Role of AMPK and its molecular intermediates in subjugating cancer survival mechanism

Life Sciences ◽  
2019 ◽  
Vol 227 ◽  
pp. 30-38 ◽  
Author(s):  
Anand Thirupathi ◽  
Yan-Zhong Chang
Placenta ◽  
2017 ◽  
Vol 57 ◽  
pp. 278-279
Author(s):  
Martina Hutabarat ◽  
Noroyono Wibowo ◽  
Berthold Huppertz
Keyword(s):  

2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
A Ostorero ◽  
A Gili ◽  
S Violi ◽  
F Stracci

Abstract Background Lung cancer is the second most common cancer worldwide and the leading cause of death for cancer (18.4%). During the last 30 years, lung cancer incidence and mortality increased in women and decreased in men, because of tobacco smoking exposure. Population survival trend reflects both the influence of disease severity at diagnosis and treatment effectiveness. Some studies reported an increase in global lung cancer survival and linked it to new treatment options. However, change in the overall survival may also reflect a shift towards morphologies with more favorable prognosis. We analyzed overall and morphology specific survival trends for lung cancer to gain insight on the role of new treatments and changing exposures. Methods We analyzed lung cancer 1 y-survival and 3 y-survival after diagnosis in Umbria (890'000 inhabitants) in the period 1994-2016. Population-based data were obtained from the Umbrian Cancer Registry (RTUP), Italy. We estimated relative net survival (Pohar-Perme approach) stratified both for sex and histotype (NSCLC, SCLC, NOS), considering six diagnostic periods from 1994 to 2016 (4 years for period, except 3 in the last one) for 5'268 lung cancer cases (26% women). Results Overall survival by gender resulted 40,5% (1y) and 16.5% (3y) in men, 47,3% (1y) and 23,2% (3y) in women. NSCLC survival increased in women during the period 1994-2016 from 41% to 53% (1y) and from 23% to 33% (3y), and remained unchanged in men. SCLC 3 year-survival did not change significantly neither in women nor in men. Conclusions We did not observe a significant increase in lung cancer survival over a 25 years period. We observed a significant increase in survival probabilities for NSCLC among women only. Thus, our data don't confirm a major role of new treatments in improving lung cancer control. We will provide further analyses for adenocarcinoma and a comparison of incidence and mortality trends to understand the influence of exposures and treatments on survival. Key messages A general increase in lung cancer survival, as could be expected after the introduction of new highly effective treatments is not present in western countries. Reducing exposure to tobacco smoking and environmental pollution remain the main intervention to improve lung cancer control.


PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e87610 ◽  
Author(s):  
Jan Blancato ◽  
Ashley Graves ◽  
Banafsheh Rashidi ◽  
Maria Moroni ◽  
Leopold Tchobe ◽  
...  

2019 ◽  
Vol 20 (6) ◽  
pp. 1486 ◽  
Author(s):  
Miguel Carracedo ◽  
Oscar Persson ◽  
Peter Saliba-Gustafsson ◽  
Gonzalo Artiach ◽  
Ewa Ehrenborg ◽  
...  

Autophagy serves as a cell survival mechanism which becomes dysregulated under pathological conditions and aging. Aortic valve thickening and calcification causing left ventricular outflow obstruction is known as calcific aortic valve stenosis (CAVS). CAVS is a chronic and progressive disease which increases in incidence and severity with age. Currently, no medical treatment exists for CAVS, and the role of autophagy in the disease remains largely unexplored. To further understand the role of autophagy in the progression of CAVS, we analyzed expression of key autophagy genes in healthy, thickened, and calcified valve tissue from 55 patients, and compared them with nine patients without significant CAVS, undergoing surgery for aortic regurgitation (AR). This revealed a upregulation in autophagy exclusively in the calcified tissue of CAVS patients. This difference in autophagy between CAVS and AR was explored by LC3 lipidation in valvular interstitial cells (VICs), revealing an upregulation in autophagic flux in CAVS patients. Inhibition of autophagy by bafilomycin-A1 led to a decrease in VIC survival. Finally, treatment of VICs with high phosphate led to an increase in autophagic activity. In conclusion, our data suggests that autophagy is upregulated in the calcified tissue of CAVS, serving as a compensatory and pro-survival mechanism.


2000 ◽  
Vol 64 (2) ◽  
pp. 157-163 ◽  
Author(s):  
Shine Chang ◽  
Julie R. Alderfer ◽  
Lina Asmar ◽  
Aman U. Buzdar

BMC Cancer ◽  
2012 ◽  
Vol 12 (1) ◽  
Author(s):  
Kate M Peters ◽  
Stacey L Edwards ◽  
Shalima S Nair ◽  
Juliet D French ◽  
Peter J Bailey ◽  
...  

Lung Cancer ◽  
1999 ◽  
Vol 25 ◽  
pp. S14
Author(s):  
P. Yang ◽  
A. Yokomizo ◽  
R. Marks ◽  
T. Lesnick ◽  
J. Sloan ◽  
...  

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