gefitinib erlotinib. A secondary mutation, T790M, has been associated with acquired resistance but not shown be sufficient render mutant/amplified cancers resistant inhibitors. We created a model for studying by prolonged exposure of gefitinib-sensitive carcinoma cell line (H3255; amplified) vitro. The resulting T790M mutation small fraction the alleles that was undetected direct sequencing identified...
We previously demonstrated the association between epithelial-to-mesenchymal transition (EMT) and drug response in lung cancer using an EMT signature derived cell lines. Given contribution of tumor microenvironments to EMT, we extended our investigation patient tumors from 11 types develop a pan-cancer signature.Using signature, conducted integrated, global analysis genomic proteomic profiles associated with across 1,934 including breast, lung, colon, ovarian, bladder cancers. Differences...