tbuckley/cabot-search huggingface dataset:
Loss of peristalsis of the esophagus due to diffuse esophageal leiomyomatosis
Authors: Kazuya Takahashi, Yui Ishii, Kazunao Hayashi, Satoshi Ikarashi, Hirokazu Kawai, Yuichi Sato, Shuji Terai
Journal: Endoscopy (2017)

A 15-year-old girl was referred to our hospital with a tumor in the mediastinum that had been found on a chest radiograph during a medical check-up. An esophagram showed a large mediastinal mass (60 mm in diameter) ([Video 1]). No peristalsis of the thoracic esophagus (smooth muscle area) was apparent, and dilatation of the esophagus and retention of the barium were observed on the proximal side of the tumor. High resolution manometry (HRM) findings showed complete loss of peristalsis of the smooth muscle area, whereas peristalsis of the striated muscle area was preserved ([Fig. 1]). Although the esophageal lumen was narrowed by the tumor, the endoscope could be passed through it ([Fig. 2]). Computed tomography (CT) scanning demonstrated a mildly enhancing tumor, which was circumferentially surrounding the lower esophagus ([Fig. 3]). On T1-weighted magnetic resonance imaging (MRI), the tumor had a relatively high signal, which was the same as that of other muscular organs ([Fig. 4]).
Adaptive NK cells can persist in patients with GATA2 mutation depleted of stem and progenitor cells
Authors: Heinrich Schlums, Moonjung Jung, Hongya Han, Jakob Theorell, Venetia Bigley, Samuel C. C. Chiang, David S. J. Allan, Jan K. Davidson-Moncada, Rachel E. Dickinson, Tim D. Holmes, Amy P. Hsu, Danielle Townsley, Thomas Winkler, Weixin Wang, Pål Aukrust, Ingvild Nordøy, Katherine R. Calvo, Steve M. Holland, Matthew Collin, Cynthia E. Dunbar, Yenan T. Bryceson
Journal: Blood (2017)
Fluorescence In Situ Hybridization (FISH) Reveals Unexpected Cryptic Chromosome 11 Defects in MDS/AML Patients.
Authors: Paolo Bernasconi, Irene Dambruoso, Marina Boni, Paola Maria Cavigliano, Ilaria Giardini, Rita Zappatore, Silvia Calatroni, Barbara Rocca, Marilena Caresana, Mario Lazzarino
Journal: Blood (2006)
C-Cbl but Not TET2 Mutations Are Present in Patients with Juvenile Myelomonocytic Leukemia.
Authors: Hideki Muramatsu, Hideki Makishima, Anna Malgorzata Jankowska, Heather Cazzolli, Christine O'Keefe, Nao Yoshida, Yinyan Xu, Nobuhiro Nishio, Asahito Hama, Hiroshi Yagasaki, Yoshiyuki Takahashi, Koji Kato, Atsushi Manabe, Seiji Kojima, Jaroslaw P. Maciejewski
Journal: Blood (2009)
Unlocking the potential of physical activity for back health
Authors: Mary O’Keeffe, Chris G Maher, Kieran O’Sullivan
Journal: British Journal of Sports Medicine (2017)

Physical activity is central to achieving better back health. Engaging in some forms of physical activity may increase the risk of low back pain (LBP), but in general a physically active lifestyle seems to be protective for LBP.1 The only known effective prevention method is exercise alone or exercise with education.2 Most guidelines for acute LBP focus on advice to increase physical activity. For persistent LBP, most effective treatments have physical activity at their core, either where it is the main component (eg, aerobic exercise) or where there is greater use of psychological principles (eg, graded exposure).

In our view, the potential value of physical activity for back health is not being realised. We address four key issues.

1. Preoccupation with the right physical activity could be holding us back 

While many clinicians confidently preach the benefits of physical activity for general health, this confidence seems to be replaced with a pause or panic when advising a patient who has …
Enhancer of zest homolog 2 (EZH2) expression in well and moderately differentiated pancreatic neuroendocrine tumor (pNET)
Authors: R. Marconcini, P. Faviana, D. Campani, L. Galli, A. Antonuzzo, C. Orlandini, A. Falcone, S. Ricci
Journal: Annals of Oncology (2016)
DDIS-16. A NOVEL EPIGENETIC PATHWAY FOR THE TREATMENT OF MEDULLOBLASTOMA
Authors: Nagi Ayad
Journal: Neuro-Oncology (2016)

We found high levels of CK1d protein in mouse models of medulloblastoma (Penas et al., 2015). Furthermore, CK1d inhibition dramatically reduced medulloblastoma tumor progression. In addition, we have recently found that CK1d phosphorylates the epigenetic reader bromodomain-containing protein 4 (BRD4). BRD4 has been identified as a therapeutic target in several cancers, including medulloblastoma. We used granule cell progenitors and medulloblastoma Ptch-/-P53-/- mouse cells to determine the effects of CK1d phosphorylation of BRD4. Cells were incubated with the CK1d inhibitor SR-1277 and the phosphorylation levels of BRD4 were determined by WB and its binding to chromatin by ChIP. In vitro phosphorylation studies with human BRD4 purified from bacteria were performed to confirm these studies. In addition, we tested whether genetic disruption of CK1d also reduced BRD4 phosphorylation. Treatment with a CK1d inhibitor (SR-1277) reduced BRD4 phosphorylation suggesting that CK1d phosphorylates BRD4. In addition knockout of CK1d also reduced BRD4 phosphorylation. In vitro phosphorylation studies with purified human BRD4 and CK1d confirmed CK1d-mediated phosphorylation of BRD4. Consistent with a functional interaction between CK1d and BRD4, we found that BRD4 association with the proximal promoter region of the Gli1 locus is inhibited by either the CK1d inhibitor SR-1277 or the BET inhibitor I-BET151. In addition, both CK1d and BET inhibition reduced Gli1 mRNA levels in mouse Ptch1+/-;Trp53-/- medulloblastoma cells when we used the brain penetrant inhibitors JQ1 and SR-1277. Since resistance to BRD4 inhibitors has been observed, we hypothesize that combined CK1d inhibition can overcome this resistance. Collectively these studies suggest that a combination therapy using CK1d and BRD4 inhibitors is more effective than single agents.
The “MarrowMiner”: A Novel, Minimally Invasive Device for the Harvest of Bone Marrow: Initial Human Experience Reveals Safety, Efficacy and Richer Cell Product Than Standard Harvest Methods
Authors: Daniel L. Kraft, Vartan Ghazarossian, Mike Crocker, Sergio Najar, Antonio A. Carrasco-YalÃ°n
Journal: Blood (2008)
5-fluorouracil degradation rate (5-FU-DR) could predict toxicity in breast cancer patients treated with capecitabine
Authors: C.E. Onesti, A. Botticelli, F. Mazzuca, S. Angelini, A. Petremolo, R. Falcone, M. Roberto, M. Occhipinti, A. Romiti, L. Lionetto, M. Simmaco, P. Marchetti
Journal: Annals of Oncology (2016)
Targeting of TNFAIP3 (A20) Links MiR-125a and MiR-125b to Constitutive Activation of the NF-KB Pathway and Lymphomagenesis
Authors: Sang-Woo Kim, Kumaraguruparan Ramasamy, Hakim Bouamar, Daifeng Jiang, Ricardo Aguiar
Journal: Blood (2011)
The combination of GDC-0980, a PI3K/mTOR kinase inhibitor and BAY-86-9766, a MEK inhibitor is able to induce cell growth inhibition of HER2 positive Trastuzumab resistant gastric cancer cell lines
Authors: B. Savastano, M.M. laterza, A. Capasso, V. Belli, J. Ventriglia, A. Petrillo, G. Tirino, L. Pompella, F. Morgillo, E. Martinelli, M. Orditura, F. Ciardiello, F. De Vita
Journal: Annals of Oncology (2016)
Patients with metastatic prostate cancer enrolled in phase 1 trials: Outcomes and molecular alterations
Authors: C. Bonnet, E. Castanon Alvarez, J.-M. Michot, F. Bigot, A. Varga, A. Gazzah, R. Bahleda, A. Marabelle, A. Hollebecque, S. Aspeslagh, E. Angevin, J.-P. Armand, L. Albiges, Y. Loriot, S. Postel-Vinay, J.-C. Soria, C. Massard
Journal: Annals of Oncology (2016)
High Frequencies of Simultaneous FLT3-ITD, WT1, and KIT mutations in NUP98-Related Hematologic Malignancies.
Authors: Takeshi Taketani, Tomohiko Taki, Seiji Fukuda, Chie Onishi, Mariko Abe, Seiji Yamaguchi, Yasuhide Hayashi
Journal: Blood (2009)
RUNX1 cooperates with FLT3-ITD to induce leukemia
Authors: Kira Behrens, Katrin Maul, Nilgün Tekin, Neele Kriebitzsch, Daniela Indenbirken, Vladimir Prassolov, Ursula Müller, Hubert Serve, Jörg Cammenga, Carol Stocking
Journal: The Journal of Experimental Medicine (2017)

Acute myeloid leukemia (AML) is induced by the cooperative action of deregulated genes that perturb self-renewal, proliferation, and differentiation. Internal tandem duplications (ITDs) in the FLT3 receptor tyrosine kinase are common mutations in AML, confer poor prognosis, and stimulate myeloproliferation. AML patient samples with FLT3-ITD express high levels of RUNX1, a transcription factor with known tumor-suppressor function. In this study, to understand this paradox, we investigated the impact of RUNX1 and FLT3-ITD coexpression. FLT3-ITD directly impacts on RUNX1 activity, whereby up-regulated and phosphorylated RUNX1 cooperates with FLT3-ITD to induce AML. Inactivating RUNX1 in tumors releases the differentiation block and down-regulates genes controlling ribosome biogenesis. We identified Hhex as a direct target of RUNX1 and FLT3-ITD stimulation and confirmed high HHEX expression in FLT3-ITD AMLs. HHEX could replace RUNX1 in cooperating with FLT3-ITD to induce AML. These results establish and elucidate the unanticipated oncogenic function of RUNX1 in AML. We predict that blocking RUNX1 activity will greatly enhance current therapeutic approaches using FLT3 inhibitors.
Concerns Over Newborn Screening
Authors: Jeff Lyon
Journal: JAMA (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
PHD Domain Deletion Mutations of ASXL1 Promote Myeloid Leukemia Transformation Through Epigenetic Dysregulation and Inhibit Megakaryocytic Differentiation Through the Inactivation of FOSB in K562 Cells.
Authors: Rabindranath Bera, Der-Cherng Liang, Ming-Chun Chiu, Ying-Jung Huang, Sung-Tzu Liang, Lee-Yung Shih
Journal: Blood (2012)
Stem Cell Transplantation in Elderly Patients with Acute Lymphoblastic Leukemia (ALL) in First Complete Remission (CR1).
Authors: Renate Arnold, Dietrich Beelen, Martin Bornhaeuser, Donald Bunjes, Juergen Finke, Nikolaus Kroeger, Michael Stadler, Matthias Stelljes, Nicola Goekbuget, Dieter Hoelzer
Journal: Blood (2008)
Pembrolizumab in patients with relapsed/refractory primary mediastinal large B-cell lymphoma (rrPMBCL) or relapsed or refractory Richter syndrome (rrRS): Phase 2 KEYNOTE-170 study
Authors: J.-M. Michot, P. Armand, W. Ding, V. Ribrag, B. Christian, A. Balakumaran, P. Marinello, S. Chlosta, Y. Zhang, M. Shipp, P.L. Zinzani
Journal: Annals of Oncology (2016)
NIMG-22. MRI CHANGES IN NEWLY DIAGNOSED GLIOBLASTOMA DURING CHEMORADIATION AND ADJUVANT TEMOZOLOMIDE
Authors: Ina Ly, Yangming Ou, Xiao Da, Tracy Batchelor, Jayashree Kalpathy-Cramer, Elizabeth Gerstner
Journal: Neuro-Oncology (2016)

Characterize anatomic and functional MRI changes in patients with newly diagnosed glioblastoma (nGBM) to more accurately measure impact of treatment. The standard of care for nGBM is maximal safe resection, six weeks of concurrent chemoradiation (CRT), followed by adjuvant monthly temozolomide. FLAIR and T1 post-contrast sequences are frequently used to assess treatment response but poorly reflect underlying tumor behavior with respect to tumor cellularity, vascular permeability, and perfusion. Following IRB approval, patients with nGBM underwent MR imaging before treatment, during week 6 of CRT, four weeks post-CRT, and before cycle 2 of adjuvant temozolomide (“pre-cycle 2”). We measured FLAIR and contrast-enhancing (CE) volumes, apparent diffusion coefficient (ADC; reflecting tumor cellularity), Ktrans (reflecting vascular permeability), and relative cerebral blood volume (rCBV) and flow (rCBF; reflecting perfusion) on spin echo (SE) and gradient echo (GE) sequences (rCBVSE, rCBFSE, rCBVGE, rCBFGE, respectively). Fourteen patients were included. Percent changes during treatment were compared to pre-treatment values. Within the CE region of interest (ROI), the respective median percent changes during CRT, post-CRT, and pre-cycle 2 were: CE volume -0.75%, 19.98%, 5.93%; ADC 10.15%, 18.03%, 27.21%; Ktrans 32.05%, 22.48%, 7.06%; rCBVSE -18.82%, -33.21%, -32.86%; rCBFSE -11.42%, -28.80%, -26.99%; rCBVGE -17.05%, -23.92%, -30.39%; and rCBFGE -21.98%, -24.29%, -32.12%. Within the peri-tumoral FLAIR ROI, the respective median percent changes during CRT, post-CRT, and pre-cycle 2 were: FLAIR volume 20.36%, 80.29%, 69.36%; ADC -3.63%, 6.59%, 11.51%; Ktrans 5.88%, -7.40%, -31.45%; rCBVSE -11.62%, -34.60%, -20.18%; rCBFSE -0.31%, -22.42%, -25.23%; rCBVGE -0.80%, -13.05%, -22.32%; and rCBFGE 6.30%, -6.25%, -19.57%. Chemoradiation in nGBM results in increased edema and permeability early during treatment, likely related to tumoral and peri-tumoral inflammation; decreased tumor cellularity, reflected by increased ADC; and decreased perfusion. ADC, Ktrans, and perfusion parameters are thus helpful in better characterizing tumor microenvironment during treatment.
Epigenetic Signatures of Obesity
Authors: Susan E. Ozanne
Journal: New England Journal of Medicine (2015)

Over the last 10 years the prevalence of obesity across the European continent has in general been rising. With the exception of a few countries where a levelling-off can be perceived, albeit at a high level, this upward trend seems likely to continue. However, considerable country to country variation is noticeable, with the proportion of people with obesity varying by 10% or more. This variation is intriguing and suggests the existence of different profiles of risk or protection factors operating in different countries. The identification of such protection factors could indicate suitable targets for interventions to help manage the obesity epidemic in Europe. This report is the output of a 2-day workshop on the 'Diversity of Obesity in Europe'. The workshop included 14 delegates from 12 different European countries. This report contains the contributions and discussions of the materials and viewpoints provided by these 14 experts; it is not the output of a single mind. However, such is the nature of scientific analysis regarding obesity that it is possible that a different set of 14 experts may have come to a different set of conclusions. Therefore the report should not be seen as a definitive statement of a stable situation. Rather it is a focus for discussion and comment, and a vehicle to drive forward further understanding and management of obesity in Europe.
Identification of Genes Which Play a Crucial Role in C/EBPβ Downstream Signalling in ALK+ ALCL Cell Lines.
Authors: Irina Bonzheim, Martin Irmler, Natasa Anastasov, Margit Klier-Richter, Sabine Schaefer, Johannes Beckers, Stefania Pittaluga, Falko Fend, Mark Raffeld, Leticia Quintanilla-Martinez
Journal: Blood (2009)
Geographical Disparities in Multiple Myeloma Survival in Three French Regions
Authors: Morgane Mounier, Nicolas Despiégel, Sophie Gauthier, Sandra Le Guyader-Peyrou, Edouard Cornet, Chantal Guilhaume, Audrey Viale, Alain Monnereau, Xavier Troussard, Marc Maynadié
Journal: Blood (2016)
Phase II study to evaluate the efficacy of regorafenib in metastatic colorectal cancer patients by the assessment using FDG-PET/CT (JACCRO CC-12) metastatic colorectal cancer (JACCRO CC-12)
Authors: H. Satake, M. Nakamura, A. Tsuji, T. Sagawa, F. Tamura, Y. Hatachi, K. Oguchi, A. Takagane, T. Kaji, T. Sekikawa, M. Furukawa, M. Kochi, W. Ichikawa, M. Takeuchi, M. Fujii, T. Nakajima
Journal: Annals of Oncology (2016)
Adherence to cisplatin-based regimens prescription in "fit" patients fulfilling platinum eligibility criteria. Impact on outcomes: a retrospective international study of invasive/advanced cancer of the urothelium (RISC) analysis
Authors: A. Bamias, K. Tzannis, M. Liontos, S.J. Crabb, L. Harshman, U. De Giorgi, J. Bellmunt, Y.-N. Wong, S.K. Pal, S. Ladoire, C.N. Sternberg, T.B. Powles, E.Y. Yu, G. Niegisch, A. Necchi, U. Vaishampayan, N. Agarwal, J. Rosenberg, R. Investigators
Journal: Annals of Oncology (2016)
Effects of HER2 immuno-histochemistry expression levels on survival in patients treated by trastuzumab at the adjuvant setting in the SIGNAL/PHARE prospective cohort
Authors: E. Curtit, A. Vincent-Salomon, S. Paget-Bailly, G. Romieu, P. Fumoleau, H. Bonnefoi, C. Jouannaud, T. Petit, A. Darut-Jouve, V. Trillet-Lenoir, C. Tarpin, J.-Y. Pierga, M. Rios, J.P. Jacquin, T. Bachelot, D. Cox, J.-F. Deleuze, I. Pauporte, J. Henriques, X. Pivot
Journal: Annals of Oncology (2016)
An extended KRAS mutation test for the detection of 28 common mutations in FFPET and plasma specimens
Authors: J. Li, C. Hoeppner, S. Gan, A. Blair, K. Min, A. Sims, A. Tietz, M. Vinas, T.T. Rehage, K. Malhotra, H. Halait, V. Brophy
Journal: Annals of Oncology (2016)
Fatty acid synthase – Modern tumor cell biology insights into a classical oncology target
Authors: Douglas Buckley, Gregory Duke, Timothy S. Heuer, Marie O'Farrell, Allan S. Wagman, William McCulloch, George Kemble
Journal: Pharmacology & Therapeutics (2017)

Decades of preclinical and natural history studies have highlighted the potential of fatty acid synthase (FASN) as a bona fide drug target for oncology. This review will highlight the foundational concepts upon which this perspective is built. Published studies have shown that high levels of FASN in patient tumor tissues are present at later stages of disease and this overexpression predicts poor prognosis. Preclinical studies have shown that experimental overexpression of FASN in previously normal cells leads to changes that are critical for establishing a tumor phenotype. Once the tumor phenotype is established, FASN elicits several changes to the tumor cell and becomes intertwined with its survival. The product of FASN, palmitate, changes the biophysical nature of the tumor cell membrane; membrane microdomains enable the efficient assembly of signaling complexes required for continued tumor cell proliferation and survival. Membranes densely packed with phospholipids containing saturated fatty acids become resistant to the action of other chemotherapeutic agents. Inhibiting FASN leads to tumor cell death while sparing normal cells, which do not have the dependence of this enzyme for normal functions, and restores membrane architecture to more normal properties thereby resensitizing tumors to killing by chemotherapies. One compound has recently reached clinical studies in solid tumor patients and highlights the need for continued evaluation of the role of FASN in tumor cell biology. Significant advances have been made and much remains to be done to optimally apply this class of pharmacological agents for the treatment of specific cancers.
SD-208, a Novel Transforming Growth Factor Beta Receptor I Kinase Inhibitor, Can Stimulate Hematopoiesis in Myelodysplastic Syndrome Progenitors.
Authors: Amit Verma, Tony A. Navas, Jing Ying, Aaron N. Nguyen, Perry Pahanish, Mahesh Seetharam, Irene Kerr, Robert Collins, Mimi Kim, Mani Mohindru, Linda S. Higgins
Journal: Blood (2005)
IMST-15. PHARMACOLOGICAL ANTAGONISM OF CCR2 IMPACTS PROGRESSION OF MURINE GLIOMAS
Authors: Defang Luo, Matthew Sarkisian, Rajon Didier, Frank Bova, James Campbell, Israel Charo, Thomas Schall, Jeffrey Harrison
Journal: Neuro-Oncology (2016)

While high numbers of microglia/macrophages are found within glioblastoma (GBM), little is known of their specific function within this tumor microenvironment. Mounting evidence indicates a role for these cells in tumor progression and therapy resistance and there is evidence for the positive correlation between numbers of infiltrating microglia/macrophages and tumor proliferation rate. Sources of these mononuclear cells include brain parenchyma (microglia) and bone marrow. Despite the potential significance of GBM-associated microglia/macrophages to tumor progression and decreased therapeutic efficacy, the mechanisms by which these cells infiltrate GBM are unknown. We hypothesize that the intratumoral localization of these cells requires the presence of chemokines within the tumor microenvironment and their cognate receptors expressed on microglia/macrophages. OBJECTIVE: To determine if chemokine receptor CCR2 contributes to GBM progression in pre-clinical mouse models of glioma. Immunohistochemical analyses of murine GL261 and KR158 gliomas in CCR2+/rfp/CX3CR1+/gfp, CCR2+/rfp, and CCR2rfp/rfp mice was performed. The impact of a CCR2 antagonist, CCX598, on the overall survival of glioma-bearing mice was also assessed. Prominent numbers of CCR2+CD11b+ macrophages were found within murine GL261 and KR158 gliomas that were distinct from CX3CR1+CD11b+ cells; ramified CX3CR1+/gfp microglia were found in normal brain while activated CX3CR1+/gfp and CCR2+/rfp were detected within the tumors. The tumor localization of the latter cells in both the GL261 and KR158 models was greatly reduced in CCR2-deficient mice. Pharmacological antagonism of CCR2, with CCX598, slowed the growth of KR158 gliomas when delivered as a monotherapy. CCX598 treatment of GL261 tumor-bearing mice slowed glioma progression when combined with either radiation or anti-PD-L1 administration. Genetic deficiency in CCR2 impacts the presence of glioma-associated macrophages, while pharmacological antagonism of this chemokine receptor slows glioma progression in murine glioma models. Thus, adjunctive therapy with CCR2 antagonists may offer a survival advantage to GBM patients.
Survival of Patients With Ovarian Cancer, Connecticut, 1935–542
Authors: Sidney J. Cutler, Fred Ederer, Matthew H. Griswold, Richard A. Greenberg
Journal: JNCI Journal of the National Cancer Institute (1960)

Journal Article Survival of Patients With Ovarian Cancer, Connecticut, 1935–54 Get access Sidney J. Cutler, Sidney J. Cutler Search for other works by this author on: Oxford Academic PubMed Google Scholar Fred Ederer, Fred Ederer Search for other works by this author on: Oxford Academic PubMed Google Scholar Matthew H. Griswold, Matthew H. Griswold Search for other works by this author on: Oxford Academic PubMed Google Scholar Richard A. Greenberg Richard A. Greenberg Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 24, Issue 3, March 1960, Pages 541–549, https://doi.org/10.1093/jnci/24.3.541 Published: 01 March 1960 Article history Received: 02 July 1959 Published: 01 March 1960
Long term efficacy and QOL data of chemohormonal therapy (C-HT) in low and high volume hormone naïve metastatic prostate cancer (PrCa): E3805 CHAARTED trial
Authors: C. Sweeney, Y.-H. Chen, G. Liu, M. Carducci, D. Jarrard, M. Eisenberger, Y.-N. Wong, L. Patrick-Miller, N. Hahn, M. Kohli, M. Conney, R. Dreicer, N.J. Vogelzang, J. Picus, D. Shevrin, M. Hussain, J. Garcia, R. Dipaola
Journal: Annals of Oncology (2016)