tbuckley/cabot-search huggingface dataset:
Ig V gene mutation status correlates well with clinical course and outcome regardless of surface membrane isotype expressed by B-CLL cells
Authors: T. Wasil, E. Albesiano, F. Ghiotto, S. L. Allen, K. R. Rai, B. Messner, N. Chiorazzi
Journal: Journal of Clinical Oncology (2004)

6562 Background: Clinical heterogeneity in B-CLL patients has been strongly correlated with the mutation status of IgV genes. Several studies have addressed the issue but these have usually involved patients whose leukemic cells express surface membrane (sm) IgM. Here, we present 25 B-CLL patients from our database whose cells expressed smIgG (n = 23) or smIgA (n = 2). Methods: VH gebe repertoire was analyzed and clinical courses of these patients were studied. Results: There was a bias in VH gene usage that differed from sIgM+ B-CLL cases as well as the normal B cell repertoire (VH4 (12) > VH3 (10) > VH1 (2) > VH7 (1) vs. VH3 > VH1 > VH4 for IgM+ cases. Strikingly, within the VH4 family, only 2 VH genes were used –4–34 and 4–39. Five patients in the VH 4–39 group expressed identical VH-D-JH and VL-JL gene segments and in all 5 cases the IgVH and VL genes were unmutated . Among the VH4–34-expressing cases, there was another set of 3 patients whose cells used the same VH-D-JH and VL-JL gene segments but these cases had mutated IgVHand IgVLgenes. Among the VH3-expressing cases, there were far fewer cases that used the VH 3–07 than would be anticipated from the known IgM+ B-CLL repertoire and no case used the VH 1–69 gene that is the predominant gene in VH1-expressing IgM+ cases. J segment use was skewed to JH6 (9) > JH5 (8) > JH4 (5), which also differs from normal B cells (JH4 > JH6 > JH5). CHγ subclass use was as follows: γ1: γ2 : γ3 = 13 : 3 : 4, which differs significantly with the normal peripheral blood and tonsillar B lymphocyte repertoires (γ1 = γ2 >> γ3). When L chain use was evaluated, all Vλ+ cases used genes from the VH3 family and all were associated with a Jλ-2 segment. Although theoretically, isotype switching and mutation go hand in hand, there were 5 cases with unmutated genes in the sIgG cases. Clinically, all of these patients with unmutated Ig V genes did extremely poorly with a median survival of <3 years despite receiving chemotherapy while those patients with mutated Ig V genes had a prolonged median survival of >15 years without requiring chemotherapy. Conclusions: These studies suggest that despite the differences in Ig V gene segment use between the non-IgM+ and IgM+ B-CLL cases, Ig V gene mutation status still correlates well with clinical course and outcome. No significant financial relationships to disclose.
Importance of Achieving Complete Remission (CR) after Intensive Therapy for Acute Myeloid Leukemia (AML) in Older Adults Age ≥60 Years: Analysis of Risk Factors for Early Mortality and Re-Induction, and Impact of Quality of Response on Overall Survival (OS) in the ECOG-ACRIN E2906 Randomized Trial
Authors: James M. Foran, Zhuoxin Sun, David F. Claxton, Hillard M. Lazarus, Mary L. Thomas, Ari Melnick, Ross L. Levine, Elisabeth Paietta, Daniel A. Arber, Yanming Zhang, Jacob M. Rowe, John E. Godwin, Jessica K Altman, Selina Luger, Aref Al-Kali, Hong Zheng, Keith W. Pratz, E. Randolph Broun, Bayard L Powell, Kristen O'Dwyer, Mark Litzow, Martin S. Tallman
Journal: Blood (2016)
A Phase II Study of Enzastaurin, a Protein Kinase C-β (PKCβ) Inhibitor, in the Treatment of Relapsed Diffuse Large B-Cell Lymphoma (DLBCL).
Authors: Michael Robertson, Brad Kahl, Julie Vose, Sven de Vos, Mary Laughlin, Patrick Flynn, Kendrith Rowland, Jose Cruz, Stuart Goldberg, Christelle Darnstein, Nathan Enas, Donna Neuberg, Kerry Savage, Donald Thornton, Christopher Slapak, Margaret Shipp
Journal: Blood (2005)
Identification of sensitivity markers for BMS-536924, an inhibitor for insulin-like growth factor-1 receptor
Authors: F. Huang, W. Hurlburt, R. Hafezi, X. Han, J. Chen, J. Carboni, R. M. Attar, L. Helman, E. Clark, A. Dongre
Journal: Journal of Clinical Oncology (2007)

3506 Background: Insulin-like growth factor-1 receptor (IGF-1R) signaling is an important regulator of mitogenesis, transformation to the oncogenic phenotype and anti-apoptotic effects in malignant cells. Over-expression of IGF-1R, seen in many tumors, may confer a growth advantage or drug resistance. A potent small-molecule inhibitor (BMS-536924) of IGF-1R tyrosine kinase showed anti-tumor activity in sarcoma, prostate, colon and pancreatic tumor models. One of the integral goals in the development of BMS-536924 as a cancer therapeutic is to identify molecular biomarkers predictive of response to the drug that ultimately will aid in selecting the patients who are most likely to benefit. Methods: The sensitivity (IC 50 ) to BMS-536924 was determined for a panel of 29 pediatric sarcoma and neuroblastoma cell lines. Both microarray and LC/MS based protein profiling were utilized to analyze the baseline gene or protein expression level. Drug treatment studies were performed using two rhabdomyosarcoma cell lines, Rh41 (sensitive to BMS-536924) and Rh36 (resistant to the drug) to identify markers that are modulated by BMS-536924. Results: (1). Sixteen out of the 29 cell lines were highly sensitive to BMS-536924; candidate markers that correlated with the sensitivity to BMS-536924 were identified by gene expression and protein profiling. (2). Histological correlation was also discovered, with specific subtypes of sarcoma having a low IC 50 to BMS-536924. (3). Pathway analysis noted that some major candidate markers are common key steps in the EGF-R pathway and the IGF1-R pathway. This observation of cross-talk between the two pathways led to the hypothesis of synergy with combined inhibition of both pathways. Combination studies of BMS-536924 and EGFR inhibitors were performed and synergism was observed. (4). Markers modulated by BMS-536924 in a sensitive cell line were identified. Conclusions: This work has identified candidate markers correlating to BMS-536924 sensitivity in vitro. The possible mechanism of synergistic activity of IGF1-R and EGFR inhibitors will be presented. No significant financial relationships to disclose.
Endothelial Protective Monocyte Patrolling in Large Arteries Intensified by Western Diet and Atherosclerosis
Authors: Amado Quintar, Sara McArdle, Dennis Wolf, Alex Marki, Erik Ehinger, Melanie Vassallo, Jacqueline Miller, Zbigniew Mikulski, Klaus Ley, Konrad Buscher
Journal: Circulation Research (2017)

Rationale: Nonclassical mouse monocyte (CX3CR1 high , Ly-6C low ) patrolling along the vessels of the microcirculation is critical for endothelial homeostasis and inflammation. Because of technical challenges, it is currently not established how patrolling occurs in large arteries. Objective: This study was undertaken to elucidate the molecular, migratory, and functional phenotypes of patrolling monocytes in the high shear and pulsatile environment of large arteries in healthy, hyperlipidemic, and atherosclerotic conditions. Methods and Results: Applying a new method for stable, long-term 2-photon intravital microscopy of unrestrained large arteries in live CX3CR1-GFP (green fluorescent protein) mice, we show that nonclassical monocytes patrol inside healthy carotid arteries at a velocity of 36 μm/min, 3× faster than in microvessels. The tracks are less straight but lead preferentially downstream. The number of patrolling monocytes is increased 9-fold by feeding wild-type mice a Western diet or by applying topical TLR7/8 (Toll-like receptor) agonists. A similar increase is seen in CX3CR1 +/GFP /apoE −/− mice on chow diet, with a further 2- to 3-fold increase on Western diet (22-fold over healthy). In plaque conditions, monocytes are readily captured onto the endothelium from free flow. Stable patrolling is unaffected in CX3CR1-deficient mice and involves the contribution of LFA-1 (lymphocyte-associated antigen 1) and α 4 integrins. The endothelial damage in atherosclerotic carotid arteries was assessed by electron microscopy and correlates with the number of intraluminal patrollers. Abolishing patrolling monocytes in Nr4a1 −/− apoE −/− mice leads to pronounced endothelial apoptosis. Conclusions: Arterial patrolling is a prominent new feature of nonclassical monocytes with unique molecular and kinetic properties. It is highly upregulated in hyperlipidemia and atherosclerosis in a CX3CR1-independent fashion and plays a potential role in endothelial protection.
Molecular subtyping of colon cancers and distinct prognostic groups [NCCTG N0147 (Alliance)].
Authors: Frank A. Sinicrope, Qian Shi, Stephen N. Thibodeau, Richard M. Goldberg, Daniel J. Sargent, Steven R. Alberts
Journal: Journal of Clinical Oncology (2014)

3512 Background: Categorization of colon cancers (CCs) into subtypes based upon pathways of tumorigenesis may improve prognostication. CCs were studied from a randomized trial of adjuvant FOLFOX ± cetuximab. Methods: Stage III CCs (N=3,018) were prospectively analyzed for BRAFV600E and KRAS (codons 12, 13) mutations by a PCR-based assay. DNA mismatch repair (MMR) proteins (MLH1, MSH2, MSH6) were analyzed; loss of any indicated deficient (dMMR) vs proficient MMR (pMMR). Sequencing-based methylation of MLH1was performed. Association with 5 yr disease-free survival (DFS) was evaluated using Cox models. Results: CCs were categorized into 5 subtypes (Table): Traditional (49%), Alternate (35%), Serrated (6.9%), Serrated dMMR (6.8%) or Familial dMMR (2.6%). Traditional vs alternate or serrated pMMR CCs were more likely left-sided (67% vs 42% or 24%; p<.0001) and from men (58% vs 51% or 41%; p< .0001). Alternate and serrated vs traditional pMMR tumors were frequently right-sided [58% and 76% vs 33%, p<.0001] and from women (p< .001). Serrated vs traditional pMMR CCs had more high grade histology (44% vs 19%, p < .0001) and N2 stage (59% vs 41%, p<.0001). Serrated vs familial dMMR CCs were older and more likely female (p <.0001). Alternate or serrated pMMR (vstraditional) tumors showed worse DFS (Table). Compared to alternate CCs, traditional [HR= 0.68 (0.58 -0.79), p<.001], serrated dMMR [HR=0.73 (0.54-.99), p=.042], and familial dMMR [HR=0.51 (0.30-.87), p=.0130] CCs showed favorable DFS. DFS of dMMR and traditional subtypes were similar. Conclusions: Subtype categorization of CCs reveals distinct clinical features and prognoses. Alternate and serrated pMMR subtypes show poor DFS whereas more prevalent traditional CCs have favorable DFS that is similar to dMMR CCs. Subtype HR (95% CI) for DFS P valuea Traditional (pMMR; wild-type BRAF and KRAS) Ref Alternate (pMMR; wild-type BRAF, mutant KRAS 1.48 (1.27-1.74) <.001 Serrated pMMR (mutant BRAFV600E, wild-type KRAS) 1.43 (1.11-1.85) .007 Serrated dMMR (mutant BRAFV600E, wild-type KRAS, hypermethylated MLH1) 1.09 (0.80-1.48) .59 Familial dMMR (wild-type BRAF, any KRAS, unmethylated MLH1 0.76 (0.45-1.29) .31 aAdjusted for age, sex, T, N stage, grade, site, # LNs, treatment.
P27 and pAKT Expression in BRCA1-associated and sporadic breast tumors
Authors: A. Blackwood-Chirchir, M. Tretiakova, W. Yuan, T. Proverbs-Singh, J.-H. Kim, T. R. Das, J. E. Garber, C. Klein, O. Olopade, B. L. Weber
Journal: Journal of Clinical Oncology (2004)

9609 Background: P27 is a tumor suppressor gene that inhibits the cyclin E/CDK2 complex. Somatic loss of p27 function may occur as a result of decreased p27 expression or as a result of nuclear exclusion of the p27 protein. Nuclear exclusion of p27 results from phosphorylation of the p27 protein. This phosphorylation is effected by activated/phosphorylated AKT (protein kinase B). Recent evidence suggests that the BRCA1 protein transactivates expression of p27. Thus, loss of BRCA1 function during carcinogenesis, is expected to be associated with decreased p27 expression. Prior studies have reported p27 loss in 40–55% of unselected breast tumors. Two series have failed to identify a difference in the rate of p27 loss between BRCA1-associated and sporadic tumors. Methods: Using a comparative case series design, we have examined p27 protein expression in the paraffin-embedded, breast tumors of 54 age-matched, BRCA1/sporadic breast tumor pairs. Conclusion: BRCA1-associated tumors are more frequently associated with p27 downregulation than sporadic breast tumors in this series. Staining for activated AKT does not differ between BRCA1-associated and unselected breast tumors, nor do differences in AKT activation appear to be associated with decreased p27 nuclear staining in BRCA1-associated tumors. These findings are consistent with the hypothesis that loss of BRCA1 function is directly responsible for loss of p27 nuclear expression. No significant financial relationships to disclose.
ALIROCUMAB EFFICACY AND SAFETY IN PATIENTS WITH HYPERCHOLESTEROLEMIA AND WITH OR WITHOUT CLINICAL ATHEROSCLEROTIC CARDIOVASCULAR DISEASE: POOLED ANALYSIS OF 10 ODYSSEY RANDOMIZED TRIALS
Authors: Peter H. Jones, Seth Martin, Harold Bays, G.B. John Mancini, Maurizio Averna, Andrei C. Sposito, Michael Koren, Rita Samuel, Alexia Letierce, Marie Baccara-Dinet, R. Scott Wright
Journal: Journal of the American College of Cardiology (2017)
REGIONAL RIGHT VENTRICULAR (RV) FUNCTION AS DETERMINED BY GATED BLOOD POOL SPECT (GBPS) PROVIDES ADDITIVE VALUE TO EVALUATION OF PATIENTS UNDERGOING LEFT VENTRICULAR ASSIST DEVICE (LVAD) IMPLANTATION
Authors: Christopher B. Link, Aditi Nayak, Robert Kormos, Marc Simon, Jeffrey Teuteberg, Luigi Lagazzi, Andrew Althouse, Prem Soman
Journal: Journal of the American College of Cardiology (2017)
RATIO OF TRANSMITTAL EARLY FILLING VELOCITY TO EARLY DIASTOLIC STRAIN RATE PREDICTS LONG TERM RISK OF CARDIOVASCULAR MORBIDITY AND MORTALITY IN A LOW RISK GENERAL POPULATION
Authors: Mats Højbjerg Lassen, Sofie R. Biering-Sørensen, Flemming Javier Olsen, Rasmus Mogelvang, Jan Jensen, Tor Biering-Sorensen
Journal: Journal of the American College of Cardiology (2017)
Estrogen plus progestin (E+P) and breast cancer incidence and mortality.
Authors: Rowan T. Chlebowski, Garnet L Anderson, Lewis H Kuller, Aaron K Aragaki, JoAnn E Manson, Marcia L Stefanick, Karen Johnson, Margery Gass, Dorothy S Lane, Judith Ockene, Gloria Sarto, Jean Wactawski-Wende, Aleksandar Rajkovic, Ross L Prentice
Journal: Journal of Clinical Oncology (2012)

1501 Background: In the WHI clinical trial, E+P increased both breast cancer incidence and breast cancer mortality (JAMA 2010;304:1684). In contrast, breast cancers associated with E+P use in most observational studies have a more favorable prognosis. To address differences, a cohort of WHI Observational Study participants with characteristics similar to the WHI clinical trial was identified to examine E+P association with invasive breast cancer incidence and outcome. Methods: 41,449 postmenopausal women with no prior hysterectomy and mammogram negative for breast cancer &lt; 2 years before who either were not hormone users (25,328) or were using E+P (16,121) were identified. Breast cancers were verified by centralized medical record review. Adjusted Cox proportional hazard regression was used to calculate hazard ratios (HRs) with 95% confidence intervals (CI). Additional analyses adjusted for breast cancer screening, censoring participants for incidence analyses who had a &gt; 2 year interval without a mammogram. Results: After a mean (SD) follow-up 11.3 (3.1) years, 2,236 breast cancers were diagnosed. Breast cancer incidence was higher in E+P users (0.60% vs 0.42%, annualized rate, respectively: HR 1.55, 95% CI 1.41-1.70, P&lt;0.001). Screening adjusted analyses had stronger breast cancer association (0.63% vs 0.39%, HR 1.72, 95% CI 1.54-1.93; P&lt;0.001). Survival following breast cancer, measured from diagnosis date, was similar in E+P users and non-users (HR 0.95, 95% CI 0.74-1.23). Breast cancer mortality, analyzed from cohort entry date, are shown in the table. Conclusions: E+P use is associated with increased breast cancer incidence. As breast cancer prognosis following diagnosis on E+P is similar to that of nonusers, the higher incidence with E+P leads to increased breast cancer mortality. [Table: see text]
ATRIAL FIBRILLATION IS ASSOCIATED WITH WORSE OUTCOMES IN PATIENTS WITH CIRRHOSIS
Authors: Subir Bhatia, Sravya Mallam, Vivek Singh, Kanishk Agnihotri, Shilpkumar Arora, Parshva Patel, Peter Noseworthy, Suraj Kapa, Sidakpal Panaich, Nileshkumar Patel, Apurva Badheka, Nilay Patel, Abhishek Deshmukh
Journal: Journal of the American College of Cardiology (2017)
The Ubiquitin Specific Peptidase 42 Gene (USP42) Is Recurrently Involved as a Fusion Gene with RUNX1 in Acute Myeloid Leukemia with the t(7;21)(p22;q22) Cryptic Translocation.
Authors: Amelie Giguere, Sawcene Hazourli, Douja Meftah, Raouf Fetni, Pierre Chagnon, Josee Hebert
Journal: Blood (2006)
UNCONTROLLED HYPERTENSION IN ACUTE AORTIC DISSECTION FOLLOW-UP
Authors: Abhinav Harish, Truls Myrmel, Marco Di Eusanio, Takeyoshi Ota, Alan Braverman, Reed Pyeritz, Toru Suzuki, G. Chad Hughes, Mark Peterson, Jehangir Appoo, Lori Conklin, Daniel Montgomery, T. Brett Reece, Christoph Nienaber, Eric Isselbacher, Kim Eagle
Journal: Journal of the American College of Cardiology (2017)
SERUM HOMOCYSTEINE LOWERING BY LONG-TERM LOW-DOSE FOLIC ACID: NEW INSIGHT ON MTHFR GENE-FOLATE INTERACTION FROM CHINA STROKE PRIMARY PREVENTION TRIAL
Authors: Xiao Huang, Hong Wang, Xianhui Qin, Wenbin Yang, Shanqun Jiang, Lishun Liu, Yun Song, Min Zhao, Yu Wang, Yan Zhang, Jianping Li, Huihui Bao, Hai Su, Ping Li, Renqiang Yang, Yanqing Wu, Kui Hong, Qinhua Wu, Genfu Tang, Binyan Wang, Fanfan Hou, Yong Huo, Xiaobin Wang, Xiaoshu Cheng
Journal: Journal of the American College of Cardiology (2017)
Clinical and prognostic implications of delta-like ligand 4 and hypoxia-inducible factors in metastatic renal cell carcinoma (mRCC) patients treated with sunitinib as first-line therapy.
Authors: Mian Xie, Chao sheng He, Zhao hui He, Qi zhan Lin
Journal: Journal of Clinical Oncology (2013)

e15567 Background: Sunitinib is recommended as the first line treatment of patients with metastatic renal cell carcinoma (mRCC). Delta-like ligand 4 (DLL4) is a Notch ligand that is upregulated by hypoxia and has a role in tumor angiogenesis. The aim of this study was to evaluate clinical and prognostic implications of DLL4 and markers of hypoxia in mRCC patients treated with sunitinib as first-line therapy. Methods: Treated-naïve, clear cell mRCC patients were received sunitinib 50 mg/d for 4 weeks followed by 2 weeks off treatment (schedule 4/2). We prospectively collected plasma samples before treatment and the expressions of DLL4, Notch1, HIF-1α, HIF-2α were measured using enzyme-linked immunosorbent (ELISA). Progression-free survival (PFS) and overall survival (OS) were determined by Kaplan-Meier method. The log-rank test was used to assess the significance of univariate survival analysis. Multivariate analysis using Cox Regression model was performed to identify independent prognostic factors. Results: Between Aug 2008 and Sep 2010, consecutive 86 patients with mRCC were enrolled. Median follow up period was 35 months. The objective response rate (ORR) was 29.3% (95% confidence interval [CI], 13.5% to 37.7%), median PFS was 10.1 months (95% CI, 8.7 to 12.1 months), and median OS was 23.6 months (95% CI, 16.8 to 26.5 months). Most treatment-related side effect were mild to moderate, including hypertension, fatigue, thrombocytopenia and hand-foot syndrome. Both high DLL4 and low HIF-1α levels significantly correlated with lower ORR (DLL4: 19.8% versus 31.7%, P &lt; 0.001; HIF-1α: 16.8% versus 33.5%, P = 0.002) and shorter PFS (DLL4: 8.6 versus 12.1 months, P = 0.01; HIF-1α: 8.3 versus 11.9 months, P = 0.01), but this was not predictive of OS. Neither survival nor ORR was associated with expressions of Notch1 and HIF-2α. Conclusions: Sunitinib has shown effective anti-tumor activity in treatment-naïve mRCC patients. High expression of DLL4 and low expression of HIF-1α may mediate resistance to sunitinib. Baseline levels of DLL4 and HIF-1α have prognostic impact on PFS for patients treated with sunitinib.
Aggregation of α-Synuclein in the Gonadal Tissue of 2 Patients With Parkinson Disease
Authors: Alicia Garrido, Iban Aldecoa, Ellen Gelpi, Eduardo Tolosa
Journal: JAMA Neurology (2017)

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A novel case of Silver Russell Syndrome (SRS) and male breast cancer
Authors: C. M. Hamm, L. Jagiello
Journal: Journal of Clinical Oncology (2007)

21178 Introduction: Silver Russell Syndome (SRS) is a heterogeneous disorder of asymmetric growth retardation and typical dysmorphic features often associated with maternal disomy 7 and chromosome 17q23–24. The BRCA1 gene is found on 17q21. The relationship between SRS and breast cancer has not been described to date. Case Presentation: We report a case of a 37 year old male diagnosed with metastatic breast cancer involving the liver and bone. Patient presented with a left proximal hip fracture related to metastatic bone disease. Biopsy of the right breast lesion revealed a moderately differentiated adenocarcinoma consistent with breast primary. Abdominal ultrasound and full body bone scan revealed extensive liver and bone metastases. There was no significant family history of cancer, specifically breast nor ovarian cancer. Discussion: The BRCA2 gene is known to be responsible for DNA repair. The SRS cases associated with chromosome 17q24–25 abnormalities are known to be associated with growth hormone deletions. Further investigations into this relationship are warranted. No significant financial relationships to disclose.
SAFETY AND EFFICACY OF ZILVER PTX DRUG ELUTING STENT IMPLANTATION FOLLOWING DRUG COATED BALLOON INFLATION VERSUS POBA IN HEALTHY SWINE MODEL
Authors: Sho Torii, Hiroyoshi Mori, Brandt Young, John Brumleve, Aloke Finn, Renu Virmani
Journal: Journal of the American College of Cardiology (2017)
DO PEDIATRIC CARDIOLOGISTS FOLLOW THE SPORTS RESTRICTION RECOMMENDATIONS FOR CHILDREN WITH A BICUSPID AORTIC VALVE?
Authors: Melissa Yamauchi, Michael Puchalski, Nelangi Pinto, Susan Etheridge, Hsin-Yi Weng, Angela Presson, L. LuAnn Minich, Richard Williams
Journal: Journal of the American College of Cardiology (2017)