tbuckley/cabot-search huggingface dataset:
Abstract OT2-07-11: Ixazomib in combination with carboplatin in pretreated women with advanced triple negative breast cancer, a phase I/II trial (AGMT MBC-10 trial)
Authors: G Rinnerthaler, SP Gampenrieder, A Petzer, R Pusch, M Fridrik, D Rossmann, M Balic, D Egle, H Rumpold, C Singer, R Bartsch, T Melchardt, H Ulmer, B Mlineritsch, R Greil
Journal: Cancer Research (2018)

Abstract Background: Triple-negative breast cancer (TNBC) comprises a heterogeneous group of diseases which are generally associated with a poor prognosis. Up to now, no targeted treatment beyond anti-VEGF therapy is approved for TNBC so far and cytotoxic agents are the mainstay for the treatment of advanced tumor stages. Ixazomib is a selective, and reversible inhibitor of the proteasome, which has been mainly investigated in the treatment of multiple myeloma. In a preclinical study triple-negative breast cancer cells were treated with bortezomib, a first generation proteaseome inhibitor, alone and in combination with cisplatin, which had a synergistic effect. Clinical data are available for carboplatin plus bortezomib in metastatic ovarian and lung cancers showing remarkable antitumor activity and good tolerability. Based on this rational, the MBC-10 trial will evaluate the toxicity profile and efficacy of ixazomib in combination with carboplatin in patients with advanced TNBC. Trial Design: Patients with metastatic TNBC pretreated with at least one prior line of chemotherapy for advanced disease with a confirmed disease progression and measurable disease are eligible for this study. Patients will receive ixazomib in combination with carboplatin on days 1, 8, and 15 in a 28-day cycle. The phase I part of this study uses an alternate dose escalation accelerated titration design. After establishing the maximum tolerated dose (MTD), accrual continues to evaluate the efficacy and safety of the combination (phase II, including 41 evaluable patients). All patients will continue on study drugs until disease progression, unacceptable toxicity or discontinuation for any other reason. Primary endpoint of the phase II is overall response rate, secondary endpoints include safety profile, progression-free survival and quality of life. This trial is open for patient enrollment since November 2016 in six Austrian cancer centers. Accrual is planned to be completed within two years. ClinicalTrials.gov Identifier: NCT02993094 Citation Format: Rinnerthaler G, Gampenrieder SP, Petzer A, Pusch R, Fridrik M, Rossmann D, Balic M, Egle D, Rumpold H, Singer C, Bartsch R, Melchardt T, Ulmer H, Mlineritsch B, Greil R. Ixazomib in combination with carboplatin in pretreated women with advanced triple negative breast cancer, a phase I/II trial (AGMT MBC-10 trial) [abstract]. In: Proceedings of the 2017 San Antonio Breast Cancer Symposium; 2017 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2018;78(4 Suppl):Abstract nr OT2-07-11.
The Propaganda for Reform
Journal: JAMA (1924)

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Sir James McGrigor (1771-1858). British army surgeon
Journal: JAMA (1970)

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The Cover
Journal: JAMA (1986)

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Die Embolie
Journal: JAMA (1934)

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Commentary
Journal: JAMA (1967)

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Long-term ethanol consumption alters the hepatic response to the regenerative effects of tumor necrosis factor-α
Authors: P Akerman
Journal: Hepatology (1993)

The pathogenesis of chronic alcoholic liver disease is uncertain, but it may reflect an impaired wound healing response to ethanol-induced liver injury. Cellto-cell communication such as that mediated by the cytokine tumor necrosis factor is necessary for successful liver regeneration and complete recovery from liver injury. Hence disruption of intercellular regenerative signaling may contribute to the pathogenesis of chronic alcoholic liver disease. To test this hypothesis, the cytokine and regenerative responses triggered by partial hepatectomy were compared in ethanol-fed rats and isocalorically maintained, pair-fed controls. To further clarify the effect of ethanol on tumor necrosis factor–modulated regenerative effects, we evaluated some of the rats in each feeding group after pretreatment with antibodies to tumor necrosis factor. As expected, ethanol inhibited DNA synthesis and liver cell proliferation after partial hepatectomy. Ethanolassociated inhibition of liver regeneration occurred despite apparently similar serum concentrations of the tumor necrosis factor–inducible cytokine interleukin-6. Treatment with antibodies to tumor necrosis factor 1 hr before partial hepatectomy inhibited post–partial hepatectomy induction of interleukin-6 and liver regeneration in ethanol-fed and pair-fed rats. However, serum interleukin-6 was reduced more in ethanol-fed rats than in control rats (93% vs. 66%; p < 0.05). Antibodies to tumor necrosis factor also inhibited hepatic DNA synthesis more in ethanol-fed rats than in controls (85% vs. 50%; p < 0.05). In ethanol-fed rats, the increased effect of tumor necrosis factor antibody on post–partial hepatectomy DNA synthesis suggests heightened sensitivity of hepatocytes to tumor necrosis factor. Tumor necrosis factor antibody decreased hepatocyte proliferation more (93%) in ethanol-fed rats than in controls (62%) (p < 0.05). In contrast, proliferation of liver nonparenchymal cells was less inhibited in ethanol-fed rats(11%) than in controls (66%) (p <0.05). These data indicate that long-term ethanol feeding alters cell responsiveness to tumor necrosis factor during liver regeneration. Such ethanol-induced alterations in cell response to cytokines may disrupt intercellular communications and impede normal liver regeneration. (HEPATOLOGY 1993;17:1066–1073).
Military Medicine, Washington
Journal: JAMA (1966)

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Incorrect Data.
Journal: JAMA (1996)

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Molecular Approaches To Analysis Of X-Linked Immunodeficiencies
Authors: M. Conley
Journal: Annual Review of Immunology (1992)

Although the X-linked immunodeficiencies—X-linked agammaglobulinemia (XLA), X-linked severe combined immunodeficiency (XSCID), Wiskott-Aldrich syndrome (WAS), X-linked lymphoproliferative syndrome and X-linked hyper IgM syndrome—have been mapped to loci distributed throughout the X chromosome, they have several features in common that suggest that they might be members of a gene family: (i) all are maintained in the population at approximately the same gene frequency; (ii) expression of each defect is limited to the hematopoieticsy stem; (iii) atypical forms of each disorder have been described; and (iv) obligate carriers of these disorders are normal by all immunologic criteria. The failure of carriers of XLA, XSCID, and WAS to show signs of their gene defects can be explained by the preferential use of the normal, nonmutant X as the active X in the cell lineages affected by the gene defects. These three disorders also share an additional feature; in boys with XLAX, SCID, or WAS there is asynchronous expression of cell surface markers of differentiation or activation. If some or all of the genes that are abnormal in the X-linked immunodeficiencies are members of a gene family, then isolation of one gene may lead to the others.
Incorrect Reference.
Journal: JAMA (1996)

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Anesthesia and Analgesia: Current Researches, Cleveland
Journal: JAMA (1962)

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Toxic Insecticides
Authors: F. D. T. Good
Journal: BMJ (1965)

be taken into the operating-theatre."Only sterile blankets should be used for this pur- pose, and we should not be prevented from using polypropylene because of an imaginary danger from static electricity.If a danger does exist polypropylene blankets appear to carry very little static and they could easily have woven into them (if the makers are told this is essential) an anti-static thread.We firmly believe that cross-infection must be fought on every front even if the effect in some cases is hard to demonstrate.We have no doubt that it will be worth while converting all our hospital linen to these autoclavable materials.Polypropylene has many uses in hospitals, and these fibres may prove to be the most advantageous of all.-Weare, etc.,
Triflupromazine Hydrochloride in Pediatric Premedication for Tonsillectomies
Journal: JAMA (1963)

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Predicting overall survival (OS) in patients (pts) with metastatic colorectal cancer (mCRC) treated with chemotherapy (CT): The British Columbia Cancer Agency (BCCA) mCRC score.
Authors: Gillian Gresham, Winson Y. Cheung, Matthew Chan, Jason Kim, Daniel John Renouf
Journal: Journal of Clinical Oncology (2013)

419 Background: Median OS of mCRC is 2 years, but the prognosis of individual pts can be highly variable. Our study objective was to develop a scoring system to improve the prognostication of mCRC pts at baseline assessment. Methods: Pts diagnosed with mCRC from 2006 to 2008, referred to 1 of 5 regional cancer centers in British Columbia, and received CT were reviewed. Pts with ECOG &gt;3 were excluded due to their uniform poor prognosis. Univariate analyses were performed on baseline variables and those significantly associated with prognosis were included in a multivariate stepwise selection. Each significant factor was given a weighted score (range 1-5) based on the regression coefficients. Patients were assigned a composite risk score (range 0-15) based on their baseline variables, and then separated into quartiles for OS using cut-point analysis and Kaplan-Meier methods. Validation was conducted with the bootstrap technique. C-index statistic was 0.75, which indicated good discrimination. Results: A total of 505 mCRC pts were included: median age 63 (range 22-86), 58% male, 75% ECOG 0-1, 58% colon primary, 34% &gt;1 metastatic site, and 46% smokers. Median pre-treatment CEA was 16.8 ng/ml. In this cohort, 64% were metastatic at presentation, 81% underwent primary tumor resection, 23% received prior adjuvant CT, and 72% were treated with palliative CT. ECOG 2-3 (HR 3.1, 95%CI 2.4-4.2), no primary resection (HR 2.3, 95%CI 1.6-3.3), colon primary (HR 1.6, 95%CI 1.2-2.1), &gt;1 metastatic site (HR 1.6, 95%CI 1.2-2.1), CEA level &gt;4 ng/ml (HR 1.2, 0.8-1.6), male (HR 1.2, 95%CI 0.8-1.6), and smoker (HR 1.4, 95%CI 1.0-1.8) were significant in the multivariate model and assigned points corresponding to their effect size. Median OS varied significantly depending on the composite risk score (Table). Conclusions: In this population-based analysis, the BCCA mCRC score was a simple method that used baseline variables to improve the prognostication of mCRC pts. This model requires external validation. [Table: see text]
IRRADIATED ANTIVIRAL VACCINES
Journal: JAMA (1941)

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