tbuckley/cabot-search huggingface dataset:
163. Hematopoietic Stem Cells Transplantation Can Normalize Thyroid Function in a Cystinosis Mouse Model
Authors: Heloise P. Gaide Chevronnay, Virginie Janssens, Patrick Van Der Smissen, Celine J. Rocca, Xiao-Hui Liao, Samuel Refetoff, Christophe E. Pierreux, Stephanie Cherqui, Pierre J. Courtoy
Journal: Molecular Therapy (2016)

Cystinosis is a multi-systemic lysosomal storage disease caused by defective transmembrane cystine transporter, cystinosin (CTNS gene). In the mouse model of cystinosis, Ctns−/− mice, it has already been shown that hematopoietic stem and progenitor cell (HSC) transplantation provides long-term protection of kidneys and eyes, which are affected early on in cystinosis. Tissue repair involves transfer of cystinosin-bearing lysosomes from HSPCs differentiated as macrophages into deficient adjacent cells, via tunnelling nanotubes (TNTs). Hypothyroidism is the most frequent and earliest endocrine complication in cystinotic patients and was recently shown as a complication in the Ctns−/− mice too. Here, we are evaluating the benefit of HSPC transplantation in the thyroid of Ctns−/− mice. Abundant engraftment of bone marrow-derived cells in Ctns−/− thyroid correlated with drastic decreased of cystine content, normalization of TSH level and correction of the structure of a large fraction of thyrocytes. In the thyroid microenvironment, HSPCs differentiated into a distinct, mixed macrophage/dendritic cell lineage expressing CD45 and MHCII, but not-detectably CD11b and F4/80. Like in cystinotic kidneys, HSPC-derived cells produced TNT-like extensions capable of crossing the follicular basement laminae. Interestingly, HSPCs themselves further squeezed into follicles, allowing extensive contact with thyrocytes, but did not transdifferentiate into Nkx2.1-expressing cells, the hallmark of thyrocytes. This is the first report demonstrating the potential of HSPC transplantation to correct thyroid disease, and supports a major multisystemic benefit of stem cells therapy for cystinosis.
Prospective cohort study of depression during androgen deprivation therapy (ADT) for nonmetastatic prostate cancer.
Authors: N. Timilshina, H. Breunis, S. M. H. Alibhai
Journal: Journal of Clinical Oncology (2011)

9085 Background: Up to 50% of prostate cancer (PC) patients receive ADT, often for 2-3 years or more. The most common side effects include fatigue, hot flashes, loss of libido, anemia, decreased muscles mass, and osteoporosis. Anxiety and depression are common after a diagnosis of cancer. Whether ADT leads to or worsens depression is not clear. Methods: Three separate cohorts were assembled. ADT users consisted of men initiating continuous ADT. PC patients who were not on ADT (PC controls) and healthy controls were also enrolled. All three cohorts were matched on age, education and baseline physical function and none had metastases. Depression was measured using the 15-item Geriatric Depression Scale (GDS). The GDS was administered at study entry and again at 3, 6 and 12 months. Our primary outcome was the development of new depressive symptoms (defined as a GDS score ≥5), analyzed as a dichotomous variable using chi-square tests and as a continuous variable in adjusted linear regression analyses. Results: Of the 257 participants (mean age 69.1 y), the majority were white (87.3%) and had a mean of 15.3 years of formal education. Most baseline characteristics (age, education, race, body mass index, smoking and alcohol use, income, and comorbidity including GDS score and a prior diagnosis of depression), were similar across cohorts at baseline. Patients who were depressed at baseline (n=18, 7%) were excluded from the main analysis. On univariate linear regression, ADT use was not a significant predictor of change in GDS score at 3 months (P=0.42), 6 months (P=0.25), or 12 months (P=0.19). Among ADT users, 8-9% of participants developed incident depression compared to 0-4% among PC controls and 4- 4.5% among healthy controls over 12 months (adjusted p>0.05 at all time points). In a separate analysis of patients with depression at baseline, there was no effect of ADT on depressive symptoms at 3, 6, or 12 months (P=0.11, 0.74, and 0.12, respectively). Conclusions: This prospective study demonstrated that 12 months of ADT use was not associated with worsening depressive symptoms among non-depressed or depressed patients with non-metastatic PC.
Abstract 3820: Ultrasensitive DNA methylation detection using sputum and plasma for early detection of NSCLC
Authors: Chen Chen, Alicia Hulbert, Alejandro Stark, Kristen Rodgers, Beverly Lee, Malcolm Brock, James Herman
Journal: Cancer Research (2015)

Abstract Purpose: The National Lung Cancer Screening Trial provides hope that early detection can result in a reduction of mortality from lung cancer. This study was to determine if molecular alterations of sputum and plasma in patients with CT detected pulmonary nodules could predict patients with malignancy from those without. Materials and Methods: We conducted a prospective case-control study obtaining cases and controls from the Lung Cancer Spore Trial at Johns Hopkins Hospital. Plasma, sputum and pre-operative CT scans were obtained from all patients. We processed the plasma, sputum and tumor by using promoter Methylation on beads followed by quantitative methylation specific real-time PCR to investigate promoter methylation status of six cancer-related genes, CDO1, TAC1, HOXA7, HOXA9, SOX17 and ZFP42. Results: 223 patients were analyzed, including 162 patients with NSCLC and 61 patients with benign lesions. The sensitivity and specificity values for lung cancer detection in plasma, sputum or in both are shown. Plasma methylation seems to be more specific than sputum methylation. Both concomitant methylation in both plasma and sputum yielded the highest specificity for all gene combinations. Promoter methylation of CDO1, TAC1, HOXA9 and SOX17 has a high specificity but low sensitivity to detect lung cancer. Sensitivity and specificity for lung cancer detection using methylation changes in plasma and sputumPlasmaPlasmaSputumSputumPlasma &amp; SputumPlasma &amp; SputumGeneSpecificitySensitivitySpecificitySensitivitySpecificitySensitivityCDO180%45%67%63%93%26%TAC167%52%40%65%80%31%HOXA7100%11%80%27%100%6%HOXA960%66%7%90%67%60%SOX1767%56%73%52%93%27%ZFP4247%69%33%74%60%52%4 or more genes67%50%67%63%97%26%CDO1, TAC1, HOXA9, SOX1787%39%80%40%93%15% Conclusion: Our gene panel of promoter methylation has a high enough specificity to be clinical useful but its sensitivity is low. The integration of this panel with other biomarkers would be needed to create a platform of high enough specificity and sensitivity to be clinically applicable. Citation Format: Chen Chen, Alicia Hulbert, Alejandro Stark, Kristen Rodgers, Beverly Lee, Malcolm Brock, James Herman. Ultrasensitive DNA methylation detection using sputum and plasma for early detection of NSCLC. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3820. doi:10.1158/1538-7445.AM2015-3820
The genome of the Gulf pipefish enables understanding of evolutionary innovations
Authors: C. M. Small, S. Bassham, J. Catchen, A. Amores, A. M. Fuiten, R. S. Brown, A. G. Jones, W. A. Cresko
Journal: Genome biology (2016)

Evolutionary origins of derived morphologies ultimately stem from changes in protein structure, gene regulation, and gene content. A well-assembled, annotated reference genome is a central resource for pursuing these molecular phenomena underlying phenotypic evolution. We explored the genome of the Gulf pipefish (Syngnathus scovelli), which belongs to family Syngnathidae (pipefishes, seahorses, and seadragons). These fishes have dramatically derived bodies and a remarkable novelty among vertebrates, the male brood pouch. We produce a reference genome, condensed into chromosomes, for the Gulf pipefish. Gene losses and other changes have occurred in pipefish hox and dlx clusters and in the tbx and pitx gene families, candidate mechanisms for the evolution of syngnathid traits, including an elongated axis and the loss of ribs, pelvic fins, and teeth. We measure gene expression changes in pregnant versus non-pregnant brood pouch tissue and characterize the genomic organization of duplicated metalloprotease genes (patristacins) recruited into the function of this novel structure. Phylogenetic inference using ultraconserved sequences provides an alternative hypothesis for the relationship between orders Syngnathiformes and Scombriformes. Comparisons of chromosome structure among percomorphs show that chromosome number in a pipefish ancestor became reduced via chromosomal fusions. The collected findings from this first syngnathid reference genome open a window into the genomic underpinnings of highly derived morphologies, demonstrating that de novo production of high quality and useful reference genomes is within reach of even small research groups.
Screening for Social Determinants of Health
Authors: Ronald Bayer, David Merritt Johns
Journal: JAMA (2016)

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
Association of HLA-G Haplotype Risk Model with Treatment Free Survival In Chronic Lymphocytic Leukemia Patients
Authors: Johanna Kapp, Crista Ochsenfarth, Magdalena Switala, Ulrich Frey, Ludger Sellmann, Jan Duerig, Peter A Horn, Ulrich Duehrsen, Vera Rebmann, Holger Nuckel
Journal: Blood (2010)
Tissue Factor Mediated Activation of Prothrombin Complex Concentrates (PCCs) Is Differently Inhibited by Dabigatran, Rivaroxaban and Apixaban. Potential Clinical Implications
Authors: Jawed Fareed, Nasir Sadeghi, Daniel Kahn, Josephine Cunanan, Kimberly Bartosiak, Job Harenberg, Debra Hoppensteadt
Journal: Blood (2012)
Comprehensive Genomic and Transcript Profiling of CBL Gene in Childhood AML: A Report from Children's Oncology Group Studies AAML03P1, AAML0531 and COG/NCI Target AML Initiative
Authors: Diana Chin, Matthew A. Kutny, Jonathan Grim, Robert B. Gerbing, Kristen Miller, Jason E. Farrar, Jaime M. Guidry Auvil, Malcolm A. Smith, Daniela S. Gerhard, Tanja M. Davidsen, Patee Gesuwan, Leandro C. Hermida, Marco A Marra, Andrew J. Mungall, Richard Moore, William Long, Yussanne Ma, Stuart Zong, E. Anders Kolb, Alan S. Gamis, Todd A. Alonzo, Soheil Meshinchi
Journal: Blood (2015)
Abstract 1033: Alternative tumor suppressor mechanisms in lung carcinomas - modulation of senescence by growth factor-induced signaling
Authors: Boyka Markova, Frank Breitenbuecher, Martin Schuler
Journal: Cancer Research (2015)

Abstract Cellular signaling pathways integrate multiple intra- and extracellular signals and thereby influence cell fate. Outcome of oncogene-targeted pharmacotherapies (cell cycle inhibition, apoptosis, senescence, autophagy) depends on variable factors (e.g. compound, dose, duration, cellular genetic background etc.). Oncogene-induced senescence is recognized as an important tumor-suppressive mechanism, bypassing of which may contribute to malignant transformation of the cells. On the other hand, senescence induction, in addition to apoptosis stimulation and proliferation suppression, is responsible for the cytostatic activity of many commonly used anticancer drugs. Therefore, senescence escape must be considered as an important drug-resistance factor. In our work we characterize,,DNA Damage-independent” senescence induced by tyrosine kinase inhibitors (TKI) and growth factor deprivation of non-small cell lung cancer (NSCLC) cell lines and other EGFR-dependent cells. Treatment of different cell lines with various concentrations of EGFR-TKIs was followed by the assessment of cell fate (i.e. apoptosis, cell cycle distribution, senescence and clonogenic survival) as well as intracellular signaling. We could show that treatment of EGFR-dependent cells with specific EGF receptor tyrosine kinase inhibitors (EGFR-TKI) can lead to generation of reactive oxygen species (ROS), activation of a DNA damage response (DDR) program and cellular senescence. Surprisingly, under certain experimental conditions DDR activation was found to be independent from detectable DNA damage. Key players of DDR signaling were shown to be essential for senescence induction. Molecular dissection of crucial signaling nodes and molecular switches involved in modulation of cell fate in oncogene dependent cells treated with specific EGFR-inhibitors is currently being performed. Furthermore, our work is focussed on the identification and characterization of cellular factors activating DNA damage response (DDR) pathways in the absence of DNA damage under certain experimental conditions. Understanding the interplay between theses decision making pathways either leading to proliferative arrest, cellular senescence or apoptosis will help improve current pharmacotherapies and develop new therapeutic approaches. Note: This abstract was not presented at the meeting. Citation Format: Boyka Markova, Frank Breitenbuecher, Martin Schuler. Alternative tumor suppressor mechanisms in lung carcinomas - modulation of senescence by growth factor-induced signaling. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1033. doi:10.1158/1538-7445.AM2015-1033
Abstract 4860: Detection of genetically distinct subclones in cancer: a novel NGS algorithm with high spatial and genetic resolution
Authors: Konstantinos Karagiannis, Konstantin Chumakov, Vahan Simonyan, Raja Mazumder
Journal: Cancer Research (2015)

Abstract Despite the large number of genome data banks, reference sequences are not always the best match for high-throughput analysis. This is especially true in studies of intratumor heterogeneity where increased mutation rates are observed; the use of a reference genome can complicate the interpretation of the results. Current techniques attempt to circumvent this obstacle by applying de novo assembly algorithms, but the process is slow and often without viable results. Here, we introduce a new technique to decrease the dependency of these pipelines on reference sequences. Our clone discovery algorithm takes advantage of existing alignment data and correlates distant mutations, reported by an alignment algorithm. The algorithm makes no statistical assumption; it extracts information from the overlapping alignments in a step-wise fashion, using reference coordinates of aligned reads. Due to the randomness of noise, the algorithm can be very sensitive and identify clones of low frequency. Citation Format: Konstantinos Karagiannis, Konstantin Chumakov, Vahan Simonyan, Raja Mazumder. Detection of genetically distinct subclones in cancer: a novel NGS algorithm with high spatial and genetic resolution. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4860. doi:10.1158/1538-7445.AM2015-4860
Dose Definition for Intravenous Cyclophosphamide in Combination with Bortezomib/Dexamethasone for Remission Induction in Patients with Newly Diagnosed Multiple Myeloma.
Authors: Martin Kropff, Peter Liebisch, Hannes Wand, Katja Weisel, Claudia-Nanette Gann, Stefan Knop, Herrmann Einsele
Journal: Blood (2007)
Association Between Human Immunodeficiency Virus Infection and Cardiovascular Diseases
Authors: Colleen Hadigan, Catharine I. Paules, Anthony S. Fauci
Journal: JAMA Cardiology (2016)

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 Cardiology 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 Cardiology journal
Cathepsin G Is Broadly Expressed By AML and Is an Effective Immunotherapeutic Target Against AML in Vivo
Authors: Gheath Alatrash, Mao Zhang, Pariya Sukhumalchandra, Yihua Qiu, Amjad H. Talukder, Vladimir Senyukov, Lisa S. St. John, Hong He, Anna Sergeeva, Jason Roszik, Karen Clise-Dwyer, Sijie Lu, Qing Ma, Elizabeth A. Mittendorf, Dean A. Lee, David H Hawke, Lizee Gregory, Jeffrey J. Molldrem, Steven M. Kornblau
Journal: Blood (2014)
Hb F Malta I in Association with Hb F Sardinia (AyT) and Hb Valletta in Heterozygotes: Quantification of the Six Globins Suggests Developmental Control of the XMN-I Site and Interplay with the (AT)xTy Sequence in Connection with Globin Gene Switching.
Authors: Alexander Felice, Joseph Borg, Wilma Cassar, Ruth Galdies, Monica Pizzuto, Maryrose Caruana, Christian Scerri
Journal: Blood (2006)
RTHP-33. OUTCOMES AFTER STEREOTACTIC RADIATION THERAPY FOR PRIMARY CNS LYMPHOMA
Authors: Gaurav Shukla, Joshua Palmer, Jon Glass, Lyndon Kim, Wenyin Shi
Journal: Neuro-Oncology (2016)

The standard of care for primary CNS lymphoma (PCNSL) typically includes high dose methotrexate systemic therapy (HD-MTX) followed by whole brain radiation therapy (WBRT). Many patients cannot tolerate this regimen, and there is increased risk of leukoencephalopathy in elderly patients receiving WBRT after HD-MTX. In our institution, we have offered stereotactic radiosurgery in 1-3 fractions for disease refractory to HD-MTX in a subset of patients who are felt to be high-risk for WBRT. Medical records of five patients who received partial brain radiation therapy for persistent CNS lymphoma were reviewed. Four patients received stereotactic radiosurgery (SRS) via single fraction or three-fraction regimen to doses of 21-24 Gy; one patient received salvage SRS three years after WBRT. Outcomes recorded were overall survival, and local control in RT field, and intracranial progression-free survival (outside of RT field). Five patients (eight lesions) were treated with stereotactic radiation therapy for PCNSL. Median follow up was 9 months (range: 4-33). Median RT dose per lesion was 21 Gy. Median time to any failure was 8.5 months, with two patients free of disease recurrence at last follow up. Median overall survival was not reached as three patients remain alive. Two patients had distant intracranial failure (salvaged with WBRT and chemo, respectively), and a third patient developed a marginal recurrence (salvaged with repeat SBRT). There was no Grade 2 or higher acute or late toxicity. Stereotactic radiation therapy may provide favorable local control in patients with refractory PCNSL at high risk with WBRT. Prospective trial is warranted to validate the efficacy of such an approach.
Absolute Monocyte Count in Follicular Lymphoma Patients Treated with Rituximab Plus Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone
Authors: Reina Watanabe, Naoto Tomita, Kumiko Kishimoto, Satoshi Koyama, Eriko Ogusa, Yoshimi Ishii, Kazuho Miyashita, Shiro Matsuura, Shin Fujisawa, Yukako Hattori, Hirotaka Takasaki, Atsuko Fujita, Rika Ohshima, Hideyuki Kuwabara, Chizuko Hashimoto, Katsumichi Fujimaki, Rika Sakai, Yoshiaki Ishigatsubo
Journal: Blood (2012)
Abstract 4242: Metformin suppresses GRP78-dependent PI3-Kinase activity in clonogenic side population to enhance the anti-myeloma benefit of bortezomib
Authors: James J. Driscoll, Sajjeev Jagannathan, Mohamed AY Abdel Malek, Nikhil Vad, Ehsan Malek
Journal: Cancer Research (2015)

Abstract Multiple myeloma (MM) patients invariably relapse through mechanisms that remain elusive. Disease recurrence after treatment suggests that rare, tumor-initiating subpopulations with chemoresistant phenotypes persist or emerge to propagate and mediate tumor regrowth. Stem cell-like side population (SP) cells were isolated from myeloma cell lines and patient samples and exhibited resistance to proteasome inhibitors relative to the main population (MP). SP cell-based high-throughput screening detected pharmacologics that enhanced the anti-proliferative effect of bortezomib and revealed the anti-diabetic agent metformin. Bortezomib treatment increased levels of the molecular chaperone glucose-regulated protein GRP78 but metformin co-treatment suppressed bortezomib-induced GRP78 upregulation. Bortezomib treatment also promoted GRP78 co-localization with the signal transducer phosphatidylinositol-3-kinase (PI3K) that activates cell growth and survival pathways. SP cells displayed greater levels of the PI3K product phosphatidylinositol (3,4,5)-trisphosphate (PIP3) and enhanced PI3K-mediated phosphorylation of protein kinase B/AKT compared to MP cells. Metformin treatment or knockdown of GRP78-encoding HSPA5 enhanced sensitivity to bortezomib preferentially in SP cells. Tumor growth was significantly delayed and overall survival prolonged after metformin co-treatment with bortezomib in mice injected with parental or SP cells. Taken together, the results support the pharmacologic repositioning of metformin to inhibit GRP78 induction in therapy-resistant cells and enhance the anti-myeloma benefit of bortezomib. Note: This abstract was not presented at the meeting. Citation Format: James J. Driscoll, Sajjeev Jagannathan, Mohamed AY Abdel Malek, Nikhil Vad, Ehsan Malek. Metformin suppresses GRP78-dependent PI3-Kinase activity in clonogenic side population to enhance the anti-myeloma benefit of bortezomib. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4242. doi:10.1158/1538-7445.AM2015-4242