POISON’s RIKKI ROCKETT Didn’t Want To Lose His Tongue In Cancer Battle – BLABBERMOUTH.NET

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BLABBERMOUTH.NET
POISON’s RIKKI ROCKETT Didn’t Want To Lose His Tongue In Cancer Battle
BLABBERMOUTH.NET
Rikki Rockett and Dr. Ezra Cohen, associate director and professor of medicine at Moores Cancer Center at UC San Diego, were interviewed by San Diego’s Fox 5 shortly after the POISON drummer was declared cancer free after undergoing an experimental …

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POISON’s RIKKI ROCKETT Didn’t Want To Lose His Tongue In Cancer Battle – BLABBERMOUTH.NET

Stephen Sinnott-Clarke interview: ‘Raising awareness literally saves lives; it’s why I’m still here today’ – The Independent

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The Independent
Stephen Sinnott-Clarke interview: ‘Raising awareness literally saves lives; it’s why I’m still here today’
The Independent
Not only did I have no immune system but I was ill and I had cancer. I was on morphine for 24 hours a day because of the high dose chemo. I caught shingles, I had ulcers inside my tongue, down my throat, in my stomach and clots were forming because my …

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Stephen Sinnott-Clarke interview: ‘Raising awareness literally saves lives; it’s why I’m still here today’ – The Independent

First-line sunitinib versus pazopanib in metastatic renal cell carcinoma: Results from the International Metastatic Renal Cell Carcinoma Database Consortium

Publication date: September 2016
Source:European Journal of Cancer, Volume 65
Author(s): Jose Manuel Ruiz-Morales, Marcin Swierkowski, J. Connor Wells, Anna Paola Fraccon, Felice Pasini, Frede Donskov, Georg A. Bjarnason, Jae-Lyun Lee, Hao-Wen Sim, Andrzej Sliwczynsk, Aneta Ptak-Chmielewska, Zbigniew Teter, Benoit Beuselinck, Lori A. Wood, Takeshi Yuasa, Carmel Pezaro, Brian I. Rini, Cezary Szczylik, Toni K. Choueiri, Daniel Y.C. Heng
BackgroundSunitinib (SU) and pazopanib (PZ) are standards of care for first-line treatment of metastatic renal cell carcinoma (mRCC). However, how the efficacy of these drugs translates into effectiveness on a population-based level is unknown.Patients and methodsWe used the International mRCC Database Consortium (IMDC) to assess overall survival (OS), progression-free survival (PFS), response rate (RR) and performed proportional hazard regression adjusting for IMDC prognostic groups. Second-line OS (OS2) and second-line PFS (PFS2) were also evaluated.ResultsWe obtained data from 7438 patients with mRCC treated with either first-line SU (n = 6519) or PZ (n = 919) with an overall median follow-up of 40.4 months (95% confidence interval [CI] 39.2–42.1). There were no significant differences in IMDC prognostic groups (p = 0.36). There was no OS difference between SU and PZ (22.3 versus 22.6 months, respectively, p = 0.65). When adjusted for IMDC criteria, the hazard ratio (HR) of death for PZ versus SU was 1.03 (95% CI 0.92–1.17, p = 0.58). There was no PFS difference between SU and PZ (8.4 versus 8.3 months, respectively, p = 0.17). When adjusted for IMDC criteria, the HR for PFS for PZ versus SU was 1.08 (95% CI 0.981–1.19, p = 0.12). There was no difference in RR between SU and PZ (30% versus 28%, respectively, p = 0.15). We also found no difference in any second-line treatment between either post-SU or post-PZ groups for OS2 (13.1 versus 11 months, p = 0.27) and PFS2 (3.7 versus 5.0 months, p = 0.07).ConclusionsWe confirmed in real-world practice that SU and PZ have similar efficacy in the first-line setting for mRCC and do not affect outcomes with subsequent second-line treatment.

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First-line sunitinib versus pazopanib in metastatic renal cell carcinoma: Results from the International Metastatic Renal Cell Carcinoma Database Consortium

Different expression levels of glycans on leukemic cells—a novel screening method with molecularly imprin ted polymers (MIP) targeting sialic acid

Abstract

Sialic acid (SA) is normally expressed on the cell membranes and is located at the terminal position of the sugar chains. SA plays an important role for regulation of the innate immunity, function as markers of the cells and can be recognized by a variety of receptors. Interestingly, the level of SA expression is increased on metastatic cancer cells. The availability of specific antibodies against SA is limited and, therefore, biomarker tools for detection of SA are lacking. We have recently presented a novel method for specific fluorescence labeling of SA molecular imprinted polymers (MIP). Here, we have performed an extended screening of SA expression by using SA-MIP and included four different chronic lymphocytic leukemia (CLL) cell lines, conveniently analyzed by flow cytometry and fluorescence microscopy. SA expression was detected in four cell lines at different levels, and the SA expression were verified with lectin-FITC. These results show that SA-MIP can be used as a plastic antibody for detection of SA using both flow cytometry and fluorescence microscopy. We suggest that SA-MIP can be used for screening of different tumor cells of various stages, including CLL cells.

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Different expression levels of glycans on leukemic cells—a novel screening method with molecularly imprin ted polymers (MIP) targeting sialic acid

A guide for the analysis of long-term population growth in cancer

Abstract

Although cancer is a chronic disease, most of the in vitro experiments to assess the effectiveness of intervention are performed in hours or a few days. Moreover, none of the available methodologies to measure cell proliferation are adapted to provide information about the growth kinetic during and after treatment. Thus, the objective of this work is to provide a guide to assess long-term changes in cell population size to be used mainly in cancer research. Cumulative population doubling (CPD) graphs based on cell counting for in vitro or tumor volume for in vivo assays were used to calculate four parameters: relative end CPD (RendCPD), to quantify the end point analysis of proliferation; relative area under curve (rAUC), to describe the global chronic effect of a treatment; relative time to cross a threshold (RTCT), to indicate the delay in cell population recovery produced by a treatment; and relative proliferation rate (RPR), to describe the relative regrowth velocity of the cells that survived after treatment. These parameters describe not only the acute and chronic effects of a treatment but also the behavior of cells that are not eliminated by the treatment, providing crucial information about the growth kinetic of the surviving population. Moreover, the proposed analysis allowed the grouping of independent CPD experiments quantified at different time points and even the direct comparison of in vitro and in vivo experiments. Therefore, this new way to analyze long-term outcomes provides a global view of the effectiveness of an intervention, as an important tool for long-term studies.

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A guide for the analysis of long-term population growth in cancer

miRNA-451 inhibits glioma cell proliferation and invasion by downregulating glucose transporter 1

Abstract

MicroRNAs play an important role in tumor development and progression. Tumor growth is closely associated with glucose metabolism. Specifically, tumor cells produce energy (ATP) under aerobic and anaerobic conditions through glycolysis and metabolites, such as lactic acid and ATP, as a result of the Warburg effect. However, the transport of glucose into cells depends on protein transporters in the cell membrane. Therefore, this area has recently become a topic of interest for research on targeted cancer therapy. We found that miRNA-451 inhibits the phosphatidylinositol-3 kinase (PI3K)/Akt signaling pathway to modify the biological behavior of glioma cells. Inhibiting the PI3K/Akt pathway may prevent glucose-addicted cancer cells from performing glycolysis. Akt directly affects glycolysis by regulating the localization of the glucose transporter 1 (GLUT1). However, how miRNA-451 regulates glucose transporters on the cell membrane and affects the regulatory mechanisms of glucose metabolism in glioma cells remains unclear. Consequently, we predict and verify related gene protein interactions. By targeting CAB 39, miRNA-451 likely triggers the LKB1/AMPK/PI3K/AKT pathway, which regulates GLUT1, to inhibit the glucose metabolism of, reduce the energy supply to, and inhibit the proliferation and invasion of glioma cells. Our results suggest a new direction for the treatment of glioma.

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miRNA-451 inhibits glioma cell proliferation and invasion by downregulating glucose transporter 1