tbuckley/cabot-search huggingface dataset:
Avoiding population exposure to carcinogens from chemotherapy.
Authors: Otis W. Brawley, Peter Boyle
Journal: Journal of Clinical Oncology (2015)

e12582 Background: Remarkable efforts are made to identify the causes of cancer. Once a cause is identified, steps are taken to avoid the population exposure wherever possible. Methods: After patients treated with certain chemotherapeutic agents were found to be at increased risk of second primary tumours, steps were introduced to decrease agent exposures of medical personnel preparing and administering these compounds. Over 20 cancer chemotherapy drugs, including widely used drugs such as cyclophosphamide, doxorubicin, 5-FU and etoposide, cause patients receiving them to excrete known human carcinogens in vomit, sweat, urine or faeces.Systems for the collection or isolation of this carcinogenic waste outside the hospital environment are not widely available. Results: As far back as 1985, accidental contamination of health care workers by one of these cytotoxic drugs, cyclophosphamide, a proven human carcinogen, was extensively studied. Nurses who working with patients treated with cycophosphamide had babies with 4.7-times the number of birth defects as nurses who did not work with such patients and 2.7-times the number of miscarriages. In the years after OSHA’s first warnings, it was still clear that employees exposed to cytotoxic drugs were still becoming contaminated with cytotoxic chemicals. Even today, in hospitals with strict procedures and advanced equipment, patients’ lavatories show high levels of cytotoxic chemicals in the splashed urine of chemotherapy patients. Conclusions: Guidelines have been prepared for hospital employees, oncologists, nurses and cancer drug producers to avoid or minimise their exposure to these carcinogenic risks. When patients are sent home following treatment, the patient is occasionally advised to restrict use of their toilet or, if not possible, to ‘flush’ twice. This will reduce the exposure to the patient and their caregivers, but will not eliminate the carcinogenic exposure. In addition, it could be foreseen that there are circumstances in which failure to deal with this source of carcinogens could lead to wider exposure in communities. Greater consideration should be given to eliminate this source of human carcinogens.
ロータブレーターのプラットフォーム時における低温ヘパリン加生理食塩水の能動的圧力ポンピングは心臓損傷を予防できるか?:包括的in vivo動物研究
Authors: Kanoh H, Misumi K, Hirose M, Itoh M, Yoshiwara H, Itakura Y, Iiduka D, Kubo T, Nitta M
Journal: Circulation (2004)
Abstract P117: Does Mammalian Target of Rapamycin Complex-2 Regulate Protein Degradation Pathways in the Heart?
Authors: Pankaj S Shende, Christian Morandi, Marijke Brink
Journal: Circulation Research (2011)

Background: Mammalian target of rapamycin (mTOR) occurs in the cell in two distinct multiprotein complexes called mTOR complex 1 (mTORC1) and mTORC2, which contain raptor and rictor, respectively. We have recently demonstrated that mTORC1 activity is required for the hypertrophic response to aortic constriction and for the normal cardiac homeostasis. Moreover, we showed that raptor deletion causes Akt hyperphosphorylation and lower gene expression of Atrogin-1 and MuRF1, two muscle specific E3 enzymes part of the proteasomal degradation pathway. These results suggested that, as a counter-regulatory response to mTORC1 inactivation, mTORC2 reduces protein degradation via phosphorylation of Akt at Ser473. It has previously been shown that the phosphorylation state of Akt regulates Atrogin-1 and MuRF1 gene expression at the transcriptional level via FoxO. In the present study, we have tested whether mTORC2 inactivation induces the ubiquitin-proteasomal degradation pathway. Methods and results: In 10 week-old male mice, transgenic for MerCreMer driven by the α-MHC promoter and homozygous for floxed rictor, deletion of the rictor gene was induced by tamoxifen. Protein and RNA extracts were analyzed at three weeks after tamoxifen by Western blotting and qPCR, respectively. The rictor gene was efficiently ablated from the heart as its protein levels were reduced. Phosphorylation of Akt and PKC-α, direct targets of mTORC2, was abolished, identifying these signaling molecules as downstream targets of mTORC2 in the heart. However, the reduced Akt phosphorylation was not associated with any changes in the mRNA levels of Atrogin-1, MuRF1, and MuRF3. Conclusion: Our study suggests that mTORC2-induced phosphorylation of Akt is not required for the maintenance of low expression levels of these genes. Further studies are ongoing to identify the factors that modulate Atrogin-1 and MuRF1 gene transcription in the heart.
Cardiovascular Risk Factors From Childhood and Midlife Cognitive Performance
Authors: Suvi P. Rovio, Katja Pahkala, Jaakko Nevalainen, Markus Juonala, Pia Salo, Mika Kähönen, Nina Hutri-Kähönen, Terho Lehtimäki, Eero Jokinen, Tomi Laitinen, Leena Taittonen, Päivi Tossavainen, Jorma S.A. Viikari, Juha O. Rinne, Olli T. Raitakari
Journal: Journal of the American College of Cardiology (2017)
Comorbidity and the receipt of curative therapy for favorable-risk prostate cancer prior to and following the publication of PIVOT.
Authors: Stephen A. Mihalcik, Ming-Hui Chen, Michelle H. Braccioforte, Brian Joseph Moran, Anthony V. D'Amico
Journal: Journal of Clinical Oncology (2016)

17 Background: On July 19, 2012, the Prostate Cancer Intervention versus Observation Trial (PIVOT) was published and reported that after a median follow up of 10 years, radical prostatectomy neither improved overall survival nor reduced prostate cancer (PC)-specific mortality in men with low-risk PC compared to watchful waiting. However, the trial’s applicability may be somewhat limited by the participants’ poorer-than-average overall health. This study aimed to evaluate the impact of the PIVOT by assessing practice patterns before and after its publication. Methods: Between October 1997 and May 2013, 6,818 men with low-risk (n = 5,081, 74.5%) or favorable intermediate-risk (N = 1,737, 25.5%) PC were treated with curative intent at the Chicago PC Foundation. We compared the proportions of these men with ≥2, 1, or 0 comorbid conditions, restricted to myocardial infarction, congestive heart failure, diabetes mellitus, and coronary artery disease. We assessed for a trend in these proportions by time tertile prior to the PIVOT’s publication and compared them one month following PIVOT to the final pre-publication time tertile. Results: Of 6,818 men treated with curative intent, 5,208 (76.5%), 1,307 (19.2%), and 293 (4.3%) had 0, 1, and ≥2 comorbidities, respectively. Prior to PIVOT, the proportion of men with the greatest comorbidity (≥2) increased by time tertile (3.5% vs. 4.2% vs. 5.4%; p = 0.002), while 1 month following publication, there was a decline in the proportion of men with the highest degree of comorbidity (5.4% vs. 2.9%; p = 0.05). In addition to the drop in men with greatest comorbidity, men treated following the publication of the PIVOT were also younger (median age 65.7 vs. 66.8 years; p = 0.04), more likely to be black or Hispanic (24.7% vs. 17.4%; p = 0.003), and more likely to have favorable intermediate than low-risk PC (36.1% vs. 28.4%; p = 0.007). Conclusions: Following the publication of the PIVOT, men with low or favorable intermediate-risk PC whose health was poorer than the national average were less likely to undergo curative treatment, whereas men at higher risk for harboring occult high grade PC despite favorable-risk indices were more likely to undergo curative treatment.
A multicenter, open-label phase II trial of liposomal doxorubicin (LD) and docetaxel (DX), followed by concurrent chemotherapy and radiation therapy in locally advanced high-risk, early breast cancer (HRBC).
Authors: Francesco Recchia, Giampiero Candeloro, Alisia Cesta, Giovambattista Desideri, Stefano Necozione, Silvio Rea
Journal: Journal of Clinical Oncology (2012)

e11041 Background: Taxanes and anthracyclines (ANs) are among the most active agents in the treatment of breast cancer. However, ANs are associated with dose-related cardiac toxicity, which can lead to progressive myocardial damage. Non-pegylated liposome-encapsulated doxorubicin (Myocet®), has been shown to significantly reduce cardiac toxicity even though providing comparable antitumor efficacy. Primary endpoint of this phase II study was the assessment of early and late cardiac toxicity of young patients with HRBC treated with LD and DX. Secondary end-points were the incidence of hematological toxicity, time to progression and overall survival in this cohort of patients. Methods: From 05-2006 to 10-2009, 60 HRBC patients were entered into the study. They were treated with LD 60 mg/m2 and DX 75 mg/m2 every three weeks for six courses. Hematological growth factors were given when indicated. Cyclophosphamide 600 mg/m2, methotrexate 60 mg/m2 and 5-fluorouracil 600 mg/m2 were given for six courses concomitantly with radiation therapy to the breast, axilla and supraclavicular nodes. After chemo-radiation therapy, a hormonal therapy was given to estrogen receptors positive (ER+) patients and trastuzumab to Herb-2 positive patients. LVEF was evaluated at baseline and after 6 months, thereafter, up to 5 years. Results: Median age was 49 years. Mean number of positive axillary nodes was 4.9 (range 0-20). 70% were ER+, 30% were ER - and progesterone receptor (PGR) negative. Median Ki-67 was 30% (range 20%-100%), 18% of patients were Herb-2 positive and 18% of patients had pre-existing hypertension. Delivered dose was 95.7% of the planned dose. No patient showed neither a decrease of EF &gt; 10%, nor congestive heart failure. Febrile neutropenia was observed in 12% of patients. At 44 months of median follow-up, 86% of patients were disease-free and 94% were alive. Conclusions: Chemotherapy with LD and DX has shown low cardiac toxicity and high activity in this group of HRBC patients.
Evaluation of Practical Interpretation Hurdles in 68Ga-PSMA PET/CT in 55 Patients
Authors: Julian Kirchner, Benedikt Michael Schaarschmidt, Lino Morris Sawicki, Philipp Heusch, Hubertus Hautzel, Johannes Ermert, Robert Rabenalt, Gerald Antoch, Christian Buchbender
Journal: Clinical Nuclear Medicine (2017)

Purpose To investigate the physiologic 68Ga-PSMA distribution and evaluate focal or diffuse radiotracer uptake in nonprostate cancer malignancies and in incidental findings. Methods 68Ga-PSMA PET/CT scans in 55 men performed for prostate cancer (49) or renal cell carcinoma (6) staging were analyzed retrospectively. Two radiologists evaluated the datasets in 2 reading sessions. First, physiological 68Ga-PSMA uptake was evaluated. Second, scans were analyzed for incidental uptake. SUVmax and SUVmean were recorded. Other imaging modalities, histopathology, or clinical follow-up served as standard of reference. Results Homogenous 68Ga-PSMA uptake of the lacrimal glands (SUVmax, 15.7 ± 7.2), parotid glands (SUVmax, 24.4 ± 8.1), submandibular glands (SUVmax, 26.7 ± 7.1), vocal cords (SUVmax, 8.4 ± 3), Waldeyer ring (SUVmax, 10.4 ± 4.3), liver (SUVmax, 8.2 ± 2.5), spleen (SUVmax, 10.9 ± 3.9), kidneys (SUVmax, 66.4 ± 25.4), and pars descendens duodeni (SUVmax, 17.6 ± 8.9) was observed in all patients. In 65% and 36%, respectively, homogenous 68Ga-PSMA uptake of the colon descendens (SUVmax, 10.6 ± 9.2) and the rectum (SUVmax, 3.7 ± 1.1) was found. Approximately 22% exhibited a 68Ga-PSMA uptake of the thyroid (SUVmax, 4.5 ± 1.2), and 21% exhibited a 68Ga-PSMA uptake of the knee's synovia (SUVmax, 2.9 ± 0.2). Furthermore, 68Ga-PSMA uptake was found in 1 patient because of fibrous dysplasia of the right os ilium (SUVmax, 7.7). Conclusions Physiologic distribution of 68Ga-PSMA comprises uptake in lacrimal and salivary glands, vocal cords, Waldeyer ring, liver, spleen, and kidneys as well as various parts of the intestine. Moreover, nonspecific tracer uptake is regularly found in the thyroid and the synovia of the knee. Incidental 68Ga-PSMA uptake can occasionally reveal nonprostate cancer–associated remodeling processes, such as fibrous dysplasia.
Funding, Institutional Conflicts of Interest, and Schools of Public Health
Authors: Sandro Galea, Richard Saitz
Journal: JAMA (2017)

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Low dose TBI based non myeloablative allografting for advanced hematological malignancies: A multicenter experience.
Authors: B Bruno, E Benedetti, B Allione, F Carnevale-Schianca, C Rosanello, M Rotta, A Capaldi, M Aglietta, A Levis, M Petrini, P Coser, R Storb, M Boccadoro
Journal: Blood (2003)
Should Low Molecular Weight PSMA Targeted Ligands Get Bigger and Use Albumin Ligands for PSMA Targeting?
Authors: Steve S. Huang, Warren D.W. Heston
Journal: Theranostics (2017)

Prostate Specific Membrane Antigen (PSMA) is strongly expressed in prostate cancer. Recently a number of low-molecular-weight inhibitors have demonstrated excellent PSMA targeting activity for both imaging as well as Lutecium-177 radiotherapy in human trials. The paper by Choy et al raises the question of whether we can further increase the effectiveness of PSMA targeted therapy by adding an albumin-binding entity to low-molecular-weight agents.
IgA pemphigus: lumping or splitting?
Authors: S. Geller, E. Sprecher
Journal: British Journal of Dermatology (2017)

Unlike the progress that has been achieved in understanding the complex molecular basis of pemphigus vulgaris (PV)1, the pathogenesis of IgA pemphigus (IGAP) remains elusive. Hashimoto et al.2 described 49 IGAP cases and their immuno-phenotype based on extensive laboratory workup. In their study, only one patient was found to have multiple myeloma and none had concomitant solid malignancies, which may bear implications regarding optimal workup in IGAP.

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De Novo Coding Variants Are Strongly Associated with Tourette Disorder
Authors: A. Jeremy Willsey, Thomas V. Fernandez, Dongmei Yu, Robert A. King, Andrea Dietrich, Jinchuan Xing, Stephan J. Sanders, Jeffrey D. Mandell, Alden Y. Huang, Petra Richer, Louw Smith, Shan Dong, Kaitlin E. Samocha, Benjamin M. Neale, Giovanni Coppola, Carol A. Mathews, Jay A. Tischfield, Jeremiah M. Scharf, Matthew W. State, Gary A. Heiman, Mohamed Abdulkadir, Julia Bohnenpoll, Yana Bromberg, Lawrence W. Brown, Keun-Ah Cheon, Barbara J. Coffey, Li Deng, Andrea Dietrich, Shan Dong, Lonneke Elzerman, Thomas V. Fernandez, Odette Fründt, Blanca Garcia-Delgar, Erika Gedvilaite, Donald L. Gilbert, Dorothy E. Grice, Julie Hagstrøm, Tammy Hedderly, Gary A. Heiman, Isobel Heyman, Pieter J. Hoekstra, Hyun Ju Hong, Chaim Huyser, Laura Ibanez-Gomez, Young Key Kim, Young-Shin Kim, Robert A. King, Yun-Joo Koh, Sodahm Kook, Samuel Kuperman, Andreas Lamerz, Bennett Leventhal, Andrea G. Ludolph, Claudia Lühr da Silva, Marcos Madruga-Garrido, Jeffrey D. Mandell, Athanasios Maras, Pablo Mir, Astrid Morer, Alexander Münchau, Tara L. Murphy, Cara Nasello, Thaïra J.C. Openneer, Kerstin J. Plessen, Petra Richer, Veit Roessner, Stephan Sanders, Eun-Young Shin, Deborah A. Sival, Louw Smith, Dong-Ho Song, Jungeun Song, Matthew W. State, Anne Marie Stolte, Nawei Sun, Jay A. Tischfield, Jennifer Tübing, Frank Visscher, Michael F. Walker, Sina Wanderer, Shuoguo Wang, A. Jeremy Willsey, Martin Woods, Jinchuan Xing, Yeting Zhang, Anbo Zhou, Samuel H. Zinner, Cathy L. Barr, James R. Batterson, Cheston Berlin, Ruth D. Bruun, Cathy L. Budman, Danielle C. Cath, Sylvain Chouinard, Giovanni Coppola, Nancy J. Cox, Sabrina Darrow, Lea K. Davis, Yves Dion, Nelson B. Freimer, Marco A. Grados, Matthew E. Hirschtritt, Alden Y. Huang, Cornelia Illmann, Robert A. King, Roger Kurlan, James F. Leckman, Gholson J. Lyon, Irene A. Malaty, Carol A. Mathews, William M. MaMahon, Benjamin M. Neale, Michael S. Okun, Lisa Osiecki, David L. Pauls, Danielle Posthuma, Vasily Ramensky, Mary M. Robertson, Guy A. Rouleau, Paul Sandor, Jeremiah M. Scharf, Harvey S. Singer, Jan Smit, Jae-Hoon Sul, Dongmei Yu
Journal: Neuron (2017)
Updating the diagnosis, classification and assessment of rosacea by effacement of subtypes
Authors: J. Wilkin
Journal: British Journal of Dermatology (2017)

Tan, et al.,(ROSCO) propose to “transition beyond a subtype classification”, which they ascribe to the National Rosacea Society's Classification of Rosacea (NRSCOR), asserting “Subtype classification may not fully cover the range of clinical presentations and is likely to confound severity assessment, whereas a phenotype-based approach could improve patient outcomes by addressing an individual patient's clinical presentation and concerns”(1). NRSCOR did not invent the phenotypic subtypes, described by expert dermatologists over preceding decades, but sought a common terminology for use in communicating ideas about rosacea (compare use in Fig. 1 by ROSCO). NRSCOR emphasized the potential evolution from one phenotypic subtype to another, and that phenotypic subtypes can occur together. ROSCO's claimed ‘phenotypic approach’ seems to be simply the elimination of these phenotypic subtypes.

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Mule Spinners Cancer: Epithelioma of the Skin in Cotton Spinners
Journal: JAMA (1942)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Autocrine activation of the IFN signaling pathway may promote immune escape in glioblastoma
Authors: Manuela Silginer, Sara Nagy, Caroline Happold, Hannah Schneider, Michael Weller, Patrick Roth
Journal: Neuro-Oncology (2017)

Interferons (IFNs) are cytokines typically induced upon viral infection but are constitutively expressed also in the absence of acute infection. The physiological role of autocrine and paracrine IFN signaling, however, remains poorly understood, and its function in glioblastoma has not been explored in depth. Using RNA interference-mediated gene silencing, we characterized constitutive type I IFN signaling and its role in human glioma cells. We observed constitutive expression of phosphorylated signal transducer and activator of transcription 1 (pSTAT1) and myxovirus resistance protein A (MxA), a classical IFN-response marker, in the absence of exogenous IFN-β. In vivo, we found higher MxA expression in gliomas than in normal tissue, suggesting that IFN signaling is constitutively active in these tumors. To demonstrate the presence of an autocrine type I IFN signaling loop in glioma cells in vitro, we first confirmed the expression of the type I alpha/beta receptor (IFNAR)1/2, and its ligands, IFN-α and IFN-β. Small interfering RNA–mediated receptor gene silencing resulted in reduced expression of MxA at mRNA and protein levels, as did gene silencing of the ligands, corroborating the hypothesis of an autocrine signaling loop in which type I IFNs induce intracellular signaling through IFNAR1/2. On a functional level, following IFNAR1 or IFNAR2 gene silencing, we observed reduced programmed death ligand 1 (PD-L1) and major histocompatibility complex (MHC) class I and II expression as well as an enhanced susceptibility to natural killer immune cell lysis, suggesting that autocrine IFN signaling contributes to the immune evasion of glioma cells. Our findings point to an important role of constitutive IFN signaling in glioma cells by modulating their interaction with the microenvironment.
Next-Generation CDK2/9 Inhibitors and Anaphase Catastrophe in Lung Cancer
Authors: Masanori Kawakami, Lisa Maria Mustachio, Jaime Rodriguez-Canales, Barbara Mino, Jason Roszik, Pan Tong, Jing Wang, J. Jack Lee, Ja Hye Myung, John V. Heymach, Faye M. Johnson, Seungpyo Hong, Lin Zheng, Shanhu Hu, Pamela Andrea Villalobos, Carmen Behrens, Ignacio Wistuba, Sarah Freemantle, Xi Liu, Ethan Dmitrovsky
Journal: JNCI Journal of the National Cancer Institute (2016)

The first generation CDK2/7/9 inhibitor seliciclib (CYC202) causes multipolar anaphase and apoptosis in lung cancer cells with supernumerary centrosomes (known as anaphase catastrophe). We investigated a new and potent CDK2/9 inhibitor, CCT68127 (Cyclacel).CCT68127 was studied in lung cancer cells (three murine and five human) and control murine pulmonary epithelial and human immortalized bronchial epithelial cells. Robotic CCT68127 cell-based proliferation screens were used. Cells undergoing multipolar anaphase and inhibited centrosome clustering were scored. Reverse phase protein arrays (RPPAs) assessed CCT68127 effects on signaling pathways. The function of PEA15, a growth regulator highlighted by RPPAs, was analyzed. Syngeneic murine lung cancer xenografts (n = 4/group) determined CCT68127 effects on tumorigenicity and circulating tumor cell levels. All statistical tests were two-sided.CCT68127 inhibited growth up to 88.5% (SD = 6.4%, P < .003) at 1 μM, induced apoptosis up to 42.6% (SD = 5.5%, P < .001) at 2 μM, and caused G1 or G2/M arrest in lung cancer cells with minimal effects on control cells (growth inhibition at 1 μM: 10.6%, SD = 3.6%, P = .32; apoptosis at 2 μM: 8.2%, SD = 1.0%, P = .22). A robotic screen found that lung cancer cells with KRAS mutation were particularly sensitive to CCT68127 ( P = .02 for IC 50 ). CCT68127 inhibited supernumerary centrosome clustering and caused anaphase catastrophe by 14.1% (SD = 3.6%, P < .009 at 1 μM). CCT68127 reduced PEA15 phosphorylation by 70% (SD = 3.0%, P = .003). The gain of PEA15 expression antagonized and its loss enhanced CCT68127-mediated growth inhibition. CCT68127 reduced lung cancer growth in vivo ( P < .001) and circulating tumor cells ( P = .004). Findings were confirmed with another CDK2/9 inhibitor, CYC065.Next-generation CDK2/9 inhibition elicits marked antineoplastic effects in lung cancer via anaphase catastrophe and reduced PEA15 phosphorylation.