MHC Class I Antigens In Malignant Cells: Immune Escape And Response To Immunotherapy (2013) (SpringerBriefs in Cancer Research #1)

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Synopsis
Abnormal expression of MHC class I molecules in malignant cells is a frequent occurrence that ranges from total loss of all class I antigens to partial loss of MHC specific haplotypes or alleles. Different mechanisms are described to be responsible for these alterations, requiring different therapeutic approaches. A complete characterization of these molecular defects is important for improvement of the strategies for the selection and follow-up of patients undergoing T-cell based cancer immunotherapy. Precise identification of the mechanism leading to MHC class I defects will help to develop new personalized patient-tailored treatment protocols. There is significant new research on the prevalence of various patterns of MHC class I defects and the underlying molecular mechanisms in different types of cancer. In contrast, few data is available on the changes in MHC class I expression during the course of cancer immunotherapy, but the authors have recently made discoveries that show the progression or regression of a tumor lesion in cancer patients undergoing immunotherapy depends on the molecular mechanism responsible for the MHC class I alteration and not on the type of immunotherapy used. According to this notion, the nature of the preexisting MHC class I lesion in the cancer cell has a crucial impact on determining the final outcome of cancer immunotherapy. This SpringerBrief will present how MHC class 1 is expressed, explain its role in tumor progression, and its role in resistance to immunotherapy. ​
Copyright:
2013

Book Details

Book Quality:
Publisher Quality
ISBN-13:
9781461465430
Related ISBNs:
9781461465423
Publisher:
Springer New York
Date of Addition:
Copyrighted By:
Natalia Aptsiauri, Angel Miguel Garcia-Lora, Teresa Cabrera
Adult content:
No
Language:
English
Has Image Descriptions:
No
Categories:
Nonfiction, Science, Medicine
Submitted By:
Bookshare Staff
Usage Restrictions:
This is a copyrighted book.

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