{"id":3188,"date":"2023-01-21T17:08:28","date_gmt":"2023-01-21T23:08:28","guid":{"rendered":"https:\/\/kermitmurray.com\/msblog\/?page_id=3188"},"modified":"2023-01-21T17:08:28","modified_gmt":"2023-01-21T23:08:28","slug":"biorxiv-cancer-biology","status":"publish","type":"page","link":"https:\/\/kermitmurray.com\/msblog\/links\/journal-feeds\/biochemistry-journal-feeds\/biorxiv\/biorxiv-cancer-biology\/","title":{"rendered":"BioRxiv Cancer Biology"},"content":{"rendered":"\n<div class=\"wp-block-caxton-grid relative\"><div class=\"absolute absolute--fill\"><div class=\"absolute absolute--fill cover bg-center\" style=\"background-color:;background-image:linear-gradient( );\"><\/div><div class=\"absolute absolute--fill\" style=\"background-color:;background-image:linear-gradient( );opacity:1;\"><\/div><\/div><div class=\"relative caxton-columns caxton-grid-block\" style=\"padding-top:0;padding-left:0;padding-bottom:0;padding-right:0;grid-template-columns:repeat(12, 1fr)\" data-tablet-css=\"padding-left:em;padding-right:em;\" data-mobile-css=\"padding-left:em;padding-right:em;\">\n<div class=\"wp-block-caxton-section relative\" style=\"grid-area:span 1\/span 8\"><div class=\"absolute absolute--fill\"><div class=\"absolute absolute--fill cover bg-center\" style=\"background-color:;background-image:linear-gradient( );\"><\/div><div class=\"absolute absolute--fill\" style=\"background-color:;background-image:linear-gradient( );opacity:1;\"><\/div><\/div><div class=\"relative caxton-section-block\" style=\"padding-top:5px;padding-left:5px;padding-bottom:5px;padding-right:5px\" data-mobile-css=\"padding-left:1em;padding-right:1em;\" data-tablet-css=\"padding-left:1em;padding-right:1em;\">\n<p><strong><a href=\"https:\/\/www.biorxiv.org\/alertsrss\" target=\"_blank\" rel=\"noreferrer noopener\">Journal Home<\/a><\/strong><\/p>\n<\/div><\/div>\n\n\n\n<div class=\"wp-block-caxton-section relative\" style=\"grid-area:span 1\/span 4\"><div class=\"absolute absolute--fill\"><div class=\"absolute absolute--fill cover bg-center\" style=\"background-color:;background-image:linear-gradient( );\"><\/div><div class=\"absolute absolute--fill\" style=\"background-color:;background-image:linear-gradient( );opacity:1;\"><\/div><\/div><div class=\"relative caxton-section-block\" style=\"padding-top:5px;padding-left:5px;padding-bottom:5px;padding-right:5px\" data-mobile-css=\"padding-left:1em;padding-right:1em;\" data-tablet-css=\"padding-left:1em;padding-right:1em;\">\n<p><strong><a href=\"http:\/\/connect.biorxiv.org\/biorxiv_xml.php?subject=cancer_biology\" target=\"_blank\" rel=\"noreferrer noopener\">RSS<\/a><\/strong><\/p>\n<\/div><\/div>\n<\/div><\/div>\n\n\n<ul class=\"has-dates has-authors has-excerpts wp-block-rss\"><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.10.724074v1?rss=1'>Astrocyte immunosuppressive activity in glioblastoma depends on ZEB1 and is counteracted by CXCL14<\/a><\/div><time datetime=\"2026-05-13T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 13, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Clement, M., Gibbs, A., Begum, A., Siebzehnrubl, D., Kaushik, S., Singh, N., Gupta, B., Eftychidis, V., Siebzehnrubl, F. A.<\/span><div class=\"wp-block-rss__item-excerpt\">Glioblastomas are incurable and lethal brain cancers. Immunotherapies offer new and promising treatment options for glioblastoma patients, but the highly immunosuppressive nature of these cancers presents a challenging clinical obstacle. Glioblastoma immune evasion is driven by cell-cell interactions in the tumor microenvironment and recent studies have identified astrocytes as important contributors to immune silencing [1, 2]. Cell plasticity is a key feature of reactive astrocytes that drives heterogeneous, pro- or anti-inflammatory states [3], but the molecular regulators of astrocyte-immune interactions [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.08.723909v1?rss=1'>Integrative Genomic, Single-Cell, and Functional Profiling of the CD48-CD244 Axis and NK-Cell Dysfunction in Multiple Myeloma<\/a><\/div><time datetime=\"2026-05-12T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 12, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Patino-Escobar, B., Steinbrunn, T., Perez-Lugo, L., Rampersaud, S., Waller, D. D., Geng, H., Salangsang, F., Paul Phojanakong, P., Camara Serrano, J. A., Steri, V., Aguilar, O. A., Mitsiades, C. S., Wiita, A.<\/span><div class=\"wp-block-rss__item-excerpt\">Multiple myeloma (MM) orchestrates immune evasion by subverting natural killer (NK) cell function. CD48, one of the most abundant NK-ligands on MM cells, paradoxically enhances NK-cell activation yet is associated with high-risk cytogenetics and poor patient survival. We integrated multi-omics (bulk and single-cell RNA-seq, ATAC-seq), genome-wide CRISPR-KO\/a screens, and machine learning to dissect CD48 regulation and function. In human MM and Vk*MYC mice scRNA-seq datasets, NK cells exhibit stepwise increases in inflammatory and exhaustion signatures and loss of cytotoxic potential [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.08.723679v1?rss=1'>Tumor-associated tissue-resident macrophages drive pancreatic cancer progression through IGF1-IGF1R signaling<\/a><\/div><time datetime=\"2026-05-12T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 12, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Yamamoto, Y., Takeuchi, K., Tabe, S., Okumura, A., Aoshima, K., Eto, R., Konishi, T., Yamamoto, N., Miyagi, Y., Ohtsuka, M., Tanimizu, N., Taniguchi, H.<\/span><div class=\"wp-block-rss__item-excerpt\">The specific contribution of tissue-resident macrophages (TRMs) to pancreatic ductal adenocarcinoma (PDAC) progression remains unclear. Here, we found that a high abundance of TRM-derived tumor-associated macrophages (TRM-TAMs) is an independent indicator of poor prognosis in patients with PDAC. To elucidate the underlying mechanism, we established an advanced organoid platform (iMac-FPCO), which incorporates macrophages derived from human induced pluripotent stem cells to reflect the differentiation process of TRMs. Single-cell transcriptomic analysis revealed this model recapitulates the transcriptional identity of TRM-TAMs in [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.08.723931v1?rss=1'>Machine Learning Analysis to Define Cell Lineage in Leiomyosarcoma<\/a><\/div><time datetime=\"2026-05-12T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 12, 2026<\/time> <span class=\"wp-block-rss__item-author\">by van IJzendoorn, D. G. P., Przybyl, J., Hastie, T., Bovee, J. V. M. G., Matusiak, M., van de Rijn, M.<\/span><div class=\"wp-block-rss__item-excerpt\">Introduction Cellular differentiation and lineage commitment are known to be associated with differences in DNA methylation. Leiomyosarcoma (LMS) is a tumor thought to originate from smooth muscle cells in the walls of vessels in the soft tissue (STLMS) or from the uterine myometrium (ULMS). Here, we identify the methylation signatures of normal smooth muscle cells from blood vessels and the uterine wall and compare these with those found in STLMS and ULMS. We hypothesized that these methylation signatures could be [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.07.721771v1?rss=1'>Tumor Protein D54 (TPD54) regulates intracellular protein trafficking, cellular function and disease progression in melanoma<\/a><\/div><time datetime=\"2026-05-12T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 12, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Bonder, C. S., Ortiz, M., Ffrench, C. B., Webb, S., Toubia, J., Nataren, N. J., Dorward, E. L., Myo Min, K. K., Lonic, A., Arts, P., Cockshell, M. P., Mahoney, M. G., Ebert, L. M., Khew-Goodall, Y.<\/span><div class=\"wp-block-rss__item-excerpt\">To facilitate survival, migration and evasion of immune surveillance, cancer cells tightly coordinate the synthesis and trafficking of a diverse repertoire of proteins to their cell surface and the surrounding tumor microenvironment. A key mechanism underlying this process is the intracellular membrane trafficking pathways, including vesicular transport systems. There remains a paucity of mechanistic insight into the regulatory components that mediate nascent protein trafficking and their dysregulation in cancer. Herein, we investigate Tumor Protein D54 (TPD54) as a central regulator [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.08.723800v1?rss=1'>Targeting an RNA Editor to Impede H3K27M+ Pediatric Gliomas<\/a><\/div><time datetime=\"2026-05-12T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 12, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Ramsoomair, C. K., Alvarez, V., Sarmiento, F., Aramburu Berckemeyer, M., Seetharam, D., Kalliecharan, K., Moorkkannur, S. N., Mitchell, J., Hudson, A., Taylor, J., Ceccarelli, M., Bayik, D., Becher, O. J., Prabahakar, R., Welford, S., Gampel, B., De Carvalho, D. D., Reinberg, D., Shah, A. H.<\/span><div class=\"wp-block-rss__item-excerpt\">Diffuse midline glioma (DMG) is a lethal pediatric brain tumor with no curative therapies. Immune checkpoint blockade (ICB) has shown limited efficacy in DMG, largely due to poor T cell infiltration, low immune checkpoint (IC) expression, and a low tumor mutational burden. Here, we identify adenosine deaminase acting on RNA (ADAR), an RNA-editing enzyme that suppresses endogenous dsRNA sensing, as a key mediator of immune evasion in H3K27M-mutant DMG. ADAR is significantly overexpressed in H3K27M tumors relative to wild-type high-grade [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.07.723573v1?rss=1'>Efficacy evaluation of glasedgib Sonic Hedgehog pathway inhibition with or without inotuzumab in B-ALL cells using a new co-culturing system model and a validated chemosensitivity assay<\/a><\/div><time datetime=\"2026-05-12T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 12, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Woolston, D. W., Churchill, M., Grandori, C., Advani, A., Yeung, C. C. S.<\/span><div class=\"wp-block-rss__item-excerpt\">Purpose: Glasdegib is a Sonic Hedgehog (SHH) pathway inhibitor used for treating newly diagnosed acute myeloid leukemia in elders or patients unfit for intensive chemotherapy. This study sought to demonstrate growth inhibition and increased apoptosis of B-cell acute lymphoblastic leukemia (B-ALL) in vitro under glasdegib, alone and combined with inotuzumab, using a novel co-culture system and validated chemosensitivity testing model to determine whether glasdegib with and without inotuzumab may represent a promising treatment strategy in B-ALL. Methods: Seven blood and [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.07.723518v1?rss=1'>Oncomimetic \u03b2-catenin activity onset, duration and region defines aberrant intestinal development<\/a><\/div><time datetime=\"2026-05-12T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 12, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Soetje, B., Ma, H., Imtiaz, S., Corbat, A., Grecco, H. E., Schroeder, L., Brueggemann, Y., Seidler, S., Reichl, M., Bastiaens, P. I. H.<\/span><div class=\"wp-block-rss__item-excerpt\">In early intestinal carcinogenesis, adenoma formation is commonly initiated by loss-of-function mutations in a tumor suppressor that lead to oncoprotein gain-of-function, like in the tumor suppressor-oncoprotein pair APC-{beta}-catenin. Small intestinal organoids provide an in vitro system to study consequences of such mutations on tissue organization. However, conventional genetic manipulations do not allow precise control over the onset and duration of oncoprotein activity to study their influence on tissue transformation. Furthermore, homogenous tissues of clonal genetic models do not readily capture [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.07.722994v1?rss=1'>Antibody Blockade of Ly49\/MHC-I interactions enhances Innate and Adaptive Immunity Against Cancer Metastasis<\/a><\/div><time datetime=\"2026-05-12T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 12, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Panda, A. K., Sinha, S., Natarajan, K., Jiang, J., Chempati, S., Kazmi, S., Kim, Y.-h., Sharma, S., Schaughency, P., Boyd, L. F., Hernandez, J. M., Margulies, D. H., Shevach, E. M.<\/span><div class=\"wp-block-rss__item-excerpt\">Background Antibody-mediated blockade of innate receptor-MHC-I interactions represents a promising strategy to enhance anti-tumor immunity, particularly against metastatic cancers resistant to conventional checkpoint inhibitors. In this study, we investigated the effects of the pan anti-MHC-I monoclonal antibody M1\/42, which targets MHC-I interactions with Ly49, selectively expressed on murine NK cell subsets. Methods We administered M1\/42 to mice and assayed the proliferation and activation immune cells. Anti-tumor activity of growth and metastasis of checkpoint inhibitor-resistant pancreatic ductal adenocarcoma (PDAC) and B16F10 [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.07.723110v1?rss=1'>Elevated Expression of MALAT1 Contributes to the Survival of Drug-Tolerant Persister Cells Following Targeted Therapy in Lung Adenocarcinoma<\/a><\/div><time datetime=\"2026-05-12T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 12, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Davis, W. J. H., Thompson, M., Farry, S. M., McKinney, C., Gimenez, G., Hatley, M., Kumar, R., Rodger, E. J., Chatterjee, A., Diermeier, S. D., Drummond, C. J., Reid, G.<\/span><div class=\"wp-block-rss__item-excerpt\">Lung adenocarcinomas frequently harbour actionable oncogenic mutations that are vulnerable to treatment with targeted therapies. While responses to targeted therapies are often initially dramatic, relapse is almost inevitable and prevents durable responses in advanced-stage patients. Relapse is, in part, caused by drug tolerant persister cells (DTPs) which are able to survive treatment by entering a reversible, dormant state. Although long non-coding RNAs (lncRNAs) regulate processes thought to allow DTPs to survive and become stably resistant, the potential roles of lncRNAs [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.08.723756v1?rss=1'>A computational model reveals that spatial localization of cancer stem cells increases radioresistance in tumorspheres<\/a><\/div><time datetime=\"2026-05-12T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 12, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Fotinos, J., Condat, C. A., Barberis, L.<\/span><div class=\"wp-block-rss__item-excerpt\">Cancer stem cells (CSCs) exhibit increased resistance to radiotherapy, contributing to tumor recurrence and progression. While CSCs are known for their intrinsic resistance, the role of their spatial organization remains poorly understood. We extend a computational model of tumorsphere growth to investigate how the spatial distribution of CSCs influences radiation response. The model explicitly tracks cell lineages and spatial positions, revealing a preferential accumulation of CSCs in the spheroid interior. Because radiosensitivity increases with oxygen availability, and oxygen levels are [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.06.723232v1?rss=1'>Integrated analysis of leukemic mutations and transcriptomes at the single-cell level<\/a><\/div><time datetime=\"2026-05-11T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 11, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Papavasileiou, S., Wu, C., Boey, D., Margerie, L., Mo, J., Olsson-Stro\u0308mberg, U., So\u0308derlund, S., Nilsson, G., Dahlin, J. S.<\/span><div class=\"wp-block-rss__item-excerpt\">Single-cell RNA-sequencing-based characterization of cells that belong to the neoplastic clone is a major challenge in hematologic neoplasms, where malignant and normal cells coexist. Confident molecular profiling requires simultaneous analysis of gene expression and genetic mutations in individual cells, an ability that is not supported by the standard 10X Genomics workflow. Here, we developed a post-hoc targeted genotyping method for samples processed with the 10X Genomics 3&#039; workflow. To establish the approach, we mixed two types of leukemic cells harboring [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.06.723237v1?rss=1'>Pan-cancer analysis of single-cell RNA sequencing data from 304 human tumors sheds light on the aneuploidy paradox<\/a><\/div><time datetime=\"2026-05-11T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 11, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Wolf-Dankovich, G., Mashiah, T., Saad, R., Somech, E., Khoury, H., Tirosh, I., Ben-David, U.<\/span><div class=\"wp-block-rss__item-excerpt\">Aneuploidy poses a central paradox in cancer biology: it impairs cellular fitness in normal cells but drives cancer progression. To resolve this, we analyzed single cell transcriptomes from &gt;665,000 cells &#8211; including ~288,000 malignant cells &#8211; across 304 tumors and 15 cancer types. Integrating transcriptomics with inferred aneuploidy profiles, we characterized cell-intrinsic programs and interactions with the tumor microenvironment. Unexpectedly, highly aneuploid single cells exhibited reduced proliferation and metabolism, contrasting sharply with tumor-bulk profiles. We show this divergence is driven [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.06.723300v1?rss=1'>Tryptophan degradation by intestinal Bacteroides induces anti-tumor immunity and limits melanoma growth<\/a><\/div><time datetime=\"2026-05-11T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 11, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Diaz Olea, X., Beede, K., Vasconcelos Pereira, G., Scott, D. A., Petucci, C., Martens, E., Rodionov, D. A., Shah, A., Martinez, M. P., Kim, H., Sharma, A. K., Martin, A., Zhang, T., Faries, M. B., Hamid, O., Devkota, S., Osterman, A., Knott, S., Voest, E. E., Ajami, N., Wargo, J., Ramer-Tait, A., Ronai, Z. A.<\/span><div class=\"wp-block-rss__item-excerpt\">Defining mechanisms used by gut microbiota to control anti-tumor immunity may offer novel therapeutic modalities. Here, we demonstrate that Bacteroides rodentium and closely related Bacteroides uniformis species induce anti-tumor immunity and limit melanoma development when colonized in either germ-free (GF) mice, mice with a complex microbiome, or WT mice. Enhanced CD8+ T cell infiltration seen in tumors of mice harboring B. rodentium coincided with increased expression of immune-stimulating pathways and activation of bone marrow-derived dendritic cells that were co-cultured with [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.06.723206v1?rss=1'>Clone-level multi-modal prediction of tumour drug response<\/a><\/div><time datetime=\"2026-05-11T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 11, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Duchemin, Q., Trejo Banos, D., Bertolini, A., Ferreira, P. F., Schill, R., Lienhard, M., Wegmann, R., Tumor Profiler Consortium,, Snijder, B., Stekhoven, D., Beerenwinkel, N., Singer, F., Obozinski, G., Kuipers, J.<\/span><div class=\"wp-block-rss__item-excerpt\">Tumour heterogeneity presents a major challenge for precision oncology, as genetically and phenotypically distinct tumour clones may respond differently to therapy. To address this, we introduce scClone2DR, a probabilistic multi-modal framework that predicts drug responses at the level of individual tumour clones by integrating single-cell DNA and RNA sequencing with ex-vivo drug-screening data. In simulations, scClone2DR substantially outperforms alternatives in recovering true drug effects and clonal sensitivities. Applied to 60 melanoma and 21 acute myeloid leukaemia patient samples, the method [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.07.723477v1?rss=1'>Differential Roles of PFDN5 Isoforms in Head and Neck Squamous Cell Carcinoma: Insights from Proximity Interactome Mapping<\/a><\/div><time datetime=\"2026-05-11T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 11, 2026<\/time> <span class=\"wp-block-rss__item-author\">by CHESNEL, F., CHERON, A., AUDIC, Y., ALUSSE, A., DUOT, M., COM, E., LAVIGNE, R., PAILLARD, L., LE GOFF, X.<\/span><div class=\"wp-block-rss__item-excerpt\">Head and neck squamous cell carcinoma (HNSCC) ranks as the seventh most common cancer, with increasing incidence and mortality rates and limited therapeutic progress. The heterohexameric prefoldin complex, a highly conserved co-chaperone assembly composed of six PFDN subunits, exhibits expression levels strongly correlated with cancer progression. Among these subunits, the PFDN5 gene presents a paradoxical role in cancer biology, demonstrating both tumor-promoting and tumor-suppressive activities. Notably, the PFDN5 gene generates two distinct protein isoforms through alternative splicing, yet their individual [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.07.723511v1?rss=1'>SLD5\/GINS4 controls dynein-dependent centrosome maturation and exposes a candidate mitotic vulnerability in cancer.<\/a><\/div><time datetime=\"2026-05-11T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 11, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Kumar, V., Singh, V., Singh, R., Kumar, P., Ghosh, T.<\/span><div class=\"wp-block-rss__item-excerpt\">Faithful proliferation requires coordinated DNA replication with centrosome maturation and spindle-pole integrity. SLD5, encoded by GINS4, is a core component of the GINS replication complex and is frequently elevated in tumors, but whether it links replication-associated cancer states to centrosome control has remained unclear. Here, we show that GINS4\/SLD5 is recurrently upregulated across human cancers at transcript and protein levels and marks tumor programs enriched for DNA replication, chromosome segregation, and mitotic control. In cancer cells, Sld5 depletion dispersed PCM1, [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.07.723296v1?rss=1'>Chemical screens identify HDAC6 as an epigenetic vulnerability in acquired Temozolomide-resistant models of glioblastoma<\/a><\/div><time datetime=\"2026-05-11T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 11, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Senbabaoglu Aksu, F., Cevatemre, B., Degirmenci, N., Kala, E. Y., Ucku, D., Philpott, M., Cribbs, A. P., Dunford, J. P., Oppermann, U., Acilan, C., Bagci-Onder, T.<\/span><div class=\"wp-block-rss__item-excerpt\">Glioblastoma (GBM) is an aggressive primary brain tumor associated with a median survival of approximately 15 months following diagnosis. Current standard-of-care treatment includes surgical resection followed by radiotherapy and chemotherapy with the DNA-alkylating agent temozolomide (TMZ). However, tumor recurrence in a therapy-resistant state remains a major driver of poor patient outcomes. To investigate the molecular mechanisms underlying TMZ resistance, we generated in vitro models of acquired resistance by exposing initially TMZ-sensitive GBM cells to escalating doses of TMZ. Transcriptomic and [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.06.723061v1?rss=1'>Epithelial mesenchymal transition initiates precancer states in BRCA1 mutation carriers<\/a><\/div><time datetime=\"2026-05-11T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 11, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Bar-Hai, N., Ben-Yishay, R., Arbili-Yarhi, S., Bernstein-Molho, R., Goldinger, G., Balint-Lahat, N., Menes, T., Herman, N., Noy, V., Mansour, A., Globus, O., Hilman, P., Zehavi, Y., Eizenberg-Magar, I., Mahammadov, E., Conrad, T., Rajewsky, N., Antebi, Y. E., Berger, R., Ishay Ronen, D.<\/span><div class=\"wp-block-rss__item-excerpt\">Epithelial-to-mesenchymal transition (EMT) is activated to equip cells with the capacity to adapt to and escape hostile conditions. While EMT is required for cancer progression, its role in breast cancer initiation remains elusive. Given the basal-like phenotype of breast cancers arising in female carriers of germline BRCA1 pathogenic variants (BRCA1 carriers), we hypothesized that enhanced EMT susceptibility underlies precancerous initiation in mammary epithelium. Perturbation of patient-derived normal mammary organoids from BRCA1 carriers and non-carriers with inflammatory cytokines induced copy number [&hellip;]<\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/www.biorxiv.org\/content\/10.64898\/2026.05.06.723215v1?rss=1'>Failure of Bacillus Calmette-Guerin Therapy in Patients with Bladder Cancer is Characterized by Immune Dysfunction Associated with Activator Protein 1<\/a><\/div><time datetime=\"2026-05-10T00:00:00-05:00\" class=\"wp-block-rss__item-publish-date\">May 10, 2026<\/time> <span class=\"wp-block-rss__item-author\">by Garven, A., Pare, J.-F., Robins, A., Vera-Rodriguez, A., Sampy, R., Bennett, A., Nauman, R. W., Craig, A. W., Greer, P. A., Koti, M., Cotechini, T., Berman, D. M., Simpson, A., Postovit, L.-M., Siemens, D. R., Graham, C. H.<\/span><div class=\"wp-block-rss__item-excerpt\">The standard-of-care for patients with higher-risk non-muscle invasive bladder cancer (NMIBC) after tumour resection is intravesical administration of Bacillus Calmette-Guerin (BCG). While this form of adjuvant immunotherapy has improved recurrence-free and progression-free survival, a large proportion of patients experience recurrences within a year of diagnosis. The reasons for this high rate of early recurrence following BCG therapy remain unclear; however, inadequate activation of systemic immunity may be a contributing factor. To address this, we analysed the transcriptomic and chromatin accessibility [&hellip;]<\/div><\/li><\/ul>\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity is-style-wide\"\/>\n\n\n\n<h4 class=\"wp-block-heading\">Related Journals<\/h4>\n\n\n<ul class=\"su-siblings\"><li class=\"page_item page-item-3099\"><a href=\"https:\/\/kermitmurray.com\/msblog\/links\/journal-feeds\/biochemistry-journal-feeds\/biorxiv\/biorxiv-biochemistry\/\">BioRxiv Biochemistry<\/a><\/li>\n<li class=\"page_item page-item-3112\"><a href=\"https:\/\/kermitmurray.com\/msblog\/links\/journal-feeds\/biochemistry-journal-feeds\/biorxiv\/biorxiv-bioinformatics\/\">BioRxiv Bioinformatics<\/a><\/li>\n<li class=\"page_item page-item-3132\"><a href=\"https:\/\/kermitmurray.com\/msblog\/links\/journal-feeds\/biochemistry-journal-feeds\/biorxiv\/biorxiv-biophysics\/\">BioRxiv Biophysics<\/a><\/li>\n<li class=\"page_item page-item-3190\"><a href=\"https:\/\/kermitmurray.com\/msblog\/links\/journal-feeds\/biochemistry-journal-feeds\/biorxiv\/biorxiv-pharmacology-and-toxicology\/\">BioRxiv Pharmacology and Toxicology<\/a><\/li>\n<li class=\"page_item page-item-3114\"><a href=\"https:\/\/kermitmurray.com\/msblog\/links\/journal-feeds\/biochemistry-journal-feeds\/biorxiv\/biorxiv-systems-biology\/\">BioRxiv Systems Biology<\/a><\/li>\n<li class=\"page_item page-item-3193\"><a href=\"https:\/\/kermitmurray.com\/msblog\/links\/journal-feeds\/biochemistry-journal-feeds\/biorxiv\/biorxiv-zoology\/\">BioRxiv Zoology<\/a><\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"<p>Related Journals<\/p>\n","protected":false},"author":1,"featured_media":2652,"parent":3087,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":"","_links_to":"","_links_to_target":""},"class_list":["post-3188","page","type-page","status-publish","has-post-thumbnail","hentry","entry"],"_links":{"self":[{"href":"https:\/\/kermitmurray.com\/msblog\/wp-json\/wp\/v2\/pages\/3188","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/kermitmurray.com\/msblog\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/kermitmurray.com\/msblog\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/kermitmurray.com\/msblog\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/kermitmurray.com\/msblog\/wp-json\/wp\/v2\/comments?post=3188"}],"version-history":[{"count":1,"href":"https:\/\/kermitmurray.com\/msblog\/wp-json\/wp\/v2\/pages\/3188\/revisions"}],"predecessor-version":[{"id":3189,"href":"https:\/\/kermitmurray.com\/msblog\/wp-json\/wp\/v2\/pages\/3188\/revisions\/3189"}],"up":[{"embeddable":true,"href":"https:\/\/kermitmurray.com\/msblog\/wp-json\/wp\/v2\/pages\/3087"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/kermitmurray.com\/msblog\/wp-json\/wp\/v2\/media\/2652"}],"wp:attachment":[{"href":"https:\/\/kermitmurray.com\/msblog\/wp-json\/wp\/v2\/media?parent=3188"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}