Imatinib : A Breakthrough of Targeted Therapy in Cancer

المؤلفون المشاركون

Iqbal, Nida
Iqbal, Naveed

المصدر

Chemotherapy Research and Practice

العدد

المجلد 2014، العدد 2014 (31 ديسمبر/كانون الأول 2014)، ص ص. 1-9، 9ص.

الناشر

Hindawi Publishing Corporation

تاريخ النشر

2014-05-19

دولة النشر

مصر

عدد الصفحات

9

التخصصات الرئيسية

علم الصيدلة

الملخص EN

Deregulated protein tyrosine kinase activity is central to the pathogenesis of human cancers.

Targeted therapy in the form of selective tyrosine kinase inhibitors (TKIs) has transformed the approach to management of various cancers and represents a therapeutic breakthrough.

Imatinib was one of the first cancer therapies to show the potential for such targeted action.

Imatinib, an oral targeted therapy, inhibits tyrosine kinases specifically BCR-ABL, c-KIT, and PDGFRA.

Apart from its remarkable success in CML and GIST, Imatinib benefits various other tumors caused by Imatinib-specific abnormalities of PDGFR and c-KIT.

Imatinib has also been proven to be effective in steroid-refractory chronic graft-versus-host disease because of its anti-PDGFR action.

This paper is a comprehensive review of the role of Imatinib in oncology.

نمط استشهاد جمعية علماء النفس الأمريكية (APA)

Iqbal, Nida& Iqbal, Naveed. 2014. Imatinib : A Breakthrough of Targeted Therapy in Cancer. Chemotherapy Research and Practice،Vol. 2014, no. 2014, pp.1-9.
https://search.emarefa.net/detail/BIM-465478

نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)

Iqbal, Nida& Iqbal, Naveed. Imatinib : A Breakthrough of Targeted Therapy in Cancer. Chemotherapy Research and Practice No. 2014 (2014), pp.1-9.
https://search.emarefa.net/detail/BIM-465478

نمط استشهاد الجمعية الطبية الأمريكية (AMA)

Iqbal, Nida& Iqbal, Naveed. Imatinib : A Breakthrough of Targeted Therapy in Cancer. Chemotherapy Research and Practice. 2014. Vol. 2014, no. 2014, pp.1-9.
https://search.emarefa.net/detail/BIM-465478

نوع البيانات

مقالات

لغة النص

الإنجليزية

الملاحظات

Includes bibliographical references

رقم السجل

BIM-465478