The objective of this study was to examine the source of advanced cancer patients’ information about their prognosis and determine whether this source of information could explain racial disparities in the accuracy of patients’ life expectancy estimates (LEEs).
Coping With Cancer was a prospective, longitudinal, multisite study of terminally ill cancer patients followed until death. In structured interviews, patients reported their LEEs and the sources of these estimates (ie, medical providers, personal beliefs, religious beliefs, and other). The accuracy of LEEs was calculated through a comparison of patients’ self-reported LEEs with their actual survival.
The sample for this analysis included 229 patients: 31 black patients and 198 white patients. Only 39.30% of the patients estimated their life expectancy within 12 months of their actual survival. Black patients were more likely to have an inaccurate LEE than white patients. A minority of the sample (18.3%) reported that a medical provider was the source of their LEEs; none of the black patients (0%) based their LEEs on a medical provider. Black race remained a significant predictor of an inaccurate LEE, even after the analysis had been controlled for sociodemographic characteristics and the source of LEEs.
The majority of advanced cancer patients have an inaccurate understanding of their life expectancy. Black patients with advanced cancer are more likely to have an inaccurate LEE than white patients. Medical providers are not the source of information for LEEs for most advanced cancer patients and especially for black patients. The source of LEEs does not explain racial differences in LEE accuracy. Additional research into the mechanisms underlying racial differences in prognostic understanding is needed. Cancer 2016;000:000-000. © 2016 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
© 2016 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society.

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The present global, open-label, single-arm, multicenter, phase IIb study was designed to determine the efficacy and tolerability of oral vorinostat combined with standard doses of bortezomib in patients with multiple myeloma considered refractory to novel myeloma agents.
Eligible patients were age ≥ 18 years, had received ≥ 2 previous regimens, had disease refractory to ≥ 1 previous bortezomib-containing regimen, and had received ≥ 1 dose of an immunomodulatory drug (thalidomide or lenalidomide)-based regimen. The patients received 21-day cycles of bortezomib (1.3 mg/m(2) intravenously on days 1, 4, 8, and 11) plus oral vorinostat (400 mg/d on days 1-14). Oral dexamethasone, 20 mg, on the day of and the day after each dose of bortezomib could be added for patients with progressive disease after 2 cycles or no change after 4 cycles. The primary endpoint was the objective response rate.
The objective response rate was 11.3% (95% confidence interval, 6.6%-17.7%), and the median duration of response was 211 days (range, 64-550 days). The median overall survival duration was 11.2 months (95% confidence interval, 8.5-14.4 months), with a 2-year survival rate of 32%. The frequently reported adverse events were thrombocytopenia (69.7%), nausea (57.0%), diarrhea (53.5%), anemia (52.1%), and fatigue (48.6%); the overall safety profile was consistent with that of bortezomib and vorinostat.
The combination of vorinostat and bortezomib is active in patients with multiple myeloma refractory to novel treatment modalities and offers a new therapeutic option for this difficult-to-treat patient population (ClinicalTrials.gov identifier, NCT00773838).
Copyright © 2016 Elsevier Inc. All rights reserved.

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Inflammation is a response of body tissues to injury and infection. Compounds that can inhibit inflammation have been shown to have potential therapeutic clinical application. Gambogenic acid (GEA) has potent antitumor and anti-inflammatory activities. Herein, the molecular mechanisms of GEA’s anti-inflammatory effect were investigated in lipopolysaccharide (LPS)-stimulated macrophage cells. The results showed that pretreatment with GEA could markedly inhibit interleukin (IL)-1α, IL-1β, tumor necrosis factor-α, IFN-β, IL-12b, and IL-23a production in a dose-dependent manner in LPS-induced model. Furthermore, this drug significantly reduced the release of nitric oxide (NO), and impaired the protein level of inducible NO synthase and the cyclooxygenase 2. The finding also showed that the effect of GEA may be related to the suppression of the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathway. These results indicate that GEA could suppress LPS-simulated inflammatory response partially by attenuating NO synthesis and NF-κB and MAPK activation, suggesting that it may become a potent therapeutic agent for the treatment of inflammatory diseases.
© The Author 2016. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

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Transcriptional activation of telomerase reverse transcriptase (TERT) gene is a rate-limiting determinant in the reactivation of telomerase expression in cancers. TERT promoter mutations represent one of the fundamental mechanisms of TERT reactivation in cancer development. We review recent studies that elucidate the molecular mechanisms underscoring activation of mutant TERT promoters.

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On March 31, 2016 Celator Pharmaceuticals, Inc. (Nasdaq: CPXX) reported that data for VYXEOS (cytarabine:daunorubicin) Liposome for Injection (also known as CPX-351), its lead product candidate, will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in New Orleans, LA, April 16-20, 2016 (Press release, Celator Pharmaceuticals, MAR 31, 2016, View Source [SID:1234510229]).

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The research was conducted in the laboratory of Dr. Jeffrey Tyner at Oregon Health & Science University. The objective of the research was to examine the ex vivo sensitivity of acute myeloid leukemia (AML) cells derived from newly diagnosed patients to VYXEOS. This work supports the observed clinical benefit of VYXEOS in high-risk AML patients and may provide a means of identifying patient genotypes/phenotypes most sensitive to VYXEOS.

"We continue to learn more about the unique activity of VYXEOS in AML and enhance our ability to match this performance with specific patient characteristics that could be predictive of improved outcomes," said Lawrence Mayer, Ph.D., President and Chief Scientific Officer at Celator. "The research being undertaken by Dr. Tyner reflects Celator’s goal to elucidate the clinical benefits of VYXEOS by expanding our scientific understanding of its mechanism of action, particularly in AML cells with important molecular phenotypes."

Details on the AACR (Free AACR Whitepaper) poster presentation:

Presentation Title:
CPX-351 cytotoxicity against fresh AML blasts is increased for FLT3-ITD+ cells and correlates with drug uptake and clinical outcomes
Date/Time:
Sunday, April 17, 2016 – 1:00pm-5:00pm
Session Category:
Poster Presentation
Session Title:
ET01-03, Combination Chemotherapy
Location:
New Orleans Convention Center, Halls G-J Poster Section 15
Abstract Number:
287

The poster will be available on Celator’s website (www.celatorpharma.com) at the conclusion of the AACR (Free AACR Whitepaper) meeting.