tbuckley/cabot-search huggingface dataset:
Imaging of rib stress fractures in elite rowers: the promise of ultrasound?
Authors: Alexandra T Roston, Mike Wilkinson, Bruce B Forster
Journal: British Journal of Sports Medicine (2017)

Stress fractures are common injuries in endurance athletes, and are due to high-intensity, repetitive training activities.1 ,2 Although these fractures occur more frequently in weight-bearing bones, the ribs are a common site for non-weight-bearing stress fractures.3 Rib stress fractures are the most common type of stress fracture in rowers, with an incidence that has been reported as being between 6.1% and 12%.2–5 This relatively large range of estimated incidence rates is likely due to both under-reporting and underdiagnosis of rib stress fractures, as well as an overall lack of epidemiological studies on musculoskeletal injury rates in rowers.3 4 6 For these reasons, the burden of rib stress fractures is likely higher than the literature suggests.3 7 In fact, there is so little epidemiological data available that some recommendations suggest that focal rib pain in any elite rower should be regarded as a stress fracture until proven otherwise.8 

Rib stress fractures are of great concern to elite-level rowers and their teams. Rib-related injuries account for the most time lost from training and competition, which can have a negative impact on the affected rower, and on crew members and coaches.3 6 8 Furthermore, because injuries can require up to 6–8 weeks of rest, a rib stress fracture can be a season-ending injury at the elite level.8 This is especially worrisome because a stress fracture that occurs during training for a major championship could prevent the injured athlete from competing altogether.3 Finally, elite level athletes may be more reluctant to abstain from training, and training despite a suspected rib stress fracture may lead to even more serious injury such as a displaced fracture and greater time lost from sport.8–10 

Much like stress fractures in weight-bearing bones, rib stress fractures are thought to result from …
HIV-associated lung cancer in New York City.
Authors: Benjamin Levy, Rangaswamy Chintapatla, Jaime Suarez, Cliff P. Connery, Faiz Y. Bhora, Andrew Evans, Walter Choi, Nicholas Rohs, Daniel Jacob Becker
Journal: Journal of Clinical Oncology (2013)

e17589 Background: Recent evidence suggests that HIV may be a risk factor of lung cancer, independent of smoking . Due to the expanding population of HIV patients with lung cancer, there is a need to define the clinical course and tumor biology of these patients. Our analysis seeks to characterize the clinical and molecular features of HIV associated non small cell lung cancer (HIV-NSCLC) and evaluate outcomes in a New York City Cancer center that serves a racially and economically diverse population. Methods: We searched the Continuum Cancer Center Registry for cases of HIV-NSCLC diagnosed from 2002 to 2012. Charts were reviewed to determine patient and tumor characteristics, treatment and outcomes. Kaplan-Meier curves were constructed for survival and compared by means of the log rank test. Patient characteristics were compared to national data from the SEER database. Mutational analysis of archival tissue was performed by OnkoMatch Tumor genotyping. Results: HIV-NSCLC was idenfied in 74 patients. Median age (MA) was 55 compared to MA of 70 for non HIV-NSCLC. Patients were predominantly male (72%). Histology distribution was reflective of the non-HIV population (SEER): adenocarcinoma [31 (42%)], squamous [18 (24%)], NSCLC NOS [8 (11%)], poorly differentiated [6 (8%)], and other [9 (15%)]. Distribution of stage was similar to SEER with 39 (53%) patients presenting with stage IV. Lowest recorded CD4 count was &lt;200 in 34 patients (68%) with available CD4 counts. Chemotherapy and radiation were administered to 28 (49%) and 19 patients (31%), respectively. Median survival was 5.2 months. Kaplan-Meier curves were not statistically different by CD4 count (&gt; or &lt; 200), or by receipt of chemo or radiation. Mutational analysis on 7 patients demonstrated 3 with cMet overexpression, 2 KRAS mutations and 1 BRAF mutation. Conclusions: Among our HIV-NSCLC cohort, patients were diagnosed at younger age, but had similar stage and histology distributions as SEER database averages. HIV associated lung cancer appears to have a poor prognosis similar to that of the general population. Rates of treatment were low in our cohort and the potential for undertreatment warrants further study. Observed increased rate of cMET overexpression should prompt further molecular profiling in this population.
Integrating a Neuroscience Perspective Into Clinical Psychiatry Today
Authors: Melissa R. Arbuckle, Michael J. Travis, David A. Ross
Journal: JAMA Psychiatry (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 Psychiatry HomeNew OnlineCurrent IssueFor Authors Podcast 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 Psychiatry journal
The Prognostic Impact of Complete Remission (CR) Plus Very Good Partial Remission (VGPR) in a Double-Transplantation Program for Newly Diagnosed Multiple Myeloma (MM). Combined Results of the IFM 99 Trials.
Authors: Jean-Luc Harousseau, Michel Attal, Philippe Moreau, Frédéric Garban, Thierry Facon, Hervé Avet-Loiseau
Journal: Blood (2006)
Inhibition of Histone Deacetylase 6 Effects on Interaction of Tumor and Immune Cells In Multiple Myeloma
Authors: Gullu Gorgun, Teru Hideshima, Naoya Mimura, Diana Cirstea, Loredana Santo, Yiguo Hu, Claire Fabre, Noopur Raje, Nikhil C. Munshi, Paul G Richardson, Kenneth C. Anderson
Journal: Blood (2010)
Abstract A17: Genomic analysis and simulation for understanding heterogenous cancer evolution
Authors: Atsushi Niida, Yusuke Takahashi, Ryutaro Uchi, Koshi Mimori, Satoru Miyano
Journal: Cancer Research (2017)

Abstract A malignant tumor harbors multiple clones generated by branching evolution. This phenomenon, called intratumor heterogeneity, could foster evolutionary adaptation and presumably causes therapeutic failure. To investigate intratumor heterogeneity in colorectal cancer, we performed whole exome sequencing of samples obtained from geographically separated regions in a single colorectal tumor. The multiregional sequencing showed early-acquired mutations, which was shared by all regions as well as late-acquired mutations, which shaped extensive intratumor heterogeneity. Next, to explore the principles underlying the intratumor heterogeneity, we built a cellular automaton model, termed the BEP model, which can simulate the branching evolution in silico. We then extensively searched for conditions that reproduce the multiregional sequencing data by performing simulations with various parameter settings on a supercomputer. The simulation analysis suggested that neutral evolution boosted by high mutation rate can extensive intratumor heterogeneity. Collectively, This study identified the possible principle underlying intratumor heterogeneity, which provides novel insights into the origin of cancer robustness and evolvability. Citation Format: Atsushi Niida, Yusuke Takahashi, Ryutaro Uchi, Koshi Mimori, Satoru Miyano. Genomic analysis and simulation for understanding heterogenous cancer evolution. [abstract]. In: Proceedings of the AACR Special Conference on Engineering and Physical Sciences in Oncology; 2016 Jun 25-28; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2017;77(2 Suppl):Abstract nr A17.
Striking Anti-Multiple Myeloma (MM) Activity with the In Vitro Use of the Multikinase Inhibitor Sorafenib (S), Cytotoxic Synergy Between Bortezomib (B) and S, but Not Between B and Epigallocatechin-3-Gallate (EGCG; E) Enlarge the Present Knowledge In MM and Promise Novel Insights for Innovative Substance Exploitation In MM-Treatment
Authors: Josefina Udi, Dagmar Wider, Julie Catusse, Gabriele Ihorst, Dominik Schnerch, Marie Follo, Meike Burger, Ralph M. Waesch, Monika Engelhardt
Journal: Blood (2010)
Randomized phase 3 study of elotuzumab for relapsed or refractory multiple myeloma: ELOQUENT-2 Japanese patient subanalysis
Authors: K Suzuki, K Sunami, K Ohashi, S Iida, T Mori, H Handa, K Matsue, M Miyoshi, E Bleickardt, M Matsumoto, M Taniwaki
Journal: Blood Cancer Journal (2017)

Elotuzumab is a humanized immunoglobulin G1 immunostimulatory monoclonal antibody targeted against signaling lymphocytic activation molecule F7 (SLAMF7).1 A phase 1 clinical study (NCT01241292) of elotuzumab in combination with lenalidomide and dexamethasone (ELd) in six patients with relapsed/refractory multiple myeloma (RRMM) was conducted in Japan. The study reported an acceptable safety and tolerability profile and an overall response rate of 83% (5/6).2 ELOQUENT-2 (NCT01239797) is a phase 3, international, randomized clinical trial that investigated the efficacy and safety of ELd compared with lenalidomide/dexamethasone (Ld) in patients with RRMM who had received one to three previous therapies.3 Patients were randomized 1:1 to ELd (n=321) or Ld (n=325). Asian patients comprised 10% (64/646) of the overall population, of which 94% (60/64) were enrolled from Japan.
Abstract P1-04-03: Cross-talk between RNA methyltransferase and demethylase regulates breast cancer growth and progression
Authors: P Subbarayalu, VK Eedunuri, S Timilsina, S Rajamanickam, S Viswanadhapalli, N Abdelfattah, BC Onyeagucha, X Cui, TA Mohammad, TH-M Huang, Y Huang, Y Chen, MK Rao
Journal: Cancer Research (2017)

Abstract The importance of RNA methylation in biological processes has just begun to emerge. However, our understanding of the role and mechanism by which RNA methylation may play a role in tumorigenesis is unclear. Here, we report that RNA N6-adenosine methyltransferase protein METTL14 supports breast cancer growth and progression. We show that METTL14 mediates its pro-tumorigenic function by activating the expression of RNA binding protein HuR and consequently inducing the transcriptional stability of key cell cycle-associated genes, TGFβ and its signaling partners as well as HMGA2, VEGF and PDGF that are known to play critical roles in cancer growth and metastasis. Importantly, m6 A RNA methylation levels of METTL14 target genes were significantly lower in breast cancer patients compared to normal matched controls. The decreased RNA methylation level resulting in increased activity of these target genes in breast cancer patients is regulated by a feedback loop between RNA demethylase ALKBH5 and METTL14. Our results reveal that ALKBH5 regulates the expression of METTL14 and HuR, which in turn transcriptionally stabilizes ALKBH5. Furthermore, we demonstrate that like METTL14, ALKBH5 also supports breast cancer growth and progression. Taken together, these findings suggest that a collaboration between RNA methylation and demethylation machinery may set up a threshold of RNA methylation that ensures the stability of genes that play a vital role in normal cell proliferation; and any perturbation of that threshold may lead to uncontrolled expression/activity of those genes resulting in tumor growth and progression. Citation Format: Subbarayalu P, Eedunuri VK, Timilsina S, Rajamanickam S, Viswanadhapalli S, Abdelfattah N, Onyeagucha BC, Cui X, Mohammad TA, Huang TH-M, Huang Y, Chen Y, Rao MK. Cross-talk between RNA methyltransferase and demethylase regulates breast cancer growth and progression [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P1-04-03.
Abstract A07: Detection of structural variants and recurrent breakpoint genes in colorectal adenoma-to-carcinoma progression
Authors: Evert van den Broek, Maurits J.J. Dijkstra, Quirinus J.M. Voorham, Beatriz Carvalho, Mark A. van de Wiel, Sanne Abeln, Gerrit A. Meijer, Remond J.A. Fijneman
Journal: Cancer Research (2017)

Abstract Background and Aim: The transition of pre-malignant colorectal adenomas (CRAs) into malignant colorectal carcinomas (CRCs) is accompanied by accumulation of somatic genetic alterations. The contribution of small nucleotide variants (SNVs, such as gene point mutations) and numerical DNA copy number aberrations (CNAs, such as gains and losses of large chromosomal segments) in tumor genomes has been studied extensively. In contrast, studies that systematically detect recurrent structural variants (SVs, such as chromosomal breaks) across large series of clinically well-defined samples are scarce. We recently developed “GeneBreak”, a computational method to identify genes that are recurrently affected by the genomic location of CNA-associated chromosomal breaks, and demonstrated high prevalence and clinical relevance of recurrent breakpoint genes in advanced CRCs (PLoS One 2015;10(9):e0138141). Using a similar approach, the present study aimed to determine what recurrent breakpoint genes contribute to colorectal adenoma-to-carcinoma progression. Methods: Differences in somatic CNA-associated gene breakpoint frequencies in 466 CRC and 118 CRA samples were examined using high-resolution array-comparative genomic hybridization (aCGH) profiles. Pearson's Chi-square statistic was applied to determine differences in gene breakpoint frequencies between CRC and CRA samples. Results: In total 21 recurrent breakpoint genes were more frequently affected in CRCs compared to CRAs (p&amp;lt;0.05). MACROD2 was affected by chromosomal breakpoints in 40% of CRCs while not being affected in CRAs. The frequencies of SVs in the other 20 recurrent breakpoint genes ranged from 5% to 29% in CRCs, and from 0% to 2% in CRAs. Conclusion: We identified 21 recurrent breakpoint genes that are frequently affected by SVs in CRCs but not in CRAs. Additional studies are needed to further elaborate the biological and clinical role of these 21 candidate driver genes for colorectal tumor progression. Citation Format: Evert van den Broek, Maurits J.J. Dijkstra, Quirinus J.M. Voorham, Beatriz Carvalho, Mark A. van de Wiel, Sanne Abeln, Gerrit A. Meijer, Remond J.A. Fijneman. Detection of structural variants and recurrent breakpoint genes in colorectal adenoma-to-carcinoma progression. [abstract]. In: Proceedings of the AACR Special Conference on Colorectal Cancer: From Initiation to Outcomes; 2016 Sep 17-20; Tampa, FL. Philadelphia (PA): AACR; Cancer Res 2017;77(3 Suppl):Abstract nr A07.
Primary Breast Diffuse Large B Cell Lymphoma in the Rituximab Era: Outcomes of a Multicenter Retrospective Study By the Lymphoma and Leukemia Committee of Chinese Geriatric Oncology Society(LLC-CGOS)
Authors: Shaoxuan Hu, Yuqin Song, Yufu Li, Xiuhua Sun, Liping Su, Wei Zhang, Jing Jia, Ou Bai, Rong Liang, Xiaoling Li, Huilai Zhang, Yuhuan Gao, Weijing Zhang, Xiubin Xiao, Huizheng Bao, Ningju Wang, Hanyun Ren, Xinan Cen, Shun'e Yang, Yu Zhao, Yinan Wang, Yalan Wang, Aichun Liu, Jingwen Wang, Yuankai Shi, Ming Yuan, Xiaohui He
Journal: Blood (2016)
Fludarabine-Induced Apoptosis in Chronic Lymphocytic Leukemia Cells Is Not Affected by Inhibitor of Apoptosis Proteins (IAPS).
Authors: Karina Lani Silva, Eric Delfraro de Paula Castro, Deborah Vidal Vasconcellos, Jolie Kiemlian Kwee, Arthur Coelho Moellman, Claudete Esteves Klumb, Raquel Ciuvalschi Maia
Journal: Blood (2004)
Abstract ES1-1: Non-cell-autonomous drivers of tumor growth and progression
Authors: K Polyak
Journal: Cancer Research (2017)

Abstract Cancer cells even within the same tumor can display startling differences for many features including migratory/invasive potential and sensitivity to therapeutic agents. This intratumor heterogeneity is a major obstacle toward understanding and treatment of cancers. In solid tumors differences in the local microenvironment, in part due to variability in blood supply and topologic differences in the distribution of leukocytes, can lead to high degree of spatial heterogeneity and also select for cancer cells with different properties. While our ability to define intratumor clonal heterogeneity has grown immensely in the past few years due to technologic advances enabling whole genome sequencing studies even at the single cell level, our understanding of the functional relevance of this heterogeneity has been lagging behind. Similarly, our definition of cancer drivers has been based on the relative frequency of the cells within tumors and based on their cell-autonomous function, thus, by definition neglecting the potential relevance of minor clones and non-cell-autonomous (e.g., paracrine and juxtracrine) effects. In experimental models there is increasing evidence for cooperation among cancer cell clones with different properties, but identifying and characterizing such interactions in clinical samples has been challenging. At the same time, emerging data suggest that intratumor clonal heterogeneity is maintained by non-cell-autonomous drivers and many of these never achieve clonal dominance due to lack of selective advantage. Thus, it is likely that non-cell-autonomous driver clones exist in human tumors and the effects of the microenvironment are mostly non-cell-autonomous as well. Because interactions among clones of cancer cells and between cancer cells and the tumor microenvironment have a major impact on overall therapeutic outcomes, understanding these interactions is necessary for the design of more effective treatment strategies for heterogeneous tumors. Citation Format: Polyak K. Non-cell-autonomous drivers of tumor growth and progression [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr ES1-1.
Phase I trial of docetaxel (D), cisplatinum (C), and continuous capecitabine (CAP) (TCX) in advanced esophagogastric cancer (AEC).
Authors: Simon Gollins, Arwel Lloyd, Jackie Morris, Nick Smith, Brian Haylock, David Smith, Angel Garcia-Alonso
Journal: Journal of Clinical Oncology (2012)

e14587 Background: This phase I study assessed the combination of D, C, and continuous CAP in AEC to develop a regimen of acceptable toxicity to take forward to phase II study. Methods: Patients with AEC were treated in cohorts of 3, at one of 3 dose levels (DL). DL0: D at 60 mg/m 2 IV on day 1, C at 60 mg/m 2 IV on day 1, CAP at 1,000 mg/m 2 per day in two divided doses days 1-21, every 3 weeks. DL1: CAP increased to 1,250 mg/m 2 per day. DL2: D increased to 75 mg/m 2 IV day 1 and CAP to 1,250 mg/m 2 per day. Prophylactic colony stimulating factors were not used. Patients received a maximum of 6 cycles. Blood counts and biochemistry were assessed twice weekly and daily for grade 3/4 abnormality. Results: Between 1.11.07 and 24.6.09 15 patients were enrolled: male/female:14/1, WHO PS:0/1:10/5, median age 63 yr (range 46-69), primary site oesophagus/GOJ/stomach:7/3/5, adeno/squamous:14/1, T2/3/4:2/9/4, N0/1/2:1/13/1, M0/1:1/14. 6 patients were treated at DL0, 6 at DL1 and 3 at DL2. All patients received 6 cycles apart from 2 at DL 1 who received 3 because of disease progression. Dose intensity: DL0: D 95%, C 100%, CAP 85%; DL1: D 91%, C 98.2%, CAP 79%; DL2: D 86%, C 100%, CAP 79%. There were no deaths on chemotherapy or within 30d of the last dose. The main dose limiting toxicity was febrile or infective neutropenia developing in 1/6 DL0, 2/6 DL1 and 3/3 DL2 (see table of most common treatment-related adverse events below: serious toxicity is gr 3 unless specified gr 4). The maximum length of gr 4 neutropenia was 5d. Best response (RECIST): 1 CR, 11PR, 2 SD and 1PD. 11 patients received second-line chemotherapy. Median and 1 yr overall survival: 17.5m and 60%. Median and 1 yr progression-free survival: 7m and 27%. Conclusions: TCX DLO is recommended for further study in a phase II trial. Encouraging response and survival were seen. [Table: see text]
Farnesyltransferase Inhibitor Tipifarnib (Zarnestra) in Refractory Mantle Cell Lymphoma (MCL): A Therapeutic Target Only for Specific Patients Categorized by the 2-Gene Classifier for Predictive Response to Tipifarnib.
Authors: Delphine Rolland, Vincent Ribrag, Corinne Haioun, Herve Ghesquieres, Fabrice Jardin, Reda Bouabdallah, Patricia Franchi, Josette Briere, Eric De Kerviler, Catherine Chassagne-Clement, Mitch Raponi, Remi Houlgatte, Jean-Philippe Jais, Catherine Thieblemont
Journal: Blood (2008)
Abstract P6-07-18: A pilot study of the impact of a single dose of zolendronic acid on biomarkers in breast cancer
Authors: M Cho, J Gong, S Chen, H Yu, L Wong, L Kruper, J Mortimer
Journal: Cancer Research (2017)

Abstract Backgrounds: In randomized trials for early stage breast cancer, patients who received adjuvant zolendronic acid (ZA) had superior disease-free survival and greater tumor shrinkage. Preclinical data suggest that ZA has anti-cancer properties by modulating angiogenesis and tumor immune environment. This is the pilot study to assess changes in tumor biomarkers and immunological function in response to a single dose of ZA in paired tumor specimens (from core biopsy and definitive surgery). Methods: Postmenopausal women with early stage invasive ductal breast carcinoma who have estrogen receptor and/or progesterone receptor positive tumor for which a lumpectomy or mastectomy was planned prior to systemic therapy were enrolled. A single dose of ZA 4mg IV was given 10-14 days prior to their planned definitive surgery. 14 biomarkers in tumor tissue was assayed; 10 by gene microarray (VEGF, IL1β, IL-6, MMP-1, MMP-2, MMP-9, TGF, Interferon α and STAT3)) and 4 by RT-PCR(P13K, PTEN, IGF-1-R, EGFR. Patient blood samples were drawn at baseline, at 48-72hrs after the single dose of ZA and at the time of surgery and assayed for cytokines and chemokines by using 30-plex Luminex panels. Results: Eight patients were enrolled in the study (median age 65 and range (57-75); 4 caucatians, 2 hispanic and 1 asian; 6 stage I, 1 stage II and 1 stage III). 30-plex luminex assays showed MIG, IP-10 and IL-12 were found to increase in Day 1-3 of ZA therapy from baseline and normalized by Day 10-24. MCP-1, IL2R, MIP-1b and Eotaxin were found to have changes in Day 1-3 from baseline and mix outcome by Day 10-24. EGF, G-CSF, HGF, IFN-alpha and IFN-gamma and RANTES showed no clear pattern among eight patients. Tumor markers and proteomics from pair tumor samples will be presented. Conclusions: Changes in multiple tumor biomarkers and immunological markers, MIG, IP-10, IL-12, MCP-1, IL2R, MIP-1b, Eotaxin, IFN-alpha and IFN-gamma are seen within 2 weeks of a single dose of ZA. Citation Format: Cho M, Gong J, Chen S, Yu H, Wong L, Kruper L, Mortimer J. A pilot study of the impact of a single dose of zolendronic acid on biomarkers in breast cancer [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P6-07-18.