cancer

Authors and Affiliations:

Gouveia MJ^1,2, Pakharukova MY^3,4, Laha T^5,6,7, Sripa B^5,6,7, Maksimova GA³, Rinaldi G⁸, Brindley PJ⁸, Mordvinov VA^3,9, Amaro T¹⁰, Santos LL¹⁰, Costa JMCD^1,11, Vale N^2,12.

¹ Center for the Study in Animal Science, ICETA, University of Porto, Rua de D. Manuel II, Apt 55142, 4051-401 Porto, Portugal.

Autores e Afiliações:

Gouveia MJ^1,2, Pakharukova MY^3,4, Laha T^5,6,7, Sripa B^5,6,7, Maksimova GA³, Rinaldi G⁸, Brindley PJ⁸, Mordvinov VA^3,9, Amaro T¹⁰, Santos LL¹⁰, Costa JMCD^1,11, Vale N^2,12.

¹ Center for the Study in Animal Science, ICETA, University of Porto, Rua de D. Manuel II, Apt 55142, 4051-401 Porto, Portugal.

Cancer survival improvements in the north region of Portugal during the 2001-2010 were not universal for all cancer sites. A significant increase in net survival was observed for stomach, colon, pancreas, larynx, melanoma, breast, brain and central nervous system, thyroid, non-Hodgkin lymphoma and multiple myeloma. No significant changes in survival were found for gynaecological tumours neither for oesophagus, rectum, liver, prostate, kidney and bladder cancer.

Cancer multidrug resistance (MDR) is a major cause of therapeutic failure in cancer. MDR is mainly due to the overexpression of drug efflux pumps, such as P-glycoprotein (P-gp). Besides overexpression of drug efflux pumps, other molecular mechanisms are involved in the MDR phenotype, including metabolic alterations. Indeed, recent studies showed that it is possible to revert the MDR phenotype by inhibition of glycolysis with specific modulators.

De Rode Hoed’s Great Hall, Amsterdam, Netherlands

4 - 6 June 2018

See more informations here: http://www.eacr.org/conference/molecularpathology2018

De Rode Hoed’s Great Hall, Amsterdam, Netherlands

4 - 6 June 2018

See more informations here: http://www.eacr.org/conference/molecularpathology2018

Major alterations in cell glycosylation occurring during cancer development and progression represent key features of tumor cell malignant behavior. In this publication, the authors preview and put in context the findings of Agrawal et al. (Cancer Cell, Vol. 31, Issue 6, 2017) that identified and characterized a novel molecular mechanism in which aberrant glycosylation actively tunes the metastatic capacity of melanoma cells by preventing the proteolytic cleavage of the L1CAM adhesion molecule.

Authors and Affiliations:

Major alterations in cell glycosylation occurring during cancer development and progression represent key features of tumor cell malignant behavior. In this publication, the authors preview and put in context the findings of Agrawal et al. (Cancer Cell, Vol. 31, Issue 6, 2017) that identified and characterized a novel molecular mechanism in which aberrant glycosylation actively tunes the metastatic capacity of melanoma cells by preventing the proteolytic cleavage of the L1CAM adhesion molecule.

Autores e Afiliações:

BT Convention Centre, Liverpool, United Kingdom

05 - 08 November, 2017

See more informations here: http://conference.ncri.org.uk/?utm_source=EACR&utm_medium=Website%20listing&utm_campaign=EACR_NCRI2017