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Oncology

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ZEB1 sensitizes lung adenocarcinoma to metastasis suppression by PI3K antagonism
Yanan Yang, … , Chad J. Creighton, Jonathan M. Kurie
Yanan Yang, … , Chad J. Creighton, Jonathan M. Kurie
Published April 24, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI72171.
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ZEB1 sensitizes lung adenocarcinoma to metastasis suppression by PI3K antagonism

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Abstract

Epithelial tumor cells that have undergone epithelial-to-mesenchymal transition (EMT) are typically prone to metastasis and drug resistance and contribute to a poor clinical outcome. The transcription factor ZEB1 is a known driver of EMT, and mediators of ZEB1 represent potential therapeutic targets for metastasis suppression. Here, we have shown that phosphatidylinositol 3-kinase–targeted (PI3K-targeted) therapy suppresses metastasis in a mouse model of Kras/Tp53-mutant lung adenocarcinoma that develops metastatic disease due to high expression of ZEB1. In lung adenocarcinoma cells from Kras/Tp53-mutant animals and human lung cancer cell lines, ZEB1 activated PI3K by derepressing miR-200 targets, including amphiregulin (AREG), betacellulin (BTC), and the transcription factor GATA6, which stimulated an EGFR/ERBB2 autocrine loop. Additionally, ZEB1-dependent derepression of the miR-200 and miR-183 target friend of GATA 2 (FOG2) enhanced GATA3-induced expression of the p110α catalytic subunit of PI3K. Knockdown of FOG2, p110α, and RHEB ameliorated invasive and metastatic propensities of tumor cells. Surprisingly, FOG2 was not required for mesenchymal differentiation, suggesting that mesenchymal differentiation and invasion are distinct and separable processes. Together, these results indicate that ZEB1 sensitizes lung adenocarcinoma cells to metastasis suppression by PI3K-targeted therapy and suggest that treatments to selectively modify the metastatic behavior of mesenchymal tumor cells are feasible and may be of clinical value.

Authors

Yanan Yang, Young-Ho Ahn, Yulong Chen, Xiaochao Tan, Lixia Guo, Don L. Gibbons, Christin Ungewiss, David H. Peng, Xin Liu, Steven H. Lin, Nishan Thilaganathan, Ignacio I. Wistuba, Jaime Rodriguez-Canales, Georgia McLendon, Chad J. Creighton, Jonathan M. Kurie

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The tumor suppressor folliculin regulates AMPK-dependent metabolic transformation
Ming Yan, … , Andrew R. Tee, Arnim Pause
Ming Yan, … , Andrew R. Tee, Arnim Pause
Published April 24, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI71749.
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The tumor suppressor folliculin regulates AMPK-dependent metabolic transformation

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Abstract

The Warburg effect is a tumorigenic metabolic adaptation process characterized by augmented aerobic glycolysis, which enhances cellular bioenergetics. In normal cells, energy homeostasis is controlled by AMPK; however, its role in cancer is not understood, as both AMPK-dependent tumor-promoting and -inhibiting functions were reported. Upon stress, energy levels are maintained by increased mitochondrial biogenesis and glycolysis, controlled by transcriptional coactivator PGC-1α and HIF, respectively. In normoxia, AMPK induces PGC-1α, but how HIF is activated is unclear. Germline mutations in the gene encoding the tumor suppressor folliculin (FLCN) lead to Birt-Hogg-Dubé (BHD) syndrome, which is associated with an increased cancer risk. FLCN was identified as an AMPK binding partner, and we evaluated its role with respect to AMPK-dependent energy functions. We revealed that loss of FLCN constitutively activates AMPK, resulting in PGC-1α–mediated mitochondrial biogenesis and increased ROS production. ROS induced HIF transcriptional activity and drove Warburg metabolic reprogramming, coupling AMPK-dependent mitochondrial biogenesis to HIF-dependent metabolic changes. This reprogramming stimulated cellular bioenergetics and conferred a HIF-dependent tumorigenic advantage in FLCN-negative cancer cells. Moreover, this pathway is conserved in a BHD-derived tumor. These results indicate that FLCN inhibits tumorigenesis by preventing AMPK-dependent HIF activation and the subsequent Warburg metabolic transformation.

Authors

Ming Yan, Marie-Claude Gingras, Elaine A. Dunlop, Yann Nouët, Fanny Dupuy, Zahra Jalali, Elite Possik, Barry J. Coull, Dmitri Kharitidi, Anders Bondo Dydensborg, Brandon Faubert, Miriam Kamps, Sylvie Sabourin, Rachael S. Preston, David Mark Davies, Taren Roughead, Laëtitia Chotard, Maurice A.M. van Steensel, Russell Jones, Andrew R. Tee, Arnim Pause

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Multifactorial ERβ and NOTCH1 control of squamous differentiation and cancer
Yang Sui Brooks, … , Karine Lefort, G. Paolo Dotto
Yang Sui Brooks, … , Karine Lefort, G. Paolo Dotto
Published April 17, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI72718.
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Multifactorial ERβ and NOTCH1 control of squamous differentiation and cancer

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Abstract

Downmodulation or loss-of-function mutations of the gene encoding NOTCH1 are associated with dysfunctional squamous cell differentiation and development of squamous cell carcinoma (SCC) in skin and internal organs. While NOTCH1 receptor activation has been well characterized, little is known about how NOTCH1 gene transcription is regulated. Using bioinformatics and functional screening approaches, we identified several regulators of the NOTCH1 gene in keratinocytes, with the transcription factors DLX5 and EGR3 and estrogen receptor β (ERβ) directly controlling its expression in differentiation. DLX5 and ERG3 are required for RNA polymerase II (PolII) recruitment to the NOTCH1 locus, while ERβ controls NOTCH1 transcription through RNA PolII pause release. Expression of several identified NOTCH1 regulators, including ERβ, is frequently compromised in skin, head and neck, and lung SCCs and SCC-derived cell lines. Furthermore, a keratinocyte ERβ–dependent program of gene expression is subverted in SCCs from various body sites, and there are consistent differences in mutation and gene-expression signatures of head and neck and lung SCCs in female versus male patients. Experimentally increased ERβ expression or treatment with ERβ agonists inhibited proliferation of SCC cells and promoted NOTCH1 expression and squamous differentiation both in vitro and in mouse xenotransplants. Our data identify a link between transcriptional control of NOTCH1 expression and the estrogen response in keratinocytes, with implications for differentiation therapy of squamous cancer.

Authors

Yang Sui Brooks, Paola Ostano, Seung-Hee Jo, Jun Dai, Spiro Getsios, Piotr Dziunycz, Günther F.L. Hofbauer, Kara Cerveny, Giovanna Chiorino, Karine Lefort, G. Paolo Dotto

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Genetic and pharmacologic inhibition of EPHA2 promotes apoptosis in NSCLC
Katherine R. Amato, … , Nathanael S. Gray, Jin Chen
Katherine R. Amato, … , Nathanael S. Gray, Jin Chen
Published April 8, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI72522.
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Genetic and pharmacologic inhibition of EPHA2 promotes apoptosis in NSCLC

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Abstract

Genome-wide analyses determined previously that the receptor tyrosine kinase (RTK) EPHA2 is commonly overexpressed in non–small cell lung cancers (NSCLCs). EPHA2 overexpression is associated with poor clinical outcomes; therefore, EPHA2 may represent a promising therapeutic target for patients with NSCLC. In support of this hypothesis, here we have shown that targeted disruption of EphA2 in a murine model of aggressive Kras-mutant NSCLC impairs tumor growth. Knockdown of EPHA2 in human NSCLC cell lines reduced cell growth and viability, confirming the epithelial cell autonomous requirements for EPHA2 in NSCLCs. Targeting EPHA2 in NSCLCs decreased S6K1-mediated phosphorylation of cell death agonist BAD and induced apoptosis. Induction of EPHA2 knockdown within established NSCLC tumors in a subcutaneous murine model reduced tumor volume and induced tumor cell death. Furthermore, an ATP-competitive EPHA2 RTK inhibitor, ALW-II-41-27, reduced the number of viable NSCLC cells in a time-dependent and dose-dependent manner in vitro and induced tumor regression in human NSCLC xenografts in vivo. Collectively, these data demonstrate a role for EPHA2 in the maintenance and progression of NSCLCs and provide evidence that ALW-II-41-27 effectively inhibits EPHA2-mediated tumor growth in preclinical models of NSCLC.

Authors

Katherine R. Amato, Shan Wang, Andrew K. Hastings, Victoria M. Youngblood, Pranav R. Santapuram, Haiying Chen, Justin M. Cates, Daniel C. Colvin, Fei Ye, Dana M. Brantley-Sieders, Rebecca S. Cook, Li Tan, Nathanael S. Gray, Jin Chen

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Excess PLAC8 promotes an unconventional ERK2-dependent EMT in colon cancer
Cunxi Li, … , Lila Solnica-Krezel, Robert J. Coffey
Cunxi Li, … , Lila Solnica-Krezel, Robert J. Coffey
Published April 1, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI71103.
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Excess PLAC8 promotes an unconventional ERK2-dependent EMT in colon cancer

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Abstract

The epithelial-to-mesenchymal transition (EMT) transcriptional program is characterized by repression of E-cadherin (CDH1) and induction of N-cadherin (CDH2), and mesenchymal genes like vimentin (VIM). Placenta-specific 8 (PLAC8) has been implicated in colon cancer; however, how PLAC8 contributes to disease is unknown, and endogenous PLAC8 protein has not been studied. We analyzed zebrafish and human tissues and found that endogenous PLAC8 localizes to the apical domain of differentiated intestinal epithelium. Colon cancer cells with elevated PLAC8 levels exhibited EMT features, including increased expression of VIM and zinc finger E-box binding homeobox 1 (ZEB1), aberrant cell motility, and increased invasiveness. In contrast to classical EMT, PLAC8 overexpression reduced cell surface CDH1 and upregulated P-cadherin (CDH3) without affecting CDH2 expression. PLAC8-induced EMT was linked to increased phosphorylated ERK2 (p-ERK2), and ERK2 knockdown restored cell surface CDH1 and suppressed CDH3, VIM, and ZEB1 upregulation. In vitro, PLAC8 directly bound and inactivated the ERK2 phosphatase DUSP6, thereby increasing p-ERK2. In a murine xenograft model, knockdown of endogenous PLAC8 in colon cancer cells resulted in smaller tumors, reduced local invasion, and decreased p-ERK2. Using MultiOmyx, a multiplex immunofluorescence-based methodology, we observed coexpression of cytosolic PLAC8, CDH3, and VIM at the leading edge of a human colorectal tumor, supporting a role for PLAC8 in cancer invasion in vivo.

Authors

Cunxi Li, Haiting Ma, Yang Wang, Zheng Cao, Ramona Graves-Deal, Anne E. Powell, Alina Starchenko, Gregory D. Ayers, Mary Kay Washington, Vidya Kamath, Keyur Desai, Michael J. Gerdes, Lila Solnica-Krezel, Robert J. Coffey

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Senescence-associated SIN3B promotes inflammation and pancreatic cancer progression
Maïté Rielland, … , George Miller, Gregory David
Maïté Rielland, … , George Miller, Gregory David
Published April 1, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI72619.
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Senescence-associated SIN3B promotes inflammation and pancreatic cancer progression

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Abstract

Pancreatic ductal adenocarcinoma (PDAC) is strikingly resistant to conventional therapeutic approaches. We previously demonstrated that the histone deacetylase–associated protein SIN3B is essential for oncogene-induced senescence in cultured cells. Here, using a mouse model of pancreatic cancer, we have demonstrated that SIN3B is required for activated KRAS-induced senescence in vivo. Surprisingly, impaired senescence as the result of genetic inactivation of Sin3B was associated with delayed PDAC progression and correlated with an impaired inflammatory response. In murine and human pancreatic cells and tissues, levels of SIN3B correlated with KRAS-induced production of IL-1α. Furthermore, evaluation of human pancreatic tissue and cancer cells revealed that Sin3B was decreased in control and PDAC samples, compared with samples from patients with pancreatic inflammation. These results indicate that senescence-associated inflammation positively correlates with PDAC progression and suggest that SIN3B has potential as a therapeutic target for inhibiting inflammation-driven tumorigenesis.

Authors

Maïté Rielland, David J. Cantor, Richard Graveline, Cristina Hajdu, Lisa Mara, Beatriz de Diego Diaz, George Miller, Gregory David

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Melanoma NOS1 expression promotes dysfunctional IFN signaling
Qiuzhen Liu, … , Ena Wang, Francesco M. Marincola
Qiuzhen Liu, … , Ena Wang, Francesco M. Marincola
Published April 1, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI69611.
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Melanoma NOS1 expression promotes dysfunctional IFN signaling

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Abstract

In multiple forms of cancer, constitutive activation of type I IFN signaling is a critical consequence of immune surveillance against cancer; however, PBMCs isolated from cancer patients exhibit depressed STAT1 phosphorylation in response to IFN-α, suggesting IFN signaling dysfunction. Here, we demonstrated in a coculture system that melanoma cells differentially impairs the IFN-α response in PBMCs and that the inhibitory potential of a particular melanoma cell correlates with NOS1 expression. Comparison of gene transcription and array comparative genomic hybridization (aCGH) between melanoma cells from different patients indicated that suppression of IFN-α signaling correlates with an amplification of the NOS1 locus within segment 12q22-24. Evaluation of NOS1 levels in melanomas and IFN responsiveness of purified PBMCs from patients indicated a negative correlation between NOS1 expression in melanomas and the responsiveness of PBMCs to IFN-α. Furthermore, in an explorative study, NOS1 expression in melanoma metastases was negatively associated with patient response to adoptive T cell therapy. This study provides a link between cancer cell phenotype and IFN signal dysfunction in circulating immune cells.

Authors

Qiuzhen Liu, Sara Tomei, Maria Libera Ascierto, Valeria De Giorgi, Davide Bedognetti, Cuilian Dai, Lorenzo Uccellini, Tara Spivey, Zoltan Pos, Jaime Thomas, Jennifer Reinboth, Daniela Murtas, Qianbing Zhang, Lotfi Chouchane, Geoffrey R. Weiss, Craig L. Slingluff Jr., Peter P. Lee, Steven A. Rosenberg, Harvey Alter, Kaitai Yao, Ena Wang, Francesco M. Marincola

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RIP140 increases APC expression and controls intestinal homeostasis and tumorigenesis
Marion Lapierre, … , Malcolm Parker, Vincent Cavailles
Marion Lapierre, … , Malcolm Parker, Vincent Cavailles
Published March 25, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI65178.
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RIP140 increases APC expression and controls intestinal homeostasis and tumorigenesis

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Abstract

Deregulation of the Wnt/APC/β-catenin signaling pathway is an important consequence of tumor suppressor APC dysfunction. Genetic and molecular data have established that disruption of this pathway contributes to the development of colorectal cancer. Here, we demonstrate that the transcriptional coregulator RIP140 regulates intestinal homeostasis and tumorigenesis. Using Rip140-null mice and mice overexpressing human RIP140, we found that RIP140 inhibited intestinal epithelial cell proliferation and apoptosis. Interestingly, following whole-body irradiation, mice lacking RIP140 exhibited improved regenerative capacity in the intestine, while mice overexpressing RIP140 displayed reduced recovery. Enhanced RIP140 expression strongly repressed human colon cancer cell proliferation in vitro and after grafting onto nude mice. Moreover, in murine tissues and human cancer cells, RIP140 stimulated APC transcription and inhibited β-catenin activation and target gene expression. Finally, RIP140 mRNA and RIP140 protein levels were decreased in human colon cancers compared with those in normal mucosal tissue, and low levels of RIP140 expression in adenocarcinomas from patients correlated with poor prognosis. Together, these results support a tumor suppressor role for RIP140 in colon cancer.

Authors

Marion Lapierre, Sandrine Bonnet, Caroline Bascoul-Mollevi, Imade Ait-Arsa, Stéphan Jalaguier, Maguy Del Rio, Michela Plateroti, Paul Roepman, Marc Ychou, Julie Pannequin, Frédéric Hollande, Malcolm Parker, Vincent Cavailles

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Tumor endothelial marker 1–specific DNA vaccination targets tumor vasculature
John G. Facciponte, … , George Coukos, Andrea Facciabene
John G. Facciponte, … , George Coukos, Andrea Facciabene
Published March 18, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI67382.
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Tumor endothelial marker 1–specific DNA vaccination targets tumor vasculature

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Abstract

Tumor endothelial marker 1 (TEM1; also known as endosialin or CD248) is a protein found on tumor vasculature and in tumor stroma. Here, we tested whether TEM1 has potential as a therapeutic target for cancer immunotherapy by immunizing immunocompetent mice with Tem1 cDNA fused to the minimal domain of the C fragment of tetanus toxoid (referred to herein as Tem1-TT vaccine). Tem1-TT vaccination elicited CD8+ and/or CD4+ T cell responses against immunodominant TEM1 protein sequences. Prophylactic immunization of animals with Tem1-TT prevented or delayed tumor formation in several murine tumor models. Therapeutic vaccination of tumor-bearing mice reduced tumor vascularity, increased infiltration of CD3+ T cells into the tumor, and controlled progression of established tumors. Tem1-TT vaccination also elicited CD8+ cytotoxic T cell responses against murine tumor-specific antigens. Effective Tem1-TT vaccination did not affect angiogenesis-dependent physiological processes, including wound healing and reproduction. Based on these data and the widespread expression of TEM1 on the vasculature of different tumor types, we conclude that targeting TEM1 has therapeutic potential in cancer immunotherapy.

Authors

John G. Facciponte, Stefano Ugel, Francesco De Sanctis, Chunsheng Li, Liping Wang, Gautham Nair, Sandy Sehgal, Arjun Raj, Efthymia Matthaiou, George Coukos, Andrea Facciabene

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CDK4 deficiency promotes genomic instability and enhances Myc-driven lymphomagenesis
Yuanzhi Lu, … , John L. Cleveland, Xianghong Zou
Yuanzhi Lu, … , John L. Cleveland, Xianghong Zou
Published March 10, 2014
Citation Information: J Clin Invest. 2014. https://doi.org/10.1172/JCI63139.
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CDK4 deficiency promotes genomic instability and enhances Myc-driven lymphomagenesis

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Abstract

The G1 kinase CDK4 is amplified or overexpressed in some human tumors and promotes tumorigenesis by inhibiting known tumor suppressors. Here, we report that CDK4 deficiency markedly accelerated lymphoma development in the Eμ-Myc transgenic mouse model of B lymphoma and that silencing or loss of CDK4 augmented the tumorigenic potential of Myc-driven mouse and human B cell lymphoma in transplant models. Accelerated disease in CDK4-deficient Eμ-Myc transgenic mice was associated with rampant genomic instability that was provoked by dysregulation of a FOXO1/RAG1/RAG2 pathway. Specifically, CDK4 phosphorylated and inactivated FOXO1, which prevented FOXO1-dependent induction of Rag1 and Rag2 transcription. CDK4-deficient Eμ-Myc B cells had high levels of the active form of FOXO1 and elevated RAG1 and RAG2. Furthermore, overexpression of RAG1 and RAG2 accelerated lymphoma development in a transplant model, with RAG1/2-expressing tumors exhibiting hallmarks of genomic instability. Evaluation of human tumor samples revealed that CDK4 expression was markedly suppressed, while FOXO1 expression was elevated, in several subtypes of human non-Hodgkin B cell lymphoma. Collectively, these findings establish a context-specific tumor suppressor function for CDK4 that prevents genomic instability, which contributes to B cell lymphoma. Furthermore, our data suggest that targeting CDK4 may increase the risk for the development and/or progression of lymphoma.

Authors

Yuanzhi Lu, Yongsheng Wu, Xiaoling Feng, Rulong Shen, Jing H. Wang, Mohammad Fallahi, Weimin Li, Chunying Yang, William Hankey, Weiqiang Zhao, Ramesh K. Ganju, Ming O. Li, John L. Cleveland, Xianghong Zou

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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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