Breast Cancer Multi-Therapy and Immune System Activation, Checkpoint Modulators, Signal Inhibitors and T Cells Reprogramming

Publish Year: 1398
نوع سند: مقاله کنفرانسی
زبان: English
View: 510

This Paper With 14 Page And PDF Format Ready To Download

  • Certificate
  • من نویسنده این مقاله هستم

این Paper در بخشهای موضوعی زیر دسته بندی شده است:

استخراج به نرم افزارهای پژوهشی:

لینک ثابت به این Paper:

شناسه ملی سند علمی:

CANCER01_010

تاریخ نمایه سازی: 11 آذر 1398

Abstract:

Cancer is one of the leading causes of death worldwide according to data from the U.S. National Cancer Institute, with approximately 14 million new cases and 8.2 million of cancer-related deaths in 2018. More than 60% of the new annual cases in the world occur in Africa, Asia, Central America, and South America, with 70% of cancer deaths in these regions. Recently they have been used for breast cancer, novel approaches among which several molecules that block signaling pathways and also reactivate the immune system by inhibiting the activities of two lymphocytes T receptor inhibitors; CTLA-4 and PD-1 in triple negative breast cancer. Although there is evidence, which supports the blocking of these inhibitory molecules, reactive the response of T cells does not always result, surely because in addition to need to reactivate the response Th1 is necessary co-activation of killer cells Natural (NK), the latter are the main actors of the anticancer response. Therefore, combining therapies with the coordinated activation of each cell of the immune response involved will probably produce better results. Through a better understanding of the interactions of the Th1 response and the action of the inhibitors of PD-1 and CTLA-4 and the intratumoral microenvironment, we believe that it would improve breast cancer therapy. In this article, recent advances in the treatment of cancer aimed at blocking signaling pathways and the use of monoclonal antibodies directed to receptors were reviewed. Likewise, it is proposed to combine therapies with antibodies that block PD-1 and CTLA-4 with the activation of the Th1 and NK response, in situ or with extracorporeal activation of autologous cells.

Authors

Miguel A Galván Morales

Dept. of Immunogenetics and Allergy. National Institute of Respiratory Diseases. Calzada de Tlalpan ۴۵۰۲, Colonia Sección XVI, Delegación Tlalpan, ۱۴۰۸۰, Mexico City.

Raúl Barrera Rodríguez

Dept. Chronic Degenerative Diseases, Lab. Autoimmunity. National Institute of Respiratory Diseases. Mexico City.

Julio R. Santiago Cruz

Laboratory of Autoimmunity, National Institute of Respiratory Diseases, Mexico. City, ۱۴۰۸۰. Department of Microbiology and Parasitology, Faculty of Medicine, National Autonomous University of México, México City.

Luis M Terán Juárez

Dept. of Immunogenetics and Allergy. National Institute of Respiratory Diseases, ۱۴۰۸۰, Mexico City,.