Cancer Research

Oncotarget

Oncotarget published this research paper on August 3, 2022 in Volume 13, entitled, "Glypican-3 (GPC3) is associated with MCPyV-negative status and impaired outcome in Merkel cell carcinoma" by researchers from SOTIO Biotech Inc., Cambridge, MA; Department of Dermatology, University Hospital of Tours, France.

DOI - https://doi.org/10.18632/oncotarget.28260

Correspondence to - Glen J. Weiss - weiss@sotio.com, and Mahtab Samimi - mahtab.samimi@univ-tours.fr
Abstract

Introduction: Merkel cell carcinoma (MCC) is an aggressive skin cancer, related to the Merkel Cell Polyomavirus (MCPyV) in 80% of cases. Immune checkpoint inhibitors provide sustained benefit in about 50% of MCC patients with advanced disease. Glypican-3 (GPC3) is an oncofetal tumor antigen that is an attractive target for chimeric antigen receptor T cell therapy due to its highly restricted expression on normal tissue and high prevalence in several solid tumors. GPC3 is known to be expressed in MCC but its association with tumor characteristics or prognosis has not been reported. We investigated MCC GPC3 expression by immunohistochemistry (IHC) and its association with tumor characteristics, MCPyV status, and patient outcome.

Methods: The GC33 antibody clone was validated for GPC3 IHC staining of tumor specimens in comparison to an established GPC3 IHC antibody. An MCC tissue microarray was stained for GPC3 by IHC using GC33 antibody. Association of GPC3+ IHC with baseline characteristics, MCPyV status (qPCR) and outcome (death from MCC/recurrence) were assessed.

Results: Forty-two of 62 samples (67.7%) were GPC3+. GPC3 expression was more frequently observed in females (p = 0.048) and MCPyV-negative tumors (p = 0.021). By multivariate analysis, GPC3 expression was associated with increased death from disease (CSS) (hazard ratio [HR] 4.05, 95% CI 1.06–15.43), together with advanced age (HR 4.85, 95% CI 1.39–16.9) and male gender (HR 4.64, 95% CI 1.31–16.41).

Conclusions: GPC3 expression is frequent in MCC tumors, especially MCPyV-negative cases, and is associated with increased risk of death. High prevalence of surface GPC3 makes it a putative drug target.

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Press release - https://www.oncotarget.com/news/pr/oncotarget-glypican-gpc-is-associated-with-mcpyv-negative-status-and-impaired-outcome-in-merkel-cell-carcinoma/

Keywords - Merkel cell carcinoma, glypican-3, Merkel cell polyomavirus, outcome

About Oncotarget

Oncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Trending With Impact: GPC3 Associated With MCPyV-negative Status and Impaired Outcome in Merkel Cell Carcinoma

Oncotarget published this priority research paper on August 3, 2022 in Volume 13, entitled, "A novel mechanism of regulation of the oncogenic transcription factor GLI3 by toll-like receptor signaling" by researchers from the Deparment of Molecular, Cellular and Biomedical Sciences, University of New Hampshire, Durham, NH; Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX; Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX.

DOI - https://doi.org/10.18632/oncotarget.28261

Correspondence to - Sherine F. Elsawa - sherine.elsawa@unh.edu

Abstract

The transcription factor GLI3 is a member of the GLI family and has been shown to be regulated by canonical hedgehog (HH) signaling through smoothened (SMO). Little is known about SMO-independent regulation of GLI3. Here, we identify TLR signaling as a novel pathway regulating GLI3 expression. We show that GLI3 expression is induced by LPS/TLR4 in human monocyte cell lines and peripheral blood CD14+ cells. Further analysis identified TRIF, but not MyD88, signaling as the adapter used by TLR4 to regulate GLI3. Using pharmacological and genetic tools, we identified IRF3 as the transcription factor regulating GLI3 downstream of TRIF. Furthermore, using additional TLR ligands that signal through TRIF such as the TLR4 ligand, MPLA and the TLR3 ligand, Poly(I:C), we confirm the role of TRIF-IRF3 in the regulation of GLI3. We found that IRF3 directly binds to the GLI3 promoter region and this binding was increased upon stimulation of TRIF-IRF3 with Poly(I:C). Furthermore, using Irf3−/− MEFs, we found that Poly(I:C) stimulation no longer induced GLI3 expression. Finally, using macrophages from mice lacking Gli3 expression in myeloid cells (M-Gli3−/−), we found that in the absence of Gli3, LPS stimulated macrophages secrete less CCL2 and TNF-α compared with macrophages from wild-type (WT) mice. Taken together, these results identify a novel TLR-TRIF-IRF3 pathway that regulates the expression of GLI3 that regulates inflammatory cytokines and expands our understanding of the non-canonical signaling pathways involved in the regulation of GLI transcription factors.

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Keywords - GLI3, inflammation, TLR, cancer research

About Oncotarget

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Paper Spotlight: Novel Regulatory Mechanism of GLI3 by Toll-like Receptor Signaling

Oncotarget published this research paper on July 28, 2022 in Volume 13, entitled, "Diverse geroprotectors differently affect a mechanism linking cellular aging to cellular quiescence in budding yeast" by researchers from the Department of Biology, Concordia University, Montreal, Quebec H4B 1R6, Canada.

DOI - https://doi.org/10.18632/oncotarget.28256

Correspondence to - Vladimir I. Titorenko - vladimir.titorenko@concordia.ca

Abstract

We propose a hypothesis of a mechanism linking cellular aging to cellular quiescence in chronologically aging budding yeast. Our hypothesis posits that this mechanism integrates four different processes, all of which are initiated after yeast cells cultured in a medium initially containing glucose consume it. Quiescent cells that develop in these cultures can be separated into the high- and low-density sub-populations of different buoyant densities. Process 1 of the proposed mechanism consists of a cell-cycle arrest in the G1 phase and leads to the formation of high-density quiescent cells. Process 2 results in converting high-density quiescent cells into low-density quiescent cells. Processes 3 and 4 cause a fast or slow decline in the quiescence of low- or high-density quiescent cells, respectively. Here, we tested our hypothesis by assessing how four different geroprotectors influence the four processes that could link cellular aging to cellular quiescence. We found that these geroprotectors differently affect processes 1 and 2 and decelerate processes 3 and 4. We also found that a rise in trehalose within quiescent yeast contributes to chronological aging and quiescence maintenance. These data collectively provide conclusive evidence for a mechanistic link between cellular aging and cellular quiescence.

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Keywords - cellular aging, cellular quiescence, longevity, gerotargets, geroprotectors

About Oncotarget

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Diverse Geroprotectors Differently Affect Mechanism Linking Cellular Aging to Cellular Quiescence in Budding Yeast

Oncotarget published this trending research paper on July 28, 2022 in Volume 13, entitled, "Chemoradiation-induced alteration of programmed death-ligand 1, CD8+ tumor-infiltrating lymphocytes and mucin expression in rectal cancer" by researchers from the Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD; Division of Biostatistics and Bioinformatics, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD; Department of Radiation Oncology and Molecular Radiation Sciences, Johns Hopkins University School of Medicine, Baltimore, MD.

DOI - https://doi.org/10.18632/oncotarget.28255

Correspondence to - Marina Baretti - mbarett1@jh.edu

Abstract

Introduction: DNA damage and resulting neoantigen formation is considered a mechanism for synergy between radiotherapy and PD-1/PD-L1 pathway inhibition to induce antitumor immune response. We investigated neoadjuvant chemoradiotherapy (nCRT)-induced changes in CD8+ tumor infiltrating lymphocyte, PD-L1 and mucin expression in rectal cancer patients.

Materials and Methods: Tumor samples of rectal adenocarcinoma patients undergoing resection between 2008-2014 with (n = 62) or without (n = 17) nCRT treatment were collected. Sections were stained with CD8 and PD-L1 antibodies for immunohistochemistry. The prevalence of CD8+ cells was recorded in the tumor, interface tumor and background rectal side. Image analysis was used to determine the density of CD8+ lymphocytes. The percentage of PD-L1 expression was manually counted in tumor cells (TC), tumor stroma (TS) and the invasive front (IF). Mucin expression was determined as the percentage of the mucin area in the whole tumor area.

Results: PD-L1 expression on TCs was identified in 7.6% (6/79) of nCRT specimens (p = 0.33) and in none of the non-nCRT patients. Median densities of CD8+ infiltrating T lymphocytes did not differ significantly between the two groups. Mucin expression was significantly higher in the nCRT cohort (p = 0.02). Higher neutrophil to lymphocytes ratio (NLR) after nCRT was associated with worse outcome (HR = 1.04, 95% CI = 1.00–1.08).

Conclusions: nCRT exposure was associated with a non-significant difference in PD-L1 expression in rectal adenocarcinoma patients, possibly due to sample size limitations. Further mechanistic investigations and comprehensive immune analysis are needed to understand nCRT-induced immunologic shift in rectal cancer and to expand the applicability of checkpoint inhibitors in this setting.

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Press release - https://www.oncotarget.com/news/pr/oncotarget-chemoradiation-induced-alteration-of-programmed-death-ligand-cd-tumor-infiltrating-lymphocytes-and-mucin-expression-in-rectal-cancer/

Keywords - programmed death ligand 1, tumor-infiltrating lymphocytes, immune checkpoints, colorectal cancer, neoadjuvant chemoradiotherapy

About Oncotarget

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Paper Spotlight: Chemoradiation Alters PD-L1, CD8+ TILs and Mucin in Rectal Cancer

Oncotarget published this trending research paper on July 19, 2022 in Volume 13, entitled, "CUDC907, a dual phosphoinositide-3 kinase/histone deacetylase inhibitor, promotes apoptosis of NF2 Schwannoma cells" by researchers from the Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL; Department of Otolaryngology, University of Miami Miller School of Medicine, Miami, FL; John P. Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, Miami, FL; Department of Pathology, University of Miami Miller School of Medicine, Miami, FL; Department of Human Genetics, University of Miami Miller School of Medicine, Miami, FL.

DOI - https://doi.org/10.18632/oncotarget.28254

Correspondence to - Cristina Fernandez-Valle - cfv@ucf.edu

Abstract

Neurofibromatosis Type 2 (NF2) is a rare tumor disorder caused by pathogenic variants of the merlin tumor suppressor encoded by NF2. Patients develop vestibular schwannomas (VS), peripheral schwannomas, meningiomas, and ependymomas. There are no approved drug therapies for NF2. Previous work identified phosphoinositide-3 kinase (PI3K) as a druggable target. Here we screened PI3K pathway inhibitors for efficacy in reducing viability of human schwannoma cells. The lead compound, CUDC907, a dual histone deacetylase (HDAC)/PI3K inhibitor, was further evaluated for its effects on isolated and nerve-grafted schwannoma model cells, and primary VS cells. CUDC907 (3 nM IG50) reduced human merlin deficient Schwann cell (MD-SC) viability and was 5–100 fold selective for MD over WT-SCs. CUDC907 (10 nM) promoted cell cycle arrest and caspase-3/7 activation within 24 h in human MD-SCs. Western blots confirmed a dose-dependent increase in acetylated lysine and decreases in pAKT and YAP. CUDC907 decreased tumor growth rate by 44% in a 14-day treatment regimen, modulated phospho-target levels, and decreased YAP levels. In five primary VS, CUDC907 decreased viability, induced caspase-3/7 cleavage, and reduced YAP levels. Its efficacy correlated with basal phospho-HDAC2 levels. CUDC907 has cytotoxic activity in NF2 schwannoma models and primary VS cells and is a candidate for clinical trials.

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Press release - https://www.oncotarget.com/news/pr/oncotarget-cudc-promotes-apoptosis-of-nf-schwannoma-cells/

Keywords - fimepinostat, Schwann cell, vestibular schwanomma, merlin, nerve allograft

About Oncotarget

Oncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Trending With Impact: CUDC907 Promotes Apoptosis of NF2 Schwannoma Cells

Oncotarget published this research paper on July 19, 2022 in Volume 13, entitled, "Predicting cancer immunotherapy response from gut microbiomes using machine learning models" by researchers from Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD; Biostatistics Branch, Division of Cancer Treatment and Diagnostics, National Cancer Institute, NIH, Bethesda, MD; Department of Medical Education, West Virginia University, Morgantown, WV; Translational and Functional Genomics Branch, National Human Genome Research Institute, NIH, Bethesda, MD; NIH Library, Division of Library Services, Office of Research Services, NIH, Bethesda, MD; Zimmerman Associates Inc., Fairfax, VA; Genitourinary Malignancies Branch, Center for Cancer Research, NCI, NIH, Bethesda, MD; Genetics and Microbiome Core, Laboratory of Integrative Cancer Immunology, Center for Cancer Research, NCI, NIH, Bethesda, MD; Department of Medicine and UPMC Hillman Cancer Center University of Pittsburgh, Pittsburgh, PA; Laboratory of Integrative Cancer Immunology, Center for Cancer Research, NCI, NIH, Bethesda, MD; Center for Immuno-Oncology, Center for Cancer Research, NCI, NIH, Bethesda, MD.

DOI - https://doi.org/10.18632/oncotarget.28252

Correspondence to - Heidi H. Kong - konghe@mail.nih.gov

Abstract

Cancer immunotherapy has significantly improved patient survival. Yet, half of patients do not respond to immunotherapy. Gut microbiomes have been linked to clinical responsiveness of melanoma patients on immunotherapies; however, different taxa have been associated with response status with implicated taxa inconsistent between studies. We used a tumor-agnostic approach to find common gut microbiome features of response among immunotherapy patients with different advanced stage cancers. A combined meta-analysis of 16S rRNA gene sequencing data from our mixed tumor cohort and three published immunotherapy gut microbiome datasets from different melanoma patient cohorts found certain gut bacterial taxa correlated with immunotherapy response status regardless of tumor type. Using multivariate selbal analysis, we identified two separate groups of bacterial genera associated with responders versus non-responders. Statistical models of gut microbiome community features showed robust prediction accuracy of immunotherapy response in amplicon sequencing datasets and in cross-sequencing platform validation with shotgun metagenomic datasets. Results suggest baseline gut microbiome features may be predictive of clinical outcomes in oncology patients on immunotherapies, and some of these features may be generalizable across different tumor types, patient cohorts, and sequencing platforms. Findings demonstrate how machine learning models can reveal microbiome-immunotherapy interactions that may ultimately improve cancer patient outcomes.

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Keywords - gut microbiome, immunotherapy, 16S rRNA, machine learning, metagenomics

About Oncotarget

Oncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Predicting Cancer Immunotherapy Response From Gut Microbiomes Using Machine Learning Models

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Oncotarget published this trending research paper on February 14, 2022 in Volume 13, entitled, "Telomere shortening accelerates tumor initiation in the L2-IL1B mouse model of Barrett esophagus and emerges as a possible biomarker" by researchers from II Medizinische Klinik, Technische Universität München, Munich, Germany; Department of Medicine, Columbia University Irving Medical Center, New York, NY; Klinik für Innere Medizin II, Universitätsklinikum Freiburg, Freiburg, Germany.

DOI - https://doi.org/10.18632/oncotarget.28198

Correspondence to - Michael Quante - michael.quante@uniklinik-freiburg.de

Abstract

Barrett’s esophagus (BE) is a precursor of the esophageal adenocarcinoma (EAC). BE- development and its progression to cancer is associated with gastroesophageal reflux disease. However, there is currently no molecular risk prediction model that accurately identifies patients at high risk for EAC. Here, we investigated the impact of shortened telomeres in a mouse model for Barrett esophagus (L2-IL1B). The L2-IL1B mouse model is characterized by IL-1β-mediated inflammation, which leads to a Barrett-like metaplasia in the transition zone between the squamous forestomach and glandular cardia/stomach. Telomere shortening was achieved by mTERC knockout. In the second generation (G2) of mTERC knockout L2-IL1B.mTERC−/− G2 mice exhibited telomere dysfunction with significantly shorter telomeres as measured by qFISH compared to L2-IL1B mice, correlating with stronger DNA damage in the form of phosphorylation of H2AX (γH2AX). Macroscopically, tumor area along the squamocolumnar junction (SCJ) was increased in L2-IL1B.mTERC−/− G2 mice, along with increased histopathological dysplasia. In vitro studies indicated increased organoid formation capacity in BE tissue from L2-IL1B.mTERC−/− G2 mice. In addition, pilot studies of human BE-, dysplasia- and EAC tissue samples confirmed that BE epithelial cells with or without dysplasia (LGD) had shorter telomeres compared to gastric cardia tissue. Of note, differentiated goblet cells retained longer telomeres than columnar lined BE epithelium. In conclusion, our studies suggest that shortened telomeres are functionally important for tumor development in a mouse model of BE and are associated with proliferating columnar epithelium in human BE. We propose that shortened telomeres should be evaluated further as a possible biomarker of cancer risk in BE patients.

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Keywords - Barrett's esophagus, telomere shortening, esophageal cancer, risk factor, TERT/TERC

About Oncotarget

Oncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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