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Oncology

  • 1,367 Articles
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High 4E-BP-1 expression associates with chromosome 8 gain and CDK4/6 sensitivity in Ewing Sarcoma
Cornelius M. Funk, … , Thomas G.P. Grünewald, Julian Musa
Cornelius M. Funk, … , Thomas G.P. Grünewald, Julian Musa
Published October 16, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI187627.
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High 4E-BP-1 expression associates with chromosome 8 gain and CDK4/6 sensitivity in Ewing Sarcoma

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Abstract

Chromosome 8 (chr8) gains are common in cancer, but their contribution to tumor heterogeneity is largely unexplored. Ewing sarcoma (EwS) is defined by FET::ETS fusions with few other recurrent mutations to explain clinical diversity. In EwS, chr8 gains are the second most frequent alteration, making it an ideal model to study their relevance in an otherwise silent genomic context. We report that chr8 gain-driven expression patterns correlate with poor overall survival of EwS patients. This effect is mainly mediated by increased expression of the translation initiation factor binding protein 4E-BP1, encoded by EIF4EBP1 on chr8. Among all chr8-encoded genes, EIF4EBP1 expression showed the strongest association with poor survival and correlated with chr8 gains in EwS tumors. Similar findings emerged across multiple TCGA cancer entities. Multi-omics profiling revealed that 4E-BP1 orchestrates a pro-proliferative proteomic network. Silencing 4E-BP1 reduced proliferation, clonogenicity, spheroidal growth in vitro, and tumor growth in vivo. Drug screens demonstrated that high 4E-BP1 expression sensitizes EwS to pharmacological CDK4/6-inhibition. Chr8 gains and elevated 4E-BP1 emerge as prognostic biomarkers in EwS, with poor outcomes driven by 4E-BP1-mediated pro-proliferative networks that sensitize tumors to CDK4/6 inhibitors. Testing for chr8 gains may enhance risk stratification and therapy in EwS and other cancers.

Authors

Cornelius M. Funk, Anna C. Ehlers, Martin F. Orth, Karim Aljakouch, Jing Li, Tilman L.B. Hoelting, Rainer Will, Florian H. Geyer, A. Katharina Ceranski, Franziska Willis, Endrit Vinca, Shunya Ohmura, Roland Imle, Jana Siebenlist, Angelina Yershova, Maximilian M.L. Knott, Felina Zahnow, Ana Sastre, Javier Alonso, Felix Sahm, Heike Peterziel, Anna Loboda, Martin Schneider, Ana Banito, Gabriel Leprivier, Wolfgang Hartmann, Uta Dirksen, Olaf Witt, Ina Oehme, Stefan M. Pfister, Laura Romero-Pérez, Jeroen Krijgsveld, Florencia Cidre-Aranaz, Thomas G.P. Grünewald, Julian Musa

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PIM3-mediated phosphorylation stabilizes myeloid leukemia factor 2 to promote metastasis in osteosarcoma
Cuiling Zeng, … , Tiebang Kang, Dan Liao
Cuiling Zeng, … , Tiebang Kang, Dan Liao
Published October 15, 2025
Citation Information: J Clin Invest. 2025;135(20):e191040. https://doi.org/10.1172/JCI191040.
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PIM3-mediated phosphorylation stabilizes myeloid leukemia factor 2 to promote metastasis in osteosarcoma

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Abstract

Osteosarcoma is the most common primary malignant bone cancer, characterized by a high incidence of lung metastasis and a lack of therapeutic targets. Here, by combining an in vivo CRISPR activation screen with the interactome of STUB1, a tumor suppressor in osteosarcoma, we identified that myeloid leukemia factor 2 (MLF2) promotes osteosarcoma metastasis. Mechanistically, MLF2 disrupted the interaction between BiP and IRE1α, thereby activating the IRE1α/XBP1-S-MMP9 axis. The E3 ligase STUB1 ubiquitinated MLF2 at Lys119 and targeted it for proteasomal degradation, whereas PIM3-mediated phosphorylation of MLF2 at Ser65 enhanced its stabilizing interaction with USP21. Our findings demonstrate that the PIM3/MLF2 axis is a critical regulator of osteosarcoma lung metastasis. We propose PIM3 as a potential therapeutic target for patients with osteosarcoma lung metastasis.

Authors

Cuiling Zeng, Xin Wang, Jinkun Zhong, Yu Zhang, Ju Deng, Wenqiang Liu, Weixuan Chen, Xinhao Yu, Dian Lin, Ruhua Zhang, Shang Wang, Jianpei Lao, Qi Zhao, Li Zhong, Tiebang Kang, Dan Liao

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RCC2 and CD24 cooperate to modulate prostate cancer progression through vimentin ubiquitination and β-catenin activation
Xuelian Cui, … , Jiangbing Zhou, Runhua Liu
Xuelian Cui, … , Jiangbing Zhou, Runhua Liu
Published October 15, 2025
Citation Information: J Clin Invest. 2025;135(20):e192883. https://doi.org/10.1172/JCI192883.
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RCC2 and CD24 cooperate to modulate prostate cancer progression through vimentin ubiquitination and β-catenin activation

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Abstract

CD24 promotes prostate cancer progression and metastasis by disrupting the ARF-NPM interaction and impairing p53 signaling. However, the mechanisms underlying CD24-driven metastasis remain unclear. This study identifies a novel interaction between CD24 and Regulator of Chromosome Condensation 2 (RCC2), a protein involved in cell proliferation and migration. IHC analysis of prostate adenocarcinoma samples showed frequent coexpression of CD24 (49%) and RCC2 (82%) with a positive correlation between coexpression of CD24 (49%) and RCC2 (82%). Functional assays revealed complex roles: RCC2 KO suppressed proliferation but increased migration and invasion, while CD24 KO reduced both proliferation and migration. Dual KO of CD24 and RCC2 further inhibited proliferation but had varied effects on migration. In mouse xenografts, RCC2 KO increased lung metastasis without significantly affecting primary tumor growth, while CD24 KO reduced both tumor growth and metastasis. Mechanistically, RCC2 controls migration by promoting ubiquitination and degradation of vimentin, affecting cytoskeletal dynamics. In contrast, CD24 targets RCC2 for degradation, thereby regulating β-catenin signaling. Notably, RCC2 KO enhances β-catenin activity by suppressing inhibitors AXIN2 and APC, whereas CD24 KO inhibits this pathway. These findings reveal a regulatory loop where CD24 and RCC2 reciprocally control proliferation and metastasis, positioning the CD24-RCC2 axis as a promising therapeutic target in prostate cancer.

Authors

Xuelian Cui, Yicun Wang, Chao Zhang, Zhichao Liu, Haiyan Yu, Lizhong Wang, Jiangbing Zhou, Runhua Liu

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C6orf223 promotes colorectal cancer growth and metastasis by facilitating PRMT5-MEP50 multiprotein complex assembling
Yufeng Qiao, … , Jinbo Liu, Pengcheng Bu
Yufeng Qiao, … , Jinbo Liu, Pengcheng Bu
Published October 15, 2025
Citation Information: J Clin Invest. 2025;135(20):e186052. https://doi.org/10.1172/JCI186052.
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C6orf223 promotes colorectal cancer growth and metastasis by facilitating PRMT5-MEP50 multiprotein complex assembling

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Abstract

Protein arginine methyltransferase 5 (PRMT5) complexes with methylosome protein 50 (MEP50) play crucial roles in tumor progress. However, the regulatory mechanism of governing the PRMT5-MEP50 hetero-octameric complex remains unclear. Here, we demonstrate that C6orf223, to our knowledge an uncharacterized protein, facilitates PRMT5-MEP50 multiprotein complex assembling, thereby promoting colorectal cancer (CRC) growth and metastasis. C6orf223 forms dimers through disulfide bonds, with its N-terminal arginine-enriched region binding to the C-terminal negatively charged groove of PRMT5, thus stabilizing PRMT5-MEP50 multiprotein and enhancing PRMT5 methyltransferase activity. Consequently, PRMT5-mediated H4R3me2s substantially decreases the expression of the tumor suppressor GATA5, leading to the upregulation of multiple oncogenic target genes including WWTR1, FGFR1, and CLU. Targeting C6orf223 using siRNAs encapsulated in ferritin protein shells effectively suppresses CRC tumor growth and metastasis. Collectively, our findings characterize the role of C6orf223 in facilitating PRMT5-MEP50 hetero-octameric complex assembling and suggest that C6orf223 could serve as a potential therapeutic target for CRC.

Authors

Yufeng Qiao, Zhenzhen Wu, Peng Wang, Yiliang Jin, Furong Bai, Fei Zhang, Yunhe An, Meiying Xue, Han Feng, Yong Zhang, Yaxin Hou, Junfeng Du, Huiyun Cai, Guizhi Shi, Bing Zhou, Pu Gao, Jizhong Lou, Peng Zhang, Kelong Fan, Jinbo Liu, Pengcheng Bu

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Cancer-associated fibroblasts enhance colorectal cancer lymphatic metastasis via CLEC11A/LGR5-mediated WNT pathway activation
Chuhan Zhang, … , Jinhai Deng, Zaoqu Liu
Chuhan Zhang, … , Jinhai Deng, Zaoqu Liu
Published October 15, 2025
Citation Information: J Clin Invest. 2025;135(20):e194243. https://doi.org/10.1172/JCI194243.
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Cancer-associated fibroblasts enhance colorectal cancer lymphatic metastasis via CLEC11A/LGR5-mediated WNT pathway activation

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Abstract

Hypoxia in the tumor microenvironment promotes lymphatic metastasis, yet the role of cancer-associated fibroblasts (CAFs) in this process remains insufficiently elucidated in colorectal cancer (CRC). In this study, we developed a large language model–based cellular hypoxia–predicting classifier to identify hypoxic CAFs (HCAFs) at single-cell resolution. Our findings revealed that HCAFs enhance CRC lymphatic metastasis by secreting CLEC11A, a protein that binds to the LGR5 receptor on tumor cells, subsequently activating the WNT/β-catenin signaling pathway. This promotes epithelial-mesenchymal transition and lymphangiogenesis, facilitating the spread of tumor cells via the lymphatic system. Furthermore, we demonstrate that the hypoxia-induced transcription factor HIF1A regulates the conversion of normoxic CAFs to HCAFs, driving CLEC11A expression and promoting metastasis. In vivo and vitro experiments confirmed the pro-metastatic role of CLEC11A in CRC, with its inhibition reducing lymphatic metastasis. This effect was markedly reversed by targeting the LGR5 receptor on tumor cells or inhibiting the WNT/β-catenin pathway, further elucidating the underlying mechanisms of CLEC11A-driven metastasis. These findings underscore the potential of targeting the CLEC11A-LGR5 axis to prevent lymphatic dissemination in CRC. Our study highlights the role of HCAFs in CRC progression and reveals mechanisms of lymphatic metastasis for intervention.

Authors

Chuhan Zhang, Teng Pan, Yuyuan Zhang, Yushuai Wu, Anning Zuo, Shutong Liu, Yuhao Ba, Benyu Liu, Shuaixi Yang, Yukang Chen, Hui Xu, Peng Luo, Quan Cheng, Siyuan Weng, Long Liu, Xing Zhou, Jingyuan Ning, Xinwei Han, Jinhai Deng, Zaoqu Liu

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A PP2A molecular glue overcomes ras/mapk inhibitor resistance in kras-mutant non-small cell lung cancer
Brynne Raines, … , Caitlin M. O'Connor, Goutham Narla
Brynne Raines, … , Caitlin M. O'Connor, Goutham Narla
Published October 14, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI193790.
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A PP2A molecular glue overcomes ras/mapk inhibitor resistance in kras-mutant non-small cell lung cancer

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Abstract

The effectiveness of RAS/MAPK inhibitors in treating metastatic KRAS-mutant NSCLC is often hindered by the development of resistance driven by disrupted negative feedback mechanisms led by phosphatases like PP2A. PP2A is frequently suppressed in lung cancer to maintain elevated RAS/MAPK activity. Despite its established role in regulating oncogenic signaling, targeting PP2A with RAS/MAPK to prevent resistance has not been previously demonstrated. In this study, we aimed to establish a treatment paradigm by combining a PP2A molecular glue with a RAS/MAPK inhibitor to restore PP2A activity and counteract resistance. We demonstrated that KRASG12C and MEK1/2 inhibitors disrupted PP2A carboxymethylation and destabilized critical heterotrimeric complexes. Furthermore, genetic disruption of PP2A carboxymethylation enhanced intrinsic resistance to MEK1/2 inhibition both in vitro and in vivo. We developed RPT04402, a PP2A molecular glue that selectively stabilizes PP2A-B56α heterotrimers. In both commercial cell lines and a patient-derived model, combining RPT04402 with a RAS/MAPK inhibitor slowed proliferation and enhanced apoptosis. In mouse xenografts, this combination induced tumor regressions, extended median survival, and delayed the onset of treatment resistance. These findings highlight that promoting PP2A stabilization and RAS/MAPK inhibition presents a promising therapeutic strategy to improve treatment outcomes and overcome resistance in metastatic KRAS-mutant NSCLC.

Authors

Brynne Raines, Stephanie Tseng-Rogenski, Amanda C. Dowdican, Irene Peris, Matthew Hinderman, Kaitlin P. Zawacki, Kelsey Barrie, Gabrielle Hodges Onishi, Alexander M. Dymond, Tahra K. Luther, Sydney Musser, Behirda Karaj Majchrowski, J. Chad Brenner, Aqila Ahmed, Derek J. Taylor, Caitlin M. O'Connor, Goutham Narla

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IL-17-producing γδ T cells in the tumor microenvironment promote radioresistance in mice
Yue Deng, … , Kunyu Yang, Chao Wan
Yue Deng, … , Kunyu Yang, Chao Wan
Published October 7, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI193945.
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IL-17-producing γδ T cells in the tumor microenvironment promote radioresistance in mice

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Abstract

The immunosuppressive tumor microenvironment (TME) drives radioresistance, but the role of γδ T cells in regulating radiosensitivity remains incompletely understood. In this study, we found that γδ T cell infiltration in the TME substantially increased after radiotherapy and contributed to radioresistance. Depletion of γδ T cells enhanced radiosensitivity. Single-cell RNA sequencing revealed that γδ T cells in the post-radiotherapy TME were characterized by the expression of Zbtb16, Il23r, and Il17a, and served as the primary source of IL-17A. These γδ T cells promoted radioresistance by recruiting myeloid-derived suppressor cells and suppressing T cell activation. Mechanistically, radiotherapy-induced tumor cell-derived microparticles containing dsDNA activated the cGAS-STING/NF-κB signaling pathway in macrophages, upregulating the expression of the chemokine CCL20, which was critical for γδ T cell recruitment. Targeting γδ T cells and IL-17A enhanced radiosensitivity and improved the efficacy of radiotherapy combined with anti-PD-1 immunotherapy, providing potential therapeutic strategies to overcome radioresistance.

Authors

Yue Deng, Xixi Liu, Xiao Yang, Wenwen Wei, Jiacheng Wang, Zheng Yang, Yajie Sun, Yan Hu, Haibo Zhang, Yijun Wang, Zhanjie Zhang, Lu Wen, Fang Huang, Kunyu Yang, Chao Wan

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S-acyl transferase ZDHHC13 modulates tumor microenvironment interactions to suppress metastasis in melanoma models
Hongjin Li, … , Colin Goding, Shuyang Chen
Hongjin Li, … , Colin Goding, Shuyang Chen
Published October 2, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI188249.
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S-acyl transferase ZDHHC13 modulates tumor microenvironment interactions to suppress metastasis in melanoma models

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Abstract

The intratumor microenvironment shapes the metastatic potential of cancer cells and their susceptibility to any immune response. Yet the nature of the signals within the microenvironment that control anti-cancer immunity and how they are regulated is poorly understood. Here, using melanoma as a model, we investigate the involvement in metastatic dissemination and the immune-modulatory microenvironment of Protein S-Acyl Transferases, as an underexplored class of potential therapeutic targets. We find that ZDHHC13, suppresses metastatic dissemination by palmitoylation of CTNND1, leading to stabilization of E-cadherin. Importantly, ZDHHC13 also reshapes the tumor immune microenvironment by suppressing lysophosphatidylcholine (LPC) synthesis in melanoma cells, leading to inhibition of M2-like tumor-associated macrophages that we show degrades E-cadherin via MMP12 expression. Consequently, ZDHHC13 activity suppresses tumor growth and metastasis in immunocompetent mice. Our study highlights the therapeutic potential of targeting the ZDHHC13-E-cadherin axis and its downstream metabolic and immune-modulatory mechanisms, offering additional strategies to inhibit melanoma progression and metastasis.

Authors

Hongjin Li, Jianke Lyu, Yu Sun, Chengqian Yin, Yuewen Li, Weiqiang Chen, Suan-Sin Foo, Xianfang Wu, Colin Goding, Shuyang Chen

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Androgen deprivation-mediated activation of AKT is enhanced in prostate cancer with TMPRSS2:ERG fusion
Fen Ma, … , Adam G. Sowalsky, Steven P. Balk
Fen Ma, … , Adam G. Sowalsky, Steven P. Balk
Published October 2, 2025
Citation Information: J Clin Invest. 2025. https://doi.org/10.1172/JCI192368.
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Androgen deprivation-mediated activation of AKT is enhanced in prostate cancer with TMPRSS2:ERG fusion

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Abstract

TMPRSS2:ERG gene fusion (T:E fusion) in prostate adenocarcinoma (PCa) puts ERG under androgen receptor (AR) regulated TMPRSS2 expression. T:E fusion is associated with PTEN loss, and is highly associated with decreased INPP4B expression, which together may compensate for ERG-mediated suppression of AKT signaling. We confirmed in PCa cells and a mouse PCa model that ERG suppresses IRS2 and AKT activation. In contrast, ERG downregulation did not increase INPP4B, suggesting its decrease is indirect and reflects selective pressure to suppress INPP4B function. Notably, INPP4B expression is decreased in PTEN-intact and PTEN-deficient T:E fusion tumors, suggesting selection for a nonredundant function. As ERG in T:E fusion tumors is AR regulated, we further assessed whether AR inhibition increases AKT activity in T:E fusion tumors. A T:E fusion positive PDX had increased AKT activity in vivo and response to AKT inhibition in vitro after androgen deprivation. Moreover, two clinical trials of neoadjuvant AR inhibition prior to radical prostatectomy showed greater increases in AKT activation in the T:E fusion positive versus negative tumors. These findings indicate that AKT activation may mitigate the efficacy of AR targeted therapy in T:E fusion PCa, and that these patients may most benefit from combination therapy targeting AR and AKT.

Authors

Fen Ma, Sen Chen, Luigi Cecchi, Betul Ersoy-Fazlioglu, Joshua W. Russo, Seiji Arai, Seifeldin Awad, Carla Calagua, Fang Xie, Larysa Poluben, Olga Voznesensky, Anson T. Ku, Fatima Karzai, Changmeng Cai, David J. Einstein, Huihui Ye, Xin Yuan, Alex Toker, Mary-Ellen Taplin, Adam G. Sowalsky, Steven P. Balk

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SOX9 drives a stem-like transcriptional state and platinum resistance in high-grade serous ovarian cancer
Alexander J. Duval, … , Daniela Matei, Mazhar Adli
Alexander J. Duval, … , Daniela Matei, Mazhar Adli
Published October 1, 2025
Citation Information: J Clin Invest. 2025;135(19):e186467. https://doi.org/10.1172/JCI186467.
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SOX9 drives a stem-like transcriptional state and platinum resistance in high-grade serous ovarian cancer

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Abstract

Chemotherapy resistance remains a formidable challenge to the treatment of high-grade serous ovarian cancer (HGSOC). The drug-tolerant cells may originate from a small population of inherently resistant cancer stem cells (CSCs) in primary tumors. In contrast, sufficient evidence suggests that drug tolerance can also be transiently acquired by nonstem cancer cells. Regardless of the route, key regulators of this plastic process are poorly understood. Here, we utilized multiomics, tumor microarrays, and epigenetic modulation to demonstrate that SOX9 is a key chemo-induced driver of chemoresistance in HGSOC. Epigenetic upregulation of SOX9 was sufficient to induce chemoresistance in multiple HGSOC lines. Moreover, this upregulation induced the formation of a stem-like subpopulation and significant chemoresistance in vivo. Mechanistically, SOX9 increased transcriptional divergence, reprogramming the transcriptional state of naive cells into a stem-like state. Supporting this, we identified a rare cluster of SOX9-expressing cells in primary tumors that were highly enriched for CSCs and chemoresistance-associated stress gene modules. Notably, single-cell analysis showed that chemo treatment results in rapid population-level induction of SOX9 that enriches for a stem-like transcriptional state. Altogether, these findings implicate SOX9 as a critical regulator of early steps of transcriptional reprogramming that lead to chemoresistance through a CSC-like state in HGSOC.

Authors

Alexander J. Duval, Fidan Seker-Polat, Magdalena Rogozinska, Meric Kinali, Ann E. Walts, Ozlem Neyisci, Yaqi Zhang, Zhonglin Li, Edward J. Tanner III, Allison E. Grubbs, Sandra Orsulic, Daniela Matei, Mazhar Adli

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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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