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Oncology

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ST6GalNAc-I regulates tumor cell sialylation via NECTIN2/MUC5AC-mediated immunosuppression and angiogenesis in non–small cell lung cancer
Muthamil Iniyan Appadurai, … , Apar Kishor Ganti, Imayavaramban Lakshmanan
Muthamil Iniyan Appadurai, … , Apar Kishor Ganti, Imayavaramban Lakshmanan
Published May 15, 2025
Citation Information: J Clin Invest. 2025;135(10):e186863. https://doi.org/10.1172/JCI186863.
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ST6GalNAc-I regulates tumor cell sialylation via NECTIN2/MUC5AC-mediated immunosuppression and angiogenesis in non–small cell lung cancer

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Abstract

Glycosylation controls immune evasion, tumor progression, and metastasis. However, how tumor cell sialylation regulates immune evasion remains poorly characterized. ST6GalNAc-I, a sialyltransferase that conjugates sialic acid to the glycans in glycoproteins, was overexpressed in an aggressive-type KPA (KrasG12D/+ Trp53R172H/+ Ad-Cre) lung adenocarcinoma (LUAD) model and patient samples. Proteomic and biochemical analysis indicated that ST6GalNAc-I mediated NECTIN2 sialylation in LUAD cells. ST6GalNAc-I–deficient tumor cells cocultured with T cells were more susceptible to T cell–mediated tumor cell killing, indicating a key role for NECTIN2 in T cell dysfunction. Mice injected with St6galnac-I–knockdown syngeneic cells showed reduced lung tumor incidence and Nectin2/Tigit-associated immunosuppression. ST6GalNAc-I–deficient cells exhibited reduced P-DMEA metabolite levels, while administration of P-DMEA promoted LUAD cell proliferation via MUC5AC. MUC5AC interacted and colocalized with PRRC1 in the Golgi, suggesting a potential role for PRRC1 in MUC5AC glycosylation. Mice injected with ST6GalNAc-I/MUC5AC-deficient cells (human LUAD) exhibited reduced lung tumor incidence, angiogenesis, and liver metastases. Mechanistically, ST6GalNAc-I/MUC5AC regulates VCAN-V1, a key factor in tumor matrix remodeling during angiogenesis and metastasis. These findings demonstrate that ST6GalNAc-I–mediated sialylation of NECTIN2/MUC5AC is critical for immune evasion and tumor angiogenesis. Targeting this pathway may prevent LUAD development and/or metastasis.

Authors

Muthamil Iniyan Appadurai, Sanjib Chaudhary, Ashu Shah, Gopalakrishnan Natarajan, Zahraa W. Alsafwani, Parvez Khan, Dhananjay D. Shinde, Subodh M. Lele, Lynette M. Smith, Mohd Wasim Nasser, Surinder Kumar Batra, Apar Kishor Ganti, Imayavaramban Lakshmanan

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Tebentafusp elicits on-target cutaneous immune responses driven by cytotoxic T-cells in uveal melanoma patients
Ramon Staeger, … , Reinhard Dummer, Barbara Meier-Schiesser
Ramon Staeger, … , Reinhard Dummer, Barbara Meier-Schiesser
Published May 1, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI181464.
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Tebentafusp elicits on-target cutaneous immune responses driven by cytotoxic T-cells in uveal melanoma patients

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Abstract

Background: Tebentafusp is the first T-cell receptor-based bispecific protein approved for clinical use in HLA-A*02:01+ adult patients with unresectable/metastatic uveal melanoma. It redirects T-cells toward gp100-expressing target cells, frequently inducing skin-related early adverse events. Methods: This study investigated immunological and cellular responses using single-cell and spatial analysis of skin biopsies from patients with metastatic uveal melanoma treated with tebentafusp. Results: 81.8% of patients developed acute cutaneous adverse events, which correlated with improved survival. Multimodal analysis revealed a brisk infiltration of CD4+ and CD8+ T-cells, while melanocyte numbers declined. Single-cell RNA-sequencing revealed T-cell activation, proliferation, and IFN-γ/cytotoxic gene upregulation. CD8+ T-cells co-localized with melanocytes and upregulated LAG3, suggesting potential for combination therapies with tebentafusp. Melanocytes upregulated antigen presentation and apoptotic pathways, while pigmentation gene expression decreased. However, gp100 remained stably expressed. Conclusion: Sequential skin biopsies enable in vivo pharmacodynamic modeling of tebentafusp, offering insights into immune activation, toxicity, and treatment response. Examining the on-target effects of bispecifics in tissues amenable to longitudinal sampling enhances our understanding of toxicity and therapeutic escape mechanisms, guiding strategies for treatment optimization.

Authors

Ramon Staeger, Aizhan Tastanova, Adhideb Ghosh, Nicola Winkelbeiner, Prachi Shukla, Isabel Kolm, Patrick Turko, Adel Benlahrech, Jane Harper, Anna Broomfield, Antonio Camera, Marianna Ambrosio, Veronika Haunerdinger, Phil F. Cheng, Egle Ramelyte, James P. Pham, Stefanie Kreutmair, Burkhard Becher, Mitchell P. Levesque, Reinhard Dummer, Barbara Meier-Schiesser

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DNA demethylating agents suppress preclinical models of synovial sarcoma
Nobuhiko Hasegawa, … , Ana Banito, Kevin B. Jones
Nobuhiko Hasegawa, … , Ana Banito, Kevin B. Jones
Published April 29, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI190855.
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DNA demethylating agents suppress preclinical models of synovial sarcoma

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Abstract

Synovial sarcoma is an aggressive soft tissue cancer driven by the chimeric SS18::SSX fusion oncoprotein, which disrupts chromatin remodeling by combining two antagonistic transcriptional regulators. SS18 participates in BAF complexes that open chromatin, while the SSX genes are cancer-testis antigens that interface with chromatin decorated with monoubiquitinated histone H2A placed by Polycomb repressive complexes (PRCs) activity. Because KDM2B brings PRC to unmethylated CpG islands, it is plausible that methylation directly determines the distribution of SS18::SSX to target loci. Given that synovial sarcoma is also characterized by a peculiarly low DNA hypomethylation profile, we hypothesized that further disturbance of DNA methylation would have a negative impact on synovial sarcoma growth. DNMT1 disruption by CRISPR/Cas9 targeting or pharmacologic inhibition with cytidine analogs 5-aza-2ʹ-deoxycytidine (decitabine) and 5-azacytidine led to decreased genome-wide methylation, redistribution of SS18::SSX, and altered gene expression profiles, most prominently including upregulation of tumor suppressor genes, immune-related genes, and mesenchymal differentiation-related genes. These drugs suppressed growth of synovial sarcoma cell lines and drove cytoreduction in mouse genetic models. DNMT1 inhibitors, already approved for treating myelodysplastic syndromes, warrant further clinical investigation for synovial sarcoma as repurposed, targeted treatments exploiting a vulnerability in the intrinsic biology of this cancer.

Authors

Nobuhiko Hasegawa, Nezha S. Benabdallah, Kyllie Smith-Fry, Li Li, Sarah McCollum, Jinxiu Li, Caelen A. Jones, Lena Wagner, Vineet Dalal, Viola Golde, Anastasija Pejkovska, Lara Carroll, Malay Haldar, Seth M. Pollack, Scott W. Lowe, Torsten O. Nielsen, Ana Banito, Kevin B. Jones

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Kinesin-like protein KIFC2 stabilizes CDK4 to accelerate growth and confer resistance in HR+/HER2- breast cancer
Shao-Ying Yang, … , A Yong Cao, Da-Qiang Li
Shao-Ying Yang, … , A Yong Cao, Da-Qiang Li
Published April 29, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI183531.
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Kinesin-like protein KIFC2 stabilizes CDK4 to accelerate growth and confer resistance in HR+/HER2- breast cancer

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Abstract

Hormone receptor-positive and human epidermal growth factor receptor 2-negative breast cancer (HR+/HER2− BC) is the most common subtype, with high risk of long-term recurrence and metastasis. Endocrine therapy (ET) combined with cyclin-dependent kinase 4/6 (CDK4/6) inhibitors is a standard treatment for advanced/metastatic HR+/HER2- BC, but resistance remains a major clinical challenge. We report that kinesin family member C2 (KIFC2) was amplified in approximately 50% HR+/HER2- BC, and its high expression was associated with poor disease outcome, increased tumor protein p53 (TP53) somatic mutation, and active pyrimidine metabolism. Function assays revealed that depletion of KIFC2 suppressed growth and enhanced sensitivity of HR+/HER2- BC cells to tamoxifen and CDK4/6 inhibitors. Mechanistically, KIFC2 stabilized CDK4 by enhancing its interaction with ubiquitin specific peptidase 9 X-linked (USP9X). Importantly, re-expression of CDK4 in KIFC2-depleted cells partially rescued the decreased growth and increased sensitivity to tamoxifen and CDK4/6 inhibitors caused by KIFC2 depletion. Clinically, high KIFC2 mRNA expression was negatively associated with survival rate of HR+/HER2- BC patients received adjuvant ET alone or in combination with CDK4/6 inhibitors. Collectively, these findings identify an important role for KIFC2 in HR+/HER2- BC growth and therapeutic resistance, and support its potential as a therapeutic target and predictive biomarker.

Authors

Shao-Ying Yang, Ming-Liang Jin, Lisa Andriani, Qian Zhao, Yun-Xiao Ling, Cai-Jin Lin, Min-Ying Huang, Jia-Yang Cai, Yin-Ling Zhang, Xin Hu, Zhi-Ming Shao, Fang-Lin Zhang, Xi Jin, A Yong Cao, Da-Qiang Li

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Disruption of Ataxia-telangiectasia mutated kinase enhances radiation therapy efficacy in spatially-directed diffuse midline glioma models
Avani Mangoli, … , Simon G. Gregory, Zachary J. Reitman
Avani Mangoli, … , Simon G. Gregory, Zachary J. Reitman
Published April 17, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI179395.
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Disruption of Ataxia-telangiectasia mutated kinase enhances radiation therapy efficacy in spatially-directed diffuse midline glioma models

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Diffuse midline gliomas (DMGs) are lethal brain tumors characterized by p53-inactivating mutations and oncohistone H3.3K27M mutations that rewire the cellular response to genotoxic stress. We used RCAS/tv-a retroviruses and Cre recombinase to inactivate p53 and induce native H3.3K27M mutations in a lineage- and spatially-directed manner. We generated primary mouse tumors that recapitulate human DMG. Disrupting ataxia-telangiectasia mutated kinase (ATM) enhanced the efficacy of radiation therapy in murine and patient-derived DMG models which increased survival. Microscopy-based in situ sequencing was used to spatially resolve transcriptional profiles in >750,000 single cells with or without ATM disruption and radiation therapy, revealing altered immune-neoplastic and endothelial cell interactions after treatment. An allelic series of primary murine DMG models with different p53 mutations confirmed that transactivation-independent p53 activity is a key mediator of radiosensitivity after ATM disruption. Our findings contribute primary DMG mouse models with deep profiling and reveal the mechanisms of treatment response to an actionable therapeutic strategy.

Authors

Avani Mangoli, Vennesa Valentine, Spencer Maingi, Sophie R. Wu, Harrison Q. Liu, Michael Aksu, Vaibhav Jain, Bronwen E. Foreman, Joshua A. Regal, Loren B. Weidenhammer, Connor E. Stewart, Maria E. Guerra Garcia, Emily Hocke, Karen Abramson, Tal Falick Michaeli, Nerissa T. Williams, Lixia Luo, Megan Romero, Katherine Deland, Samantha Gadd, Eita Uchida, Laura Attardi, Kouki Abe, Rintaro Hashizume, David M. Ashley, Oren J. Becher, David G. Kirsch, Simon G. Gregory, Zachary J. Reitman

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IL-7-mediated expansion of autologous lymphocytes increases CD8+ VLA-4 expression and accumulation in glioblastoma models
Kirit Singh, … , Mustafa Khasraw, Peter E. Fecci
Kirit Singh, … , Mustafa Khasraw, Peter E. Fecci
Published April 17, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI181471.
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IL-7-mediated expansion of autologous lymphocytes increases CD8+ VLA-4 expression and accumulation in glioblastoma models

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The efficacy of T cell-activating therapies against glioma is limited by an immunosuppressive tumor microenvironment and tumor-induced T cell sequestration. We investigated whether peripherally infused non-antigen specific autologous lymphocytes (ALT) could accumulate in intracranial tumors. We observed that non-specific autologous CD8+ ALT cells can indeed accumulate in this context, despite endogenous T cell sequestration in bone marrow. Rates of intratumoral accumulation were markedly increased when expanding lymphocytes with IL-7 compared to IL-2. Pre-treatment with IL-7 ALT also enhanced the efficacy of multiple tumor-specific and non-tumor-specific T cell-dependent immunotherapies against orthotopic murine and human xenograft gliomas. Mechanistically, we detected increased VLA-4 on mouse and human CD8+ T cells following IL-7 expansion, with increased transcription of genes associated with migratory integrin expression (CD9). We also observed that IL-7 increases S1PR1 transcription in human CD8+ T cells, which we have shown to be protective against tumor-induced T cell sequestration. These observations demonstrate that expansion with IL-7 enhances the capacity of ALT to accumulate within intracranial tumors, and that pre-treatment with IL-7 ALT can boost the efficacy of subsequent T cell-activating therapies against glioma. Our findings will inform the development of future clinical trials where ALT pre-treatment can be combined with T cell-activating therapies.

Authors

Kirit Singh, Kelly M. Hotchkiss, Sarah L. Cook, Pamy Noldner, Ying Zhou, Eliese M. Moelker, Chelsea O. Railton, Emily E. Blandford, Bhairavy J. Puviindran, Shannon E. Wallace, Pamela K. Norberg, Gary E. Archer, Beth H. Shaz, Katayoun Ayasoufi, John H. Sampson, Mustafa Khasraw, Peter E. Fecci

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Off-the-shelf invariant NKT cells expressing anti-PSCA CAR and IL-15 promote pancreatic cancer regression in mice
Zhenyu Dai, … , Michael A. Caligiuri, Jianhua Yu
Zhenyu Dai, … , Michael A. Caligiuri, Jianhua Yu
Published April 15, 2025
Citation Information: J Clin Invest. 2025;135(8):e179014. https://doi.org/10.1172/JCI179014.
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Off-the-shelf invariant NKT cells expressing anti-PSCA CAR and IL-15 promote pancreatic cancer regression in mice

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Abstract

Pancreatic ductal adenocarcinoma cancer (PDAC) continues to pose a significant health burden, with a 5-year survival rate of only 10%. Prostate stem cell antigen (PSCA) is highly expressed on the surface of tumor cells of most PDAC patients, with minimum expression in most normal tissues. Here, we generated cryopreserved, off-the-shelf, allogeneic PSCA chimeric antigen receptor (CAR) invariant NKT (iNKT) cells using human peripheral blood mononuclear cells as a cell source. In multiple in vitro and in vivo PDAC models, freshly manufactured PSCA CAR_sIL-15 iNKT cells and frozen-thawed, off-the-shelf PSCA CAR_sIL-15 iNKT cells demonstrate comparable efficacies, and both show remarkable suppression of PSCA-positive and gemcitabine-resistant PDAC. Importantly, off-the-shelf cryopreserved PSCA CAR_sIL-15 iNKT cells show equivalent efficacy when compared with PSCA CAR T cells using the same PSCA CAR and in the same PDAC model; however, PSCA CAR_sIL-15 iNKT cells do not appear to induce systemic toxicity or graft-versus-host disease, thus allowing for multiple infusions to control recurrent disease. Collectively, our study suggests that PSCA CAR_sIL-15 iNKT cells merit clinical investigation for PDAC patients exhibiting positive PSCA expression. The therapy could be given as a single agent or in combination with established therapeutic modalities for PDAC.

Authors

Zhenyu Dai, Zheng Zhu, Zhiyao Li, Lei Tian, Kun-Yu Teng, Hanyu Chen, Li-Shu Wang, Jianying Zhang, Laleh Melstrom, Michael A. Caligiuri, Jianhua Yu

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Addiction of primary cutaneous γδ T cell lymphomas to JAK/STAT signaling
Yue Zhang, … , Naiem T. Issa, Jaehyuk Choi
Yue Zhang, … , Naiem T. Issa, Jaehyuk Choi
Published April 15, 2025
Citation Information: J Clin Invest. 2025;135(8):e180417. https://doi.org/10.1172/JCI180417.
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Addiction of primary cutaneous γδ T cell lymphomas to JAK/STAT signaling

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Abstract

Authors

Yue Zhang, Julia A. Yescas, Kristy Tefft, Spencer Ng, Kevin Qiu, Erica B. Wang, Shifa Akhtar, Addie Walker, Macartney Welborn, Martin Zaiac, Joan Guitart, Aamir M. Qureshi, Youn H. Kim, Michael S. Khodadoust, Naiem T. Issa, Jaehyuk Choi

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A small-molecule inhibitor of BCL10-MALT1 interaction abrogates progression of diffuse large B cell lymphoma
Heejae Kang, … , Linda M. McAllister-Lucas, Peter C. Lucas
Heejae Kang, … , Linda M. McAllister-Lucas, Peter C. Lucas
Published April 15, 2025
Citation Information: J Clin Invest. 2025;135(8):e164573. https://doi.org/10.1172/JCI164573.
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A small-molecule inhibitor of BCL10-MALT1 interaction abrogates progression of diffuse large B cell lymphoma

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Abstract

Diffuse large B cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma, and the activated B cell–like subtype (ABC-DLBCL) is associated with particularly poor outcome. Many ABC-DLBCLs harbor gain-of-function mutations that cause inappropriate assembly of the CARMA1-BCL10-MALT1 (CBM) signalosome, a cytoplasmic complex that drives downstream NF-κB signaling. MALT1 is the effector protein of the CBM signalosome such that its recruitment to the signalosome via interaction with BCL10 allows it to exert both protease and scaffolding activities that together synergize in driving NF-κB. Here, we demonstrate that a molecular groove located between two adjacent immunoglobulin-like domains within MALT1 represents a binding pocket for BCL10. Leveraging this discovery, we performed an in silico screen to identify small molecules that dock within this MALT1 groove and act as BCL10-MALT1 protein-protein interaction (PPI) inhibitors. We report the identification of M1i-124 as a first-in-class compound that blocks BCL10-MALT1 interaction, abrogates MALT1 scaffolding and protease activities, promotes degradation of BCL10 and MALT1 proteins, and specifically targets ABC-DLBCLs characterized by dysregulated MALT1. Our findings demonstrate that small-molecule inhibitors of BCL10-MALT1 interaction can function as potent agents to block MALT1 signaling in selected lymphomas, and provide a road map for clinical development of a new class of precision-medicine therapeutics.

Authors

Heejae Kang, Lisa M. Maurer, Jing Cheng, Mei Smyers, Linda R. Klei, Dong Hu, Juliana Hofstatter Azambuja, Marcelo J. Murai, Ahmed Mady, Ejaz Ahmad, Matthew Trotta, Hanna B. Klei, Minda Liu, Prasanna Ekambaram, Zaneta Nikolovska-Coleska, Bill B. Chen, Linda M. McAllister-Lucas, Peter C. Lucas

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Precision screening facilitates clinical classification of BRCA2-PALB2 binding variants with benign and pathogenic functional effects
Muthiah Bose, … , Claus S. Sørensen, Maria Rossing
Muthiah Bose, … , Claus S. Sørensen, Maria Rossing
Published April 15, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI181879.
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Precision screening facilitates clinical classification of BRCA2-PALB2 binding variants with benign and pathogenic functional effects

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Abstract

BACKGROUND. Decoding the clinical impact of genetic variants is particularly important for precision medicine in cancer. Genetic screening of mainly breast and ovarian cancer patients has identified numerous BRCA1/BRCA2 ‘variants of uncertain significance’ (VUS) that remain unclassified due to a lack of pedigrees and functional data. METHODS. Here, we used CRISPR-Select — a technology that exploits unique inbuilt controls at the endogenous locus — to assess 54 rare ClinVar VUS located in the PALB2-binding domain (PBD) of BRCA2. Variant deleteriousness was examined in the absence and presence of PARPi, Cisplatin, or Mitomycin C. RESULTS. Marked functional deficiency was observed for variants in the exon 2-donor splice region (A22 = (c.66A>C), A22 = (c.66A>G), A22 = (c.66A>T), and D23H) and Trp31 amino acid (W31G, W31L, and W31C), both critical for BRCA2 function. Moreover, T10K and G25R resulted in an intermediate phenotype, suggesting these variants are hypomorphic in nature. Combining our functional results with the latest ClinGen BRCA1/2 Variant Curation Expert Panel recommendations, we could classify 49 of the 54 VUS as either likely benign (n = 45) or likely pathogenic (n = 4). CONCLUSION. Hence, CRISPR-Select is an important tool for efficient variant clinical classification. Application of this technology in the future will ultimately improve patient care. FUNDING. Danish Cancer Society, Novo Nordisk Foundation, Sygeforsikring Danmark, Børnecancerfonden, Neye-Fonden, Roche, Novartis, Pfizer, AstraZeneca, MSD, and Daiichi Sankyo Europe GmbH.

Authors

Muthiah Bose, Manika Indrajit Singh, Morten Frödin, Bent Ejlertsen, Claus S. Sørensen, Maria Rossing

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E2F8 keeps liver cancer at bay
Alain de Bruin, Gustavo Leone, and colleagues find that the E2F8-mediated transcriptional repression in the developing liver suppresses hepatocellular carcinoma later in life …
Published July 25, 2016
Scientific Show StopperOncology

AIDing and abetting UV-independent skin cancer
Taichiro Nonaka and colleagues find that AID plays a role in the development of inflammation-driven, non-UV skin cancer
Published March 14, 2016
Scientific Show StopperOncology

CD37 keeps B cell lymphoma at bay
Charlotte de Winde, Sharon Veenbergen, and colleagues demonstrate that loss of CD37 expression relieves SOCS3-mediated suppression of IL-6 signaling and supports the development of B cell lymphoma…
Published January 19, 2016
Scientific Show StopperOncology

Maintaining endometrial epithelial barrier function
Jessica Bowser and colleagues identify a mechanism by which loss of CD73 promotes endometrial cancer progression…
Published December 7, 2015
Scientific Show StopperOncology

Sleuthing out the cellular source of hepatocellular carcinoma
Xueru Mu, Regina Español-Suñer, and colleagues show that tumors in murine hepatocellular carcinoma models are derived from hepatocytes and not from other liver resident cells …
Published September 8, 2015
Scientific Show StopperOncology

Live animal imaging in the far red
Ming Zhang and colleagues developed a far-red-absorbing reporter/probe system that can be used to image live animals and overcomes imaging limitations associated with conventional systems that use lower wavelengths of light…
Published September 8, 2015
Scientific Show StopperTechnical AdvanceOncology

Cancer cells fight off stress with ATF4
Souvik Dey, Carly Sayers, and colleagues reveal that activation of heme oxygenase 1 by ATF4 protects cancer cells from ECM detachment-induced death and promotes metastasis…
Published May 26, 2015
Scientific Show StopperOncology

Smothering Von Hippel-Lindau syndrome-associated phenotypes
Ana Metelo and colleagues demonstrate that specific inhibition of HIF2a ameliorates VHL-associated phenotypes and improves survival in a zebrafish model of disease…
Published April 13, 2015
Scientific Show StopperOncology

Blazing the trail for metastasis
Jill Westcott, Amanda Prechtl, and colleagues identify an epigenetically distinct population of breast cancer cells that promotes collective invasion…
Published April 6, 2015
Scientific Show StopperOncology

Dynamic focal adhesions
Wies van Roosmalen, Sylvia E. Le Dévédec, and colleagues screen for genes that alter cancer cell migration and demonstrate that SRPK1 promotes metastasis...
Published March 16, 2015
Scientific Show StopperOncology
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