For researchers with little time and a lot of important content in the field to digest, Oncotarget will present unabridged audio versions of its key papers. While driving home from the lab, or pipetting, the key content of Oncotarget will be at a researcher's disposal.

Subscribers to the new podcast series will gain access to the journal's most important discoveries through full readings of published papers, interviews with outstanding authors, and selected readings from the Oncotarget blog. The podcast will highlight topics in oncology and beyond, including aging, pathology, immunology and microbiology, autophagy, chromosome, neuroscience, endocrinology, cardiology, metabolism, cell biology, pharmacology and more on Stitcher, Blubrry, and Soundcloud.

"Our mission has always been to make exceptional discoveries rapidly and widely available, eliminate borders between specialties by linking different fields of biomedical science and foster applications of basic and clinical science," said Mikhail Blagosklonny, Oncotarget's editor-in-chief. "This new podcast series will be another way to deliver people free access to the research published in this journal."

Audiopapers & Press releases

Audiopaper - Published in Volume 8 Issue 42 of Oncotarget - "A global comparison of the cost of patented cancer drugs in relation to global differences in wealth" by Daniel A. Goldstein from the Davidoff Cancer Center, Rabin Medical Center, Petach Tikvah, Israel and the Winship Cancer Institute, Emory University, Atlanta, GA, USA

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A global comparison of the cost of patented cancer drugs in relation to global differences in wealth

Full Text: bit.ly/2xufwZQ

Critically, our findings suggest for the first time that targeting BRAFWT/V600E and CDK4/6 represents a novel therapeutic strategy to treat vemurafenib-resistant or vemurafenib-naïve radioiodine-refractory BRAFWT/V600E-PTC. This combined therapy could prevent selection and expansion of aggressive PTC cell sub-clones with intrinsic resistance, targeting tumor cells either with primary or secondary resistance to BRAFV600E inhibitor.

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Combined therapy with vemurafenib and palbociclib

The Featured Cover Paper for the most recent issue of @Oncotarget -http://bit.ly/2yG5wlh

A Priority Research Paper by Pongas, et al. titled “PI3Kδ inhibition causes feedback activation of PI3Kα in the ABC subtype of diffuse large B-cell lymphoma”

The corresponding author is Dr. Louis M. Staudt from the Lymphoid Malignancies Branch of the National Cancer Institute at National Institutes of Health in Bethesda, MD, USA.

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PI3Kδ inhibition causes feedback activation of PI3Kα in the ABC subtype of diffuse large B-cell...

Title - Screening of cancer tissue arrays identifies CXCR4 on adrenocortical carcinoma: correlates with expression and quantification on metastases using 64Cu-plerixafor PET

Abstract - Expression of the chemokine receptor CXCR4 by many cancers correlates with aggressive clinical behavior. As part of the initial studies in a project whose goal was to quantify CXCR4 expression on cancers non-invasively, we examined CXCR4 expression in cancer samples by immunohistochemistry using a validated anti-CXCR4 antibody. Among solid tumors, we found expression of CXCR4 on significant percentages of major types of kidney, lung, and pancreatic adenocarcinomas, and, notably, on metastases of clear cell renal cell carcinoma and squamous cell carcinoma of the lung. We found particularly high expression of CXCR4 on adrenocortical cancer (ACC) metastases. Microarrays of ACC metastases revealed correlations between expression of CXCR4 and other chemokine system genes, particularly CXCR7/ACKR3, which encodes an atypical chemokine receptor that shares a ligand, CXCL12, with CXCR4. A first-in-human study using 64Cu-plerixafor for PET in an ACC patient prior to resection of metastases showed heterogeneity among metastatic nodules and good correlations among PET SUVs, CXCR4 staining, and CXCR4 mRNA. Additionally, we were able to show that CXCR4 expression correlated with the rates of growth of the pulmonary lesions in this patient. Further studies are needed to understand better the role of CXCR4 in ACC and whether targeting it may be beneficial. In this regard, non-invasive methods for assessing CXCR4 expression, such as PET using 64Cu-plerixafor, should be important investigative tools.

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Screening of cancer tissue arrays identifies CXCR4 on adrenocortical carcinoma

Full text - http://bit.ly/2mlYU6k

"ERβ inhibits cyclin dependent kinases 1 and 7 in triple negative breast cancer"

Abstract - Triple negative breast cancer (TNBC), which comprises approximately 15% of all primary breast cancer diagnoses, lacks estrogen receptor alpha, progesterone receptor and human epidermal growth factor receptor 2 expression. However, we, and others, have demonstrated that approximately 30% of TNBCs express estrogen receptor beta (ERβ), a nuclear hormone receptor and potential drug target. Treatment of ERβ expressing MDA-MB-231 cells with estrogen or the ERβ selective agonist, LY500307, was shown to result in suppression of cell proliferation. This inhibitory effect was due to blockade of cell cycle progression. In vivo, estrogen treatment significantly repressed the growth of ERβ expressing MDA-MB-231 cell line xenografts. Gene expression studies and ingenuity pathway analysis identified a network of ERβ down-regulated genes involved in cell cycle progression including CDK1, cyclin B and cyclin H. siRNA mediated knockdown or drug inhibition of CDK1 and CDK7 in TNBC cells resulted in substantial decreases in proliferation regardless of ERβ expression. These data suggest that the tumor suppressive effects of ERβ in TNBC result from inhibition of cell cycle progression, effects that are in part mediated by suppression of CDK1/7. Furthermore, these data indicate that blockade of CDK1/7 activity in TNBC may be of therapeutic benefit, an area of study that has yet to be explored.

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ERβ inhibits cyclin dependent kinases 1 and 7 in triple negative breast cancer

Full Text- http://bit.ly/2DnHaPQ

We, the scientists, should change the situation and change the policies of Indexes such as Clarivate's Web of Science, and Medline, and make indexes work for us. Otherwise, why should all of these organizations exist?

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Librarians Against Scientists: Oncotarget lesson

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

Librarians Against Scientists: Oncotarget lesson

Oncotarget Podcast