دانلود رایگان مقاله انگلیسی دوگانگی ژنتیکی / غیر ژنتیکی مقاومت دارویی در سرطان - الزویر 2018

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عنوان فارسی

دوگانگی ژنتیکی / غیر ژنتیکی مقاومت دارویی در سرطان

عنوان انگلیسی

The Genetic/Non-genetic Duality of Drug ‘Resistance’ in Cancer

صفحات مقاله فارسی

0

صفحات مقاله انگلیسی

9

سال انتشار

2018

نشریه

الزویر - Elsevier

فرمت مقاله انگلیسی

PDF

نوع مقاله

ISI

نوع نگارش

مقالات مروری

رفرنس

دارد

پایگاه

اسکوپوس

کد محصول

E9506

رشته های مرتبط با این مقاله

داروسازی

گرایش های مرتبط با این مقاله

داروشناسی

مجله

روند سرطان - Trends in Cancer

دانشگاه

Department of Medical Oncology and Therapeutics Research - City of Hope National Medical Center - USA

doi یا شناسه دیجیتال

https://doi.org/10.1016/j.trecan.2018.01.001

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۰.۰ (بدون امتیاز)

امتیاز دهید

چکیده

Drug resistance is a serious impediment to the treatment of cancer. However, the mechanisms involved remain poorly understood. While it is widely held that the phenomenon is genetic in nature, emerging evidence suggests that nongenetic mechanisms may also be important. Furthermore, at least in some cases, refractoriness to treatment can be reversed by epigenetic reprogramming, and combination and intermittent therapies, as opposed to sustained monotherapy, appear more effective in attenuating it. Here we iterate the confusion in understanding the phenomenon by which cancer cells evade drug response and underscore the need to recognize the genetic/non-genetic duality of drug resistance in cancer. We discuss how ecological and evolutionary principles may help to reconcile the duality and may even offer new treatment strategies.

نتیجه گیری

Concluding Remarks

Tumor cells are complex adaptive systems governed by nonlinear dynamics. Recent studies integrating mathematics, physics, and the biology of such systems have underscored the multifaceted, heterogeneous nature of drug resistance, which evolves dynamically with changes in therapy [34,35]. The results from these thought-provoking theoretical and empirical studies collectively demonstrate that multiple mechanisms regulating phenotypic switching exist even within a given cancer type that can be genetic or non-genetic in nature. Thus, it may be prudent to understand the mechanism involved before considering a therapeutic approach (see Outstanding Questions). For example, including epigenetic modifiers in combination with targeted therapies may help to alter the ability of the cancer cell to switch phenotypes to acquire a drug-resistant state while rendering it more susceptible to adaptive therapy. Although several questions remain (see Outstanding Questions) and a deeper understanding is required, incorporating this new thinking in treatment protocols may help to enhance the precision with which we deliver personalized medicine.

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