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Kopetz, S.

Publications and source records attributed to Kopetz, S..

At least 19 recordsLinked to original sources

Biological rationales from language models enable leakage-resistant forecasts of target-indication success

Identifying which target-indication (T-I) hypotheses can translate into clinical success remains a central challenge in drug discovery. We present PRIORITI (Prospective Rationale-Informed Outcome Reasoning for Integrated Target-indication Intelligence), a leakage-resistant framework that separates upstream biological evidence synthesis from outcome prediction. Given only a target gene and disease indication, a domain-instructed large language model (LLM) synthesizes drug-agnostic human genetics across prespecified channels. These evidence were embedded and combined with static entity context derived from gene summaries and disease definitions. The resulting representation is used to fit a supervised model trained on 6,784 temporally curated historical T-I outcomes, which is one of the largest cohorts assembled for this task. On a held-out historical test set of 1,696 T-I pairs, PRIORITI achieved a ROC-AUC of 0.883 and an expected calibration error (ECE) of 0.023, outperforming both a static target and indication context baseline and a human-curated genetic-evidence reference. On a strictly post-cutoff out-of-time benchmark of 765 T-I pairs, the largest such evaluation cohort reported to date, performance remained robust, with ROC-AUC 0.817, PR-AUC 0.357 and ECE 0.044, exceeding static target and indication context baseline and direct zero-shot LLM forecasting. A label-blinded LLM-based explainer further converted locked predictions into auditable prioritization rationales. Together, PRIORITI provides a calibrated, biology-first probability together with decision-oriented rationales for T-I prioritization before downstream translational investment.

bioinformatics↗

Ex vivo human tumor slices more accurately predict patient responses to an oncolytic virus than in vivo mouse models

Immunotherapies, including oncolytic viruses (OV), are promising therapies that can enhance anti-tumor immune responses. However, preclinical success of immunotherapies in mouse models has not always translated to clinical benefit in cancer patients. This study compared preclinical efficacy and mechanism of action for ASP9801, a vaccinia virus expressing IL-7 and IL-12, using mouse models of colorectal cancer (CRC) in vivo and in human organotypic tumor slice models ex vivo. The murine surrogate for ASP9801 significantly reduced tumor volumes in treated and abscopal tumors in two different CRC models in vivo (MC38 and RO100). Treatment efficacy was accentuated when combined with anti-PD1 treatment, and single-cell RNA sequencing analysis revealed depletion of tumor cells and increased T cell infiltration and activation in both treated and abscopal tumors. However, human tissue analysis ex vivo (E-slices) using PDX models and patient samples showed that ASP9801 is not effective in CRC, consistent with clinical trial results. On the other hand, ASP9801 was highly effective in GBM, indicating indication-specific efficacy of ASP9801, and how E-slice assays can be used to identify treatment-sensitive indications. This study demonstrates the superiority of E-slices over mouse models for predicting clinical response and its utility in planning clinical trials.

cancer biology↗

The Y chromosome gene KDM5D restrains CD8+ T cell antitumor immunity through TCR and cholesterol-exhaustion programs

Sex differences in immunity shape cancer risk, autoimmunity, and responses to immunotherapy, yet the sex-chromosome genes that regulate antitumor T cell function remain incompletely defined. Here, we identify the Y chromosome-encoded KDM5D histone demethylase as a male-specific suppressor of CD8+ T cell antitumor immunity. In murine colorectal cancer (CRC) models, male CD8+ T cells displayed reduced cytokine production, proliferation, cytotoxicity, TCR{beta} abundance, and proximal TCR signaling relative to female CD8+ T cells. CRISPR-RNP-mediated KDM5D depletion in male CD8+ T cells enhanced effector function, increased TCR{beta} expression, augmented TCR signaling, and improved tumor control after adoptive transfer. Transcriptomic and functional analyses further linked KDM5D to cholesterol biosynthesis and exhaustion-associated programs, with KDM5D depletion reducing SREBP2/XBP1-associated cholesterol and exhaustion signatures. Correspondingly, human CRC single-cell analyses supported the clinical relevance of this axis, showing enrichment of exhausted and cholesterol-associated CD8+ T cell states in male tumors. Pharmacologic inhibition of cholesterol biosynthesis with lovastatin partially attenuated select exhaustion-associated markers in male CD8+ T cells and delayed tumor growth in vivo. Together, these findings define KDM5D as a sex chromosome-encoded regulator of male CD8+ T cell dysfunction and point to cholesterol-exhaustion programs as a potential therapeutic vulnerability in male CRC.

cancer biology↗

Tumor cell specific total mRNA expression informed neural networks predicts cancer progression

Inferring tumor molecular phenotypes from high-dimensional multi-omic data is a fundamental challenge in computational biology. Current methods for estimating tumor cell-specific total mRNA expression (TmS) require matched DNA and RNA sequencing data and rely on computationally intensive deconvolution pipelines. We present TmSNet, a deep learning framework that predicts TmS using mRNA, DNA methylation, miRNA, and immune cell proportions as input features. TmSNet integrates structured feature selection (gradient boosting, LASSO, elastic net) with specialized neural architectures to predict continuous TmS. Across 12 TCGA cancer types, TmSNet achieved cross-validated performance up to concordance correlation coefficient (CCC) = 0.93 and correlation R{superscript 2} = 0.88 and generalized to external cohorts with correlations of 0.54 (SCAN-B) and 0.43 (FUSCC). Predicted TmS values effectively stratify patients by risk and preserve known transcriptional profiles across tumor subtypes. These results demonstrate that TmSNet can infer biologically meaningful phenotypes from multi-omic data and provide a scalable framework for modeling tumor transcriptional activity in heterogeneous cohorts.

bioinformatics↗

Functional modules predict cancer-relevant genetic interactions in mammalian cells

Genetic interactions can reveal gene function and identify disease-relevant synthetic lethals, but resource-intensive screening in human cells constrains experimental scope and limits our understanding of how generalizable sparse hits are. Here, we leverage principles from yeast genetic networks to identify human gene modules involved in receptor tyrosine kinase signaling and DNA damage response that are predicted to be enriched for genetic interactions, then use our enCas12a-based In4mer combinatorial knockout platform to efficiently screen these modules across diverse cancer cell lines. We identify hundreds of unreported synthetic lethals, including a dense network within the protein N-linked glycosylation machinery that shows both evolutionary conservation and network rewiring, and we confirm that interactions discovered in 2D cell culture are maintained in more physiologically relevant models. Critically, a meta-analysis within and between screens highlights sources of variation in published results, reveals the potential for false positives in screens with many essential genes, and demonstrates the need to move beyond DDR for actionable synthetic lethalities.

systems biology↗

Deconvolution of Sparse-count RNA Sequencing Data for Tumor Cells Using Embedded Negative Binomial Distributions

Estimating tumor-specific transcript proportions from mixed bulk samples has potential to inform novel biology. However, estimation accuracy using existing methods in sparse-count data such as microRNA-seq and spatial transcriptomics has yet to be established. We generated a mixed small RNA benchmark dataset to demonstrate analytical challenges. To resolve them, we developed DeMixNB, a semi-reference-based deconvolution model assuming a sum of negative binomial distributions. Applications to miRNA-seq from 856 patients with breast cancer and 3,755 spatial spots from lung cancer generated either clinical or mechanistic insights into tumor cell plasticity. This supports the important utility of DeMixNB to investigate cancer RNomes.

bioinformatics↗

Cooperativity between Ras pathway mutations in colonic tumorigenesis

The Kirsten rat sarcoma (KRAS) gene is the most frequently mutated oncogene in colorectal cancer (CRC). We previously characterized two activating alleles of KRAS, A59T and A59E, that show impaired BRAF dimerization. These alleles of KRAS are enriched in CRC tumors with genetic alterations in genes that regulate MAPK signaling (e.g. EGFR, NF1). Using a new conditional mouse model of K-Ras (LSL-K-Ras A59E) we show that, despite its inability to universally activate RAF kinases, K-Ras A59E disturbs colon epithelium and decreases mouse survival in a tumor model. By combining LSL-K-Ras A59E mice with a conditional knockout of Nf1, we demonstrate cooperation between these alleles at multiple levels. Consistent with cooperation and clinical observations, we show that K-Ras A59E neither promotes EGF independence of organoid growth, nor confers intrinsic resistance to EGFR inhibition. Thus, our data provide a deeper understanding of the role of RAF isoforms in mutant KRAS driven CRC and argue for the use of anti-EGFR therapies against some Ala59 mutant alleles of KRAS. Statement of significanceOur studies on oncogenic K-RAS mutants demonstrate that the biochemical properties of a mutant oncoprotein are reflected in the somatic genetics of cancer, in particular in the cooperating mutations that occur. These mutant-specific genetic interactions influence therapeutic responses. As such, KRAS mutation may not be a univariate predictor of response to EGFR inhibition.

cancer biology↗

Reprogramming of Cellular Plasticity via ETS and MYC Core-regulatory Circuits During Response to MAPK Inhibition in BRAF-mutant Colorectal Cancer

BackgroundAberrant enhancer dynamics play a critical role in the initiation and progression of colorectal cancer (CRC). BRAFV600E-mutated metastatic CRC may be a unique subtype, exhibiting a strong epigenetic phenotype. Interestingly, bromodomain 2, a reader protein for H3K27ac-marked enhancers, was found to be synthetically lethal in CRC with BRAF + EGFR inhibition. DesignWe evaluated the effectiveness of targeting aberrant enhancers with bromodomain and extraterminal (BET) + MAPK pathway inhibitors in patient-derived xenograft models of metastatic CRC, followed by comprehensive profiling of transcriptomic and chromatin dynamics upon BET inhibitor combination treatment. ResultsThe combination of BET and standard MAPK inhibitors has demonstrated improved efficacy against BRAFV600E CRC and selective improvements against RAS-mutant CRC in vivo. We showed that BET + MAPK inhibition induced a profound downregulation of the MAPK signaling pathway compared to MAPK inhibition alone. The loss of activation signal on enhancers, as determined by H3K27ac, led to dysregulation of core-regulatory circuitries of CRC, especially loss of the auto-regulatory mechanism of the MAPK downstream E26 transformation-specific transcription factor family. Single nucleus multiome (RNA + ATAC) sequencing further distinguished differential transcriptomic and chromatin dynamics at cell type levels. Profound downregulation of well-differentiated cell types confirmed deep inhibition of MAPK signaling and downstream transcription factors. On the other hand, dedifferentiated cell populations were abundant after MAPK or combination inhibition, suggesting therapy-induced cell state switching and adaptation. ConclusionWe are evaluating BET + BRAF + EGFR inhibition in patients with treatment-refractory BRAFV600E metastatic CRC. ClinicalTrial.gov identifier: NCT06102902. What is already known on this topicEnhancer aberrations emerge as critical epigenetic features in the progression of colorectal cancer (CRC). However, the dynamics of active enhancer and the therapeutic potential of enhancer blockade, particularly in CRC tumors with BRAFV600E mutation, is not well understood. What this study addsThis study demonstrates improved efficacy of BET inhibitor combination therapies in diverse patient-derived models and reveals epigenetic reprogramming driven cellular plasticity in BRAFV600E-mutated CRC. How this study might affect research, practice or policyOur findings support treatment with BET + BRAF + EGFR inhibitors for patients with BRAFV600E-mutant mCRC [NCT06102902]. This study also highlights the potential of combining epigenetic agents to standard targeted therapy, offering a novel treatment option for this subset of patients.

cancer biology↗

IL-1R1 Blockade Enhances CD40 Agonist-Mediated Immune Responses but Fails to Increase Efficacy or Mitigate Hepatotoxicity in Pancreatic Cancer

Pancreatic ductal adenocarcinoma (PDAC) has a poor survival rate and limited treatments. Agonistic CD40 antibodies are promising, but clinical trials have shown only modest efficacy and significant hepatotoxicity. We previously reported that IL-1 pathway blockade enhances agonistic CD40 antibody efficacy against melanoma by depleting polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs; CD11b+Ly6C+Ly6G+). Because PMN-MDSCs also cause liver toxicity, we investigated the impact of IL-1R1 blockade on the efficacy and toxicity of agonistic CD40 antibody therapy in PDAC. Agonistic CD40 antibody therapy induced immune activation and significantly prolonged survival in orthotopic PDAC-bearing mice. IL-1R1 blockade monotherapy downregulated innate and adaptive immune response and exacerbated tumor growth. Although combination therapy upregulated several immune-related pathways and boosted innate and adaptive immune responses. IL-1R1 blockade failed to improve the overall antitumor efficacy of agonistic CD40 antibody therapy and exacerbated liver toxicity. Ly6G+ cell depletion in mice reduced the efficacy of agonistic CD40 antibody therapy, suggesting that Ly6G immune cells (PMN-MDSCs or neutrophils) exhibit an antitumor rather than immunosuppressive role in PDAC. Our findings underscore the complex role of IL-1 signaling in modulating immune responses in PDAC and caution against pursuing IL-1R1 blockade, either as monotherapy or combined with agonistic CD40 antibodies, in clinical trials for PDAC.

cancer biology↗

Adaptive Plasticity Tumor Cells Modulate MAPK-Targeting Therapy Response in Colorectal Cancer

MAPK pathway inhibitors (MAPKi) are increasingly used in the treatment of advanced colorectal cancer, but often produce short-lived responses in patients. Although acquired resistance by de novo mutations in tumors have been found to reduce response in some patients, additional mechanisms underlying the limited response durability of MAPK targeting therapy remain unknown. Here, we denote new contributory tumor biology and provide insight on the impact of tumor plasticity on therapy response. Analysis of MAPKi treated patients revealed activation of stemness programs and increased ASCL2 expression, which are associated with poor outcomes. Greater ASCL2 with MAPKi treatment was also seen in patient-derived CRC models, independent of driver mutations. We find ASCL2 denotes a distinct cell population, arising from phenotypic plasticity, with a proliferative, stem-like phenotype, and decreased sensitivity to MAPKi therapy, which were named adaptive plasticity tumor (APT) cells. MAPK pathway suppression induces the APT phenotype in cells, resulting in APT cell enrichment in tumors and limiting therapy response in preclinical and clinical data. APT cell depletion improved MAPKi treatment efficacy and extended MAPKi response durability in mice. These findings uncover a cellular program that mitigates the impact of MAPKi therapies and highlights the importance of addressing tumor plasticity to improve clinical outcomes.

cancer biology↗

Enhancing efficacy of the MEK inhibitor trametinib with paclitaxel in KRAS-mutated colorectal cancer

BackgroundKRAS is frequently mutated in the tumors of patients with metastatic colorectal cancer (mCRC) and thus represents a valid target for therapy. However, the strategies of targeting KRAS directly and targeting the downstream effector mitogen-activated protein kinase kinase (MEK) via monotherapies have shown limited efficacy. Thus, there is a strong need for novel, effective combination therapies to improve MEK-inhibitor efficacy in patients with KRAS-mutated mCRC. ObjectiveOur objective was to identify novel drug combinations that enhance MEK-inhibitor efficacy in patients with KRAS-mutated mCRC. DesignIn this study, we performed unbiased high-throughput screening (HTS) to identify drugs that enhance the efficacy of MEK inhibitors in vitro, and we validated the efficacy of the drugs in vivo. MethodsHTS was performed using 3-dimensional CRC spheroids. Trametinib, the anchor drug, was probed with 2 clinically ready libraries of 252 drugs to identify effective drug combinations. The effects of the drug combinations on CRC cell proliferation and apoptosis were further validated using cell growth assays, flow cytometry, and biochemical assays. Proteomic and immunostaining studies were performed to determine the effects of the drugs on molecular signaling and cell division. The effects of the drug combinations were examined in vivo using CRC patient-derived xenografts. ResultsHTS identified paclitaxel as being synergistic with trametinib. In vitro validation showed that, compared with monotherapies, this drug combination demonstrated strong inhibition of cell growth, reduced colony formation, and enhanced apoptosis in multiple KRAS-mutated CRC cell lines. Mechanistically, combining trametinib with paclitaxel led to alterations in signaling mediators that block cell cycle progression and increases in microtubule stability that resulted in significantly higher defects in the mitosis. Finally, the combination of trametinib with paclitaxel exhibited significant inhibition of tumor growth in several KRAS-mutant patient-derived xenograft mouse models. ConclusionOur data provide evidence supporting clinical trials of trametinib with paclitaxel as a novel therapeutic option for patients with KRAS-mutated, metastatic CRC.

cancer biology↗

Therapeutic targeting of Syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers

The therapeutic benefit of recently developed mutant KRAS (mKRAS) inhibitors has been limited by the rapid onset of resistance. Here, we aimed to delineate the mechanisms underlying acquired resistance to mKRAS inhibition and identify actionable targets for overcoming this clinical challenge. Previously, we identified Syndecan-1 (SDC1) as a key effector for pancreatic cancer progression whose surface expression is driven by mKRAS. By leveraging both pancreatic and colorectal cancer models, we found that surface SDC1 expression was initially diminished upon mKRAS inhibition, but recovered in tumor cells that bypass mKRAS dependency. Functional studies showed that these tumors depended on SDC1 for survival, further establishing SDC1 as a driver for the acquired resistance to mKRAS inhibition. Mechanistically, we revealed that the YAP1-SDC1 axis was the major driving force for bypassing mKRAS dependency to sustain nutrient salvage machinery and tumor maintenance. Specifically, YAP1 activation mediated the recovery of SDC1 localization on cell surface that sustained macropinocytosis and enhanced the activation of multiple RTKs, promoting resistance to KRAS-targeted therapy. Overall, our study has provided the rationale for targeting the YAP-SDC1 axis to overcome resistance to mKRAS inhibition, thereby revealing new therapeutic opportunities for improving the clinical outcome of patients with KRAS-mutated cancers.

cancer biology↗

Pan-cancer subclonal mutation analysis of 7,827 tumors predicts clinical outcome

Intra-tumor heterogeneity is characterized by a diverse population of tumor clones and subclones which are important drivers of tumor evolution and therapeutic response. However, accurate subclonal reconstruction at scale remains challenging. We developed a machine learning tool, CliPP, and surveyed 9,972 tumors from 32 cancer types. We found that high subclonal mutation load (sML), the fraction of subclonal single nucleotide variants (SNVs) to all SNVs in the coding region, was prognostic of survival (progression free survival or overall survival) in 18 cancer types. In 14 cancers with low to moderate tumor mutation burden (TMB), high sML was associated with better prognosis. In immunotherapy trials for 42 metastatic prostate cancer (mCRPC), high sML was predictive of favorable response to ipilimumab and associated with increased CD8+ T-cell infiltration and decreased macrophage population. A validation using 613 whole-genomes of esophageal adenocarcinoma confirms the favorable effect of high sML and the observed tumor-associated macrophage. Our study identifies sML as a key feature of cancer, suggesting a biphasic relationship between evolutionary dynamics and differential immune environments. Finally, sML may serve as an orthogonal approach to identify likely responders of immune checkpoint blockade in low to moderate TMB tumors.

genomics↗

Oncogenic KRAS Mutations Confer a Unique Mechanotransduction Response to Peristalsis in Colorectal Cancer Cells

Colorectal cancer (CRC) tumors start as precancerous polyps on the inner lining of the colon or rectum, where they are exposed to the mechanics of colonic peristalsis. Our previous work leveraged a custom-built peristalsis bioreactor to demonstrate that colonic peristalsis led to cancer stem cell enrichment in colorectal cancer cells. However, this malignant mechanotransductive response was confined to select CRC lines that harbored an oncogenic mutation in the KRAS gene. In this work, therefore, we explored the involvement of activating KRAS mutations on peristalsis-associated mechanotransduction in CRC. Peristalsis enriched the cancer stem cell marker LGR5 in KRAS mutant (G13D, etc.) lines, in a Wnt-independent manner. Conversely, LGR5 enrichment in wild type KRAS lines exposed to peristalsis were minimal. LGR5 enrichment downstream of peristalsis translated to increased tumorigenicity in vivo in KRAS mutant vs. wild type lines. Differences in mechanotransduction response was additionally apparent via unbiased gene set enrichment analysis, where many unique pathways were enriched in wild type vs. mutant lines, in response to peristalsis. Interestingly, peristalsis also triggered {beta}-catenin nuclear localization independent of Wnt, particularly in KRAS mutant lines. The central involvement of KRAS in the mechanotransductive responses was validated via gain and loss of function strategies. {beta}-catenin activation and LGR5 enrichment downstream of peristalsis converged to the activation of the MEK/ERK kinase cascade, that remains active in cells that harbor oncogenic KRAS mutations. Taken together, our results demonstrated that oncogenic KRAS mutations conferred a unique peristalsis-associated mechanotransduction response to colorectal cancer cells, resulting in cancer stem cell enrichment and increased tumorigenicity. These mechanosensory connections can be leveraged in improving the sensitivity of emerging therapies that target oncogenic KRAS.

bioengineering↗

The DeMixSC deconvolution framework uses single-cell sequencing plus a small benchmark dataset for improved analysis of cell-type ratios in complex tissue samples

Bulk deconvolution with single-cell/nucleus RNA-seq data is critical for understanding heterogeneity in complex biological samples, yet the technological discrepancy across sequencing platforms limits deconvolution accuracy. To address this, we introduce an experimental design to match inter-platform biological signals, hence revealing the technological discrepancy, and then develop a deconvolution framework called DeMixSC using the better-matched, i.e., benchmark, data. Built upon a novel weighted nonnegative least-squares framework, DeMixSC identifies and adjusts genes with high technological discrepancy and aligns the benchmark data with large patient cohorts of matched-tissue-type for large-scale deconvolution. Our results using a benchmark dataset of healthy retinas suggest much-improved deconvolution accuracy. Further analysis of a cohort of 453 patients with age-related macular degeneration supports the broad applicability of DeMixSC. Our findings reveal the impact of technological discrepancy on deconvolution performance and underscore the importance of a well-matched dataset to resolve this challenge. The developed DeMixSC framework is generally applicable for deconvolving large cohorts of disease tissues, and potentially cancer.

bioinformatics↗

The oncogenic role of Streptococcus gallolyticus subsp. gallolyticus is linked to activation of multiple cancer-related signaling pathways

Streptococcus gallolyticus subsp. gallolyticus (SGG), an opportunistic gram-positive pathogen responsible for septicemia and endocarditis in the elderly, is often associated with colon cancer (CRC). In this work, we investigated the oncogenic role of SGG strain UCN34 using the azoxymethane (AOM)-induced CRC model in vivo, organoid formation ex vivo and proteomic and phosphoproteomic analyses from murine colons. We showed that SGG UCN34 accelerates colon tumor development in the murine CRC model. Full proteome and phosphoproteome analysis of murine colons chronically colonized by SGG UCN34 or the closely related non-pathogenic S. gallolyticus subsp. macedonicus (SGM) revealed that 164 proteins and 725 phosphorylation sites were differentially regulated following colonization by SGG UCN34. Ingenuity Pathway Analysis (IPA) indicates a pro-tumoral shift specifically induced following colonization by SGG UCN34, as most proteins and phosphoproteins identified were associated with digestive cancer. Comprehensive analysis of the altered phosphoproteins using ROMA software revealed significantly elevated activities in several cancer hallmark pathways affecting tumoral cells and their microenvironment, i.e. MAPK (ERK, JNK and p38), mTOR and integrin/ILK/actin signaling, in SGG UCN34 colonized colon. Importantly, analysis of protein arrays of human colon tumors colonized with SGG showed up-regulation of PI3K/Akt/mTOR and MAPK pathways, providing clinical relevance to our findings. To test SGGs capacity to induce pre-cancerous transformation of the murine colonic epithelium, we grew ex vivo organoids which revealed unusual structures with compact morphology following exposure to SGG. Taken together, our results reveal that the oncogenic role of SGG UCN34 is associated with activation of multiple cancer-related signaling pathways. Author SummaryColorectal cancer is the third most common cause of cancer mortality worldwide. The colon is a very singular organ, colonized by a vast and complex community of microorganisms, known as the gut microbiota. Strong evidence supports a role of the microbiota in colon cancer development. Streptococcus gallolyticus subsp. gallolyticus (SGG), a gut commensal, was one of the first bacteria to be associated with colorectal cancer. A better understanding of the role of SGG in colon cancer development is critical to developing novel strategies to improve clinical diagnosis and treatment of this disease. Here, using a global proteomic analysis of mouse colonic tissue colonized by SGG, we show that over 90% of the proteins with altered levels are involved in cancer. SGG colonization promotes autocrine and paracrine pro-tumor signals contributing to transformation of the colonic epithelium but also modifying the stromal microenvironment, which in turn sustains tumor development. Importantly, two tumor hallmark pathways (PI3K/Akt/mTOR and MAPK) identified in our mouse model were also found in human colon tumor biopsies colonized by SGG, strengthening the clinical relevance to our study.

microbiology↗

Combined KRASG12C and SOS1 inhibition enhances and extends the anti-tumor response in KRASG12C-driven cancers by addressing intrinsic and acquired resistance

Efforts to improve the anti-tumor response to KRASG12C targeted therapy have benefited from leveraging combination approaches. Here, we compare the anti-tumor response induced by the SOS1-KRAS interaction inhibitor, BI-3406, combined with a KRASG12C inhibitor (KRASG12Ci) to those induced by KRASG12Ci alone or combined with SHP2 or EGFR inhibitors. In lung cancer and colorectal cancer (CRC) models, BI-3406 plus KRASG12Ci induces an anti-tumor response stronger than that observed with KRASG12Ci alone and comparable to those by the other combinations. This enhanced anti-tumor response is associated with a stronger and extended suppression of RAS-MAPK signaling. Importantly, BI-3406 plus KRASG12Ci treatment delays the emergence of acquired adagrasib resistance in both CRC and lung cancer models and is associated with re-establishment of anti-proliferative activity in KRASG12Ci-resistant CRC models. Our findings position KRASG12C plus SOS1 inhibition therapy as a promising strategy for treating both KRASG12C-mutated tumors as well as for addressing acquired resistance to KRASG12Ci.

cancer biology↗

Chromatin Remodeling in Patient-Derived Colorectal Cancer Models

Patient-Derived Organoids (PDO) and Xenografts (PDX) are the current gold standards for patient derived models of cancer (PDMC). Nevertheless, how patient tumor cells evolve in these models and the impact on drug response remains unclear. Herein, we compared the transcriptomic and chromatin accessibility landscapes of six matched sets of colorectal cancer (CRC) PDO, PDX, PDO-derived PDX (PDOX), and original patient tumors (PT) and discovered two major remodeling axes. The first axis delineates PDX and PDO from PT, and the second axis distinguishes PDX and PDO. PDOX were more similar to PDX than they were to PDO, indicating that the growth environment is a driving force for chromatin adaptation. Using bivariate genomic footprinting analysis, we identified transcription factors (TF) that differentially bind to open chromatins between matched PDO and PDOX. Among them, KLF14 and EGR2 footprints were enriched in all six PDOX relative to matched PDO, and silencing of KLF14 or EGR2 promoted tumor growth. Furthermore, EPHA4, a shared downstream target gene of KLF14 and EGR2, altered tumor sensitivity to MEK inhibitor treatment. Altogether, patient-derived CRC cells undergo both common and distinct chromatin remodeling in PDO and PDX/PDOX, driven largely by their respective microenvironments, which results in differences in growth and drug sensitivity and needs to be taken into consideration when interpreting their ability to predict clinical outcome.

cancer biology↗