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Oncology

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Atorvastatin is associated with reduced cisplatin-induced hearing loss
Katharine A. Fernandez, … , Nicole C. Schmitt, Lisa L. Cunningham
Katharine A. Fernandez, … , Nicole C. Schmitt, Lisa L. Cunningham
Published January 4, 2021
Citation Information: J Clin Invest. 2021;131(1):e142616. https://doi.org/10.1172/JCI142616.
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Atorvastatin is associated with reduced cisplatin-induced hearing loss

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Abstract

BACKGROUND Cisplatin is widely used to treat adult and pediatric cancers. It is the most ototoxic drug in clinical use, resulting in permanent hearing loss in approximately 50% of treated patients. There is a major need for therapies that prevent cisplatin-induced hearing loss. Studies in mice suggest that concurrent use of statins reduces cisplatin-induced hearing loss.METHODS We examined hearing thresholds from 277 adults treated with cisplatin for head and neck cancer. Pretreatment and posttreatment audiograms were collected within 90 days of initiation and completion of cisplatin therapy. The primary outcome measure was a change in hearing as defined by the National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE).RESULTS Among patients on concurrent atorvastatin, 9.7% experienced a CTCAE grade 2 or higher cisplatin-induced hearing loss compared with 29.4% in nonstatin users (P < 0.0001). A mixed-effect model analysis showed that atorvastatin use was significantly associated with reduced cisplatin-induced hearing loss (P ≤ 0.01). An adjusted odds ratio (OR) analysis indicated that an atorvastatin user is 53% less likely to acquire a cisplatin-induced hearing loss than a nonstatin user (OR = 0.47; 95% CI, 0.30–0.78). Three-year survival rates were not different between atorvastatin users and nonstatin users (P > 0.05).CONCLUSIONS Our data indicate that atorvastatin use is associated with reduced incidence and severity of cisplatin-induced hearing loss in adults being treated for head and neck cancer.TRIAL REGISTRATION ClinicalTrials.gov identifier NCT03225157.FUNDING Funding was provided by the Division of Intramural Research at the National Institute on Deafness and Other Communication Disorders (1 ZIA DC000079, ZIA DC000090).

Authors

Katharine A. Fernandez, Paul Allen, Maura Campbell, Brandi Page, Thomas Townes, Chuan-Ming Li, Hui Cheng, Jaylon Garrett, Marcia Mulquin, Anna Clements, Deborah Mulford, Candice Ortiz, Carmen Brewer, Judy R. Dubno, Shawn Newlands, Nicole C. Schmitt, Lisa L. Cunningham

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RGS2-mediated translational control mediates cancer cell dormancy and tumor relapse
Jaebeom Cho, … , Mien-Chie Hung, Ho-Young Lee
Jaebeom Cho, … , Mien-Chie Hung, Ho-Young Lee
Published January 4, 2021
Citation Information: J Clin Invest. 2021;131(1):e136779. https://doi.org/10.1172/JCI136779.
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RGS2-mediated translational control mediates cancer cell dormancy and tumor relapse

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Abstract

Slow-cycling/dormant cancer cells (SCCs) have pivotal roles in driving cancer relapse and drug resistance. A mechanistic explanation for cancer cell dormancy and therapeutic strategies targeting SCCs are necessary to improve patient prognosis, but are limited because of technical challenges to obtaining SCCs. Here, by applying proliferation-sensitive dyes and chemotherapeutics to non–small cell lung cancer (NSCLC) cell lines and patient-derived xenografts, we identified a distinct SCC subpopulation that resembled SCCs in patient tumors. These SCCs displayed major dormancy-like phenotypes and high survival capacity under hostile microenvironments through transcriptional upregulation of regulator of G protein signaling 2 (RGS2). Database analysis revealed RGS2 as a biomarker of retarded proliferation and poor prognosis in NSCLC. We showed that RGS2 caused prolonged translational arrest in SCCs through persistent eukaryotic initiation factor 2 (eIF2α) phosphorylation via proteasome-mediated degradation of activating transcription factor 4 (ATF4). Translational activation through RGS2 antagonism or the use of phosphodiesterase 5 inhibitors, including sildenafil (Viagra), promoted ER stress–induced apoptosis in SCCs in vitro and in vivo under stressed conditions, such as those induced by chemotherapy. Our results suggest that a low-dose chemotherapy and translation-instigating pharmacological intervention in combination is an effective strategy to prevent tumor progression in NSCLC patients after rigorous chemotherapy.

Authors

Jaebeom Cho, Hye-Young Min, Ho Jin Lee, Seung Yeob Hyun, Jeong Yeon Sim, Myungkyung Noh, Su Jung Hwang, Shin-Hyung Park, Hye-Jin Boo, Hyo-Jong Lee, Sungyoul Hong, Rang-Woon Park, Young Kee Shin, Mien-Chie Hung, Ho-Young Lee

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DYRK1A regulates B cell acute lymphoblastic leukemia through phosphorylation of FOXO1 and STAT3
Rahul S. Bhansali, … , Sébastien Malinge, John D. Crispino
Rahul S. Bhansali, … , Sébastien Malinge, John D. Crispino
Published January 4, 2021
Citation Information: J Clin Invest. 2021;131(1):e135937. https://doi.org/10.1172/JCI135937.
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DYRK1A regulates B cell acute lymphoblastic leukemia through phosphorylation of FOXO1 and STAT3

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Abstract

DYRK1A is a serine/threonine kinase encoded on human chromosome 21 (HSA21) that has been implicated in several pathologies of Down syndrome (DS), including cognitive deficits and Alzheimer’s disease. Although children with DS are predisposed to developing leukemia, especially B cell acute lymphoblastic leukemia (B-ALL), the HSA21 genes that contribute to malignancies remain largely undefined. Here, we report that DYRK1A is overexpressed and required for B-ALL. Genetic and pharmacologic inhibition of DYRK1A decreased leukemic cell expansion and suppressed B-ALL development in vitro and in vivo. Furthermore, we found that FOXO1 and STAT3, transcription factors that are indispensable for B cell development, are critical substrates of DYRK1A. Loss of DYRK1A-mediated FOXO1 and STAT3 signaling disrupted DNA damage and ROS regulation, respectively, leading to preferential cell death in leukemic B cells. Thus, we reveal a DYRK1A/FOXO1/STAT3 axis that facilitates the development and maintenance of B-ALL.

Authors

Rahul S. Bhansali, Malini Rammohan, Paul Lee, Anouchka P. Laurent, Qiang Wen, Praveen Suraneni, Bon Ham Yip, Yi-Chien Tsai, Silvia Jenni, Beat Bornhauser, Aurélie Siret, Corinne Fruit, Alexandra Pacheco-Benichou, Ethan Harris, Thierry Besson, Benjamin J. Thompson, Young Ah Goo, Nobuko Hijiya, Maria Vilenchik, Shai Izraeli, Jean-Pierre Bourquin, Sébastien Malinge, John D. Crispino

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Targeting the mitochondrial trifunctional protein restrains tumor growth in oxidative lung carcinomas
Nivea Dias Amoedo, … , Matthieu Thumerel, Rodrigue Rossignol
Nivea Dias Amoedo, … , Matthieu Thumerel, Rodrigue Rossignol
Published January 4, 2021
Citation Information: J Clin Invest. 2021;131(1):e133081. https://doi.org/10.1172/JCI133081.
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Targeting the mitochondrial trifunctional protein restrains tumor growth in oxidative lung carcinomas

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Abstract

Metabolic reprogramming is a common hallmark of cancer, but a large variability in tumor bioenergetics exists between patients. Using high-resolution respirometry on fresh biopsies of human lung adenocarcinoma, we identified 2 subgroups reflected in the histologically normal, paired, cancer-adjacent tissue: high (OX+) mitochondrial respiration and low (OX–) mitochondrial respiration. The OX+ tumors poorly incorporated [18F]fluorodeoxy-glucose and showed increased expression of the mitochondrial trifunctional fatty acid oxidation enzyme (MTP; HADHA) compared with the paired adjacent tissue. Genetic inhibition of MTP altered OX+ tumor growth in vivo. Trimetazidine, an approved drug inhibitor of MTP used in cardiology, also reduced tumor growth and induced disruption of the physical interaction between the MTP and respiratory chain complex I, leading to a cellular redox and energy crisis. MTP expression in tumors was assessed using histology scoring methods and varied in negative correlation with [18F]fluorodeoxy-glucose incorporation. These findings provide proof-of-concept data for preclinical, precision, bioenergetic medicine in oxidative lung carcinomas.

Authors

Nivea Dias Amoedo, Saharnaz Sarlak, Emilie Obre, Pauline Esteves, Hugues Bégueret, Yann Kieffer, Benoît Rousseau, Alexis Dupis, Julien Izotte, Nadège Bellance, Laetitia Dard, Isabelle Redonnet-Vernhet, Giuseppe Punzi, Mariana Figueiredo Rodrigues, Elodie Dumon, Walid Mafhouf, Véronique Guyonnet-Dupérat, Lara Gales, Tony Palama, Floriant Bellvert, Nathalie Dugot-Senan, Stéphane Claverol, Jean-Marc Baste, Didier Lacombe, Hamid Reza Rezvani, Ciro Leonardo Pierri, Fatima Mechta-Grigoriou, Matthieu Thumerel, Rodrigue Rossignol

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BCL6 confers KRAS-mutant non–small-cell lung cancer resistance to BET inhibitors
Jiawei Guo, … , Mingyao Liu, Xiufeng Pang
Jiawei Guo, … , Mingyao Liu, Xiufeng Pang
Published January 4, 2021
Citation Information: J Clin Invest. 2021;131(1):e133090. https://doi.org/10.1172/JCI133090.
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BCL6 confers KRAS-mutant non–small-cell lung cancer resistance to BET inhibitors

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Abstract

The bromodomain and extra-terminal domain (BET) proteins are promising therapeutic targets to treat refractory solid tumors; however, inherent resistance remains a major challenge in the clinic. Recently, the emerging role of the oncoprotein B cell lymphoma 6 (BCL6) in tumorigenesis and stress response has been unveiled. Here, we demonstrate that BCL6 was upregulated upon BET inhibition in KRAS-mutant cancers, including non–small-cell lung cancer (NSCLC). We further found that BRD3, not BRD2 or BRD4, directly interacted with BCL6 and maintained the negative autoregulatory circuit of BCL6. Disrupting this negative autoregulation by BET inhibitors (BETi) resulted in a striking increase in BCL6 transcription, which further activated the mTOR signaling pathway through repression of the tumor suppressor death-associated protein kinase 2. Importantly, pharmacological inhibition of either BCL6 or mTOR improved the tumor response and enhanced the sensitivity of KRAS-mutant NSCLC to BETi in both in vitro and in vivo settings. Overall, our findings identify a mechanism of BRD3-mediated BCL6 autoregulation and further develop an effective combinatorial strategy to circumvent BETi resistance in KRAS-driven NSCLC.

Authors

Jiawei Guo, Yanan Liu, Jing Lv, Bin Zou, Zhi Chen, Kun Li, Juanjuan Feng, Zhenyu Cai, Lai Wei, Mingyao Liu, Xiufeng Pang

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Cyclin A2 maintains colon homeostasis and is a prognostic factor in CRC
Yuchen Guo, … , Bénédicte Lemmers, Michael Hahne
Yuchen Guo, … , Bénédicte Lemmers, Michael Hahne
Published December 17, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI131517.
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Cyclin A2 maintains colon homeostasis and is a prognostic factor in CRC

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Abstract

To clarify the function of cyclin A2 in colon homeostasis and colorectal cancer (CRC), we generated mice deficient for cyclin A2 in colonic epithelial cells (CEC). Colons of those mice displayed architectural changes in the mucosa, and signs of inflammation as well as an increased proliferation of CEC associated with the appearance of low- and high-grade dysplasia. The main initial events triggering those alterations in cyclin A2 deficient CEC appear to be abnormal mitoses and DNA damage. Cyclin A2 deletion in CEC promoted the development of dysplasia and adenocarcinomas in the murine colitis-associated cancer model. We next explored the status of cyclin A2 expression in clinical CRC samples at the mRNA and protein level and found higher expression in tumors of stage I and II patients compared to those of stage III and IV. A meta-analysis of 11 transcriptome datasets comprising 2,239 primary CRC tumors displayed different CCNA2 (the mRNA coding for cyclin A2) expression levels among the CRC tumor subtypes with highest in CMS1 and lowest in CMS4. Moreover, high expression of CCNA2 was found to be a new independent prognosis factor for CRC tumors.

Authors

Yuchen Guo, Monica Gabola, Rossano Lattanzio, Conception Paul, Valérie Pinet, Ruizhi Tang, Hulya Turali, Julie Bremond, Ciro Longobardi, Chloé Maurizy, Quentin Da Costa, Pascal Finetti, Florence Boissière-Michot, Benjamin Rivière, Céline Lemmers, Séverine Garnier, François Bertucci, Inti Zlobec, Karim Chebli, Jamal Tazi, Rania Azar, Jean-Marie Blanchard, Peter Sicinski, Emilie Mamessier, Bénédicte Lemmers, Michael Hahne

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Regulation and targeting of androgen receptor nuclear localization in castration-resistant prostate cancer
Shidong Lv, … , Wenhua Huang, Zhou Wang
Shidong Lv, … , Wenhua Huang, Zhou Wang
Published December 17, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI141335.
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Regulation and targeting of androgen receptor nuclear localization in castration-resistant prostate cancer

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Abstract

Androgen receptor (AR) nuclear localization is necessary for its activation as a transcription factor. Defining the mechanisms regulating AR nuclear localization in androgen-sensitive cells, and how these mechanisms are dysregulated in castration-resistant prostate cancer (CRPC) cells are fundamentally important and clinically relevant. According to the classical model of AR intracellular trafficking, androgens induce AR nuclear import and androgen withdrawal causes AR nuclear export. The present study led to an updated model that AR could be imported in the absence of androgens, ubiquitinated, and degraded in the nucleus. Androgen withdrawal caused nuclear AR degradation but not export. In comparison to their parental androgen-sensitive LNCaP prostate cancer cells, castration-resistant C4-2 cells exhibited reduced nuclear AR polyubiquitination and increased nuclear AR level. We previously identified 3-(4-chlorophenyl)-6,7-dihydro-5H-pyrrolo[1,2-a]imidazole (CPPI) in a high throughput screen for its inhibition of androgen-independent AR nuclear localization in CRPC cells. The current study showed that CPPI was a novel competitive AR antagonist capable of enhancing AR interaction with its E3 ligase MDM2, and degradation of AR in the nuclei of CRPC cells. Also, CPPI blocked androgen-independent AR nuclear import. Overall, these findings suggest the feasibility of targeting androgen-independent AR nuclear import and stabilization, two necessary steps leading to AR nuclear localization and activation in CRPC cells, with small molecule inhibitors.

Authors

Shidong Lv, Qiong Song, Guang Chen, Erdong Cheng, Wei Chen, Ryan Cole, Zeyu Wu, Laura E. Pascal, Ke Wang, Peter Wipf, Joel B. Nelson, Qiang Wei, Wenhua Huang, Zhou Wang

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An unbiased approach to defining bona fide cancer neoepitopes that elicit immune-mediated cancer rejection
Cory A. Brennick, … , Ion I. Mandoiu, Pramod K. Srivastava
Cory A. Brennick, … , Ion I. Mandoiu, Pramod K. Srivastava
Published December 15, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI142823.
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An unbiased approach to defining bona fide cancer neoepitopes that elicit immune-mediated cancer rejection

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Abstract

Identification of neoepitopes that are effective in cancer therapy is a major challenge in creating cancer vaccines. Here, using an entirely unbiased approach, we queried all possible neoepitopes in a mouse cancer model and asked which of those are effective in mediating tumor rejection, and independently, in eliciting a measurable CD8 response. This analysis uncovered a large trove of effective anticancer neoepitopes which have strikingly different properties from conventional epitopes and suggested an algorithm to predict them. It also revealed that our current methods of prediction discard the overwhelming majority of true anticancer neoepitopes. These results from a single mouse model were validated in another, antigenically distinct mouse cancer model, and are consistent with data reported in human studies. Structural modeling showed how the MHC I-presented neoepitopes have an altered conformation, higher stability, or increased exposure to T cell receptors as compared to the un-mutated counterparts. T cells elicited by the active neoepitopes identified here demonstrated a stem-like early dysfunctional phenotype associated with effective responses against viruses and tumors of transgenic mice. These abundant anticancer neoepitopes, which have not been tested in human studies thus far, can be exploited for the generation of personalized human cancer vaccines.

Authors

Cory A. Brennick, Mariam M. George, Marmar R. Moussa, Adam T. Hagymasi, Sahar Al Seesi, Tatiana V. Shcheglova, Ryan P. Englander, Grant L.J. Keller, Jeremy L. Balsbaugh, Brian M. Baker, Andrea Schietinger, Ion I. Mandoiu, Pramod K. Srivastava

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Selective glutamine metabolism inhibition in tumor cells improves anti-tumor T lymphocyte activity in triple-negative breast cancer
Deanna N. Edwards, … , Mark R. Boothby, Jin Chen
Deanna N. Edwards, … , Mark R. Boothby, Jin Chen
Published December 15, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI140100.
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Selective glutamine metabolism inhibition in tumor cells improves anti-tumor T lymphocyte activity in triple-negative breast cancer

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Abstract

Rapidly proliferating tumor and immune cells need metabolic programs that support energy and biomass production. The amino acid glutamine is consumed by effector T cells and glutamine-addicted triple-negative breast cancer (TNBC) cells, suggesting that a metabolic competition for glutamine may exist within the tumor microenvironment, potentially serving as a therapeutic intervention strategy. Here, we report that there is an inverse correlation between glutamine metabolic genes and markers of T cell-mediated cytotoxicity in human basal-like breast cancer (BLBC) patient datasets, with increased glutamine metabolism and decreased T cell cytotoxicity associated with poor survival. We found that tumor cell-specific loss of glutaminase (GLS), a key enzyme for glutamine metabolism, improved anti-tumor T cell activation in both a spontaneous mouse TNBC model and orthotopic grafts. The glutamine transporter inhibitor V-9302 selectively blocked glutamine uptake by TNBC cells but not CD8+ T cells, driving synthesis of GSH, a major cellular antioxidant, to improve CD8+ T cell effector function. We propose a “glutamine steal” scenario, in which cancer cells deprive tumor-infiltrating lymphocytes of needed glutamine, thus impairing anti-tumor immune responses. Therefore, tumor-selective targeting of glutamine metabolism may be a promising therapeutic strategy in TNBC.

Authors

Deanna N. Edwards, Verra M. Ngwa, Ariel L. Raybuck, Shan Wang, Yoonha Hwang, Laura C. Kim, Sung Hoon Cho, Yeeun Paik, Qingfei Wang, Siyuan Zhang, H. Charles Manning, Jeffrey C. Rathmell, Rebecca S. Cook, Mark R. Boothby, Jin Chen

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ATM inhibition enhances cancer immunotherapy by promoting mtDNA leakage/cGAS-STING activation
Mengjie Hu, … , Fang Li, Chuan-Yuan Li
Mengjie Hu, … , Fang Li, Chuan-Yuan Li
Published December 8, 2020
Citation Information: J Clin Invest. 2020. https://doi.org/10.1172/JCI139333.
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ATM inhibition enhances cancer immunotherapy by promoting mtDNA leakage/cGAS-STING activation

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Abstract

Novel approaches are needed to boost the efficacy of immune checkpoint blockade (ICB) therapy. Ataxia Telangiectasia Mutated (ATM) protein plays a central role in sensing DNA double strand breaks and coordinating their repair. Recent data indicated that ATM might be a promising target to enhance immune checkpoint blockade (ICB) therapy. However, the molecular mechanism involved is not clearly elucidated. Here we show that ATM inhibition could potentiate ICB therapy by promoting cytoplasmic leakage of mitochondrial DNA and activation of the cGAS/STING pathway. Genetic depletion of ATM in murine cancer cells significantly delayed tumor growth in syngeneic mouse hosts in a T-cell dependent manner. Furthermore, chemical inhibition of ATM significantly potentiated anti-PD1 therapy of mouse tumors. ATM inhibition potently activated the cGAS/STING pathway and enhanced lymphocyte infiltration into the tumor microenvironment by downregulating TFAM, which led to mitochondrial DNA leakage into the cytoplasm. Moreover, our analysis of data from a large patient cohort indicated that ATM mutations, especially nonsense mutations, predicted for clinical benefits for ICB therapy. Our study therefore provides strong evidence that ATM may serve both as a therapeutic target and a biomarker to enable ICB therapy

Authors

Mengjie Hu, Min Zhou, Xuhui Bao, Dong Pan, Meng Jiao, Xinjian Liu, Fang Li, Chuan-Yuan Li

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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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