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The tumor microenvironment controls drug sensitivity

Nature Medicine volume 18, pages 1332–1334 (2012)Cite this article

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A better understanding of mechanisms involved in regulation of drug sensitivity is crucial for improved cancer treatment. New studies show that cells of the tumor microenvironment modulate the response of cancer cells to chemotherapy and targeted therapies through production of secreted factors (pages 1359–1368).

The goal for cancer research is to provide personalized and effective cancer treatments. An important part of these studies is to better understand the biological basis for variations in response to treatment, as well as to identify markers for drug sensitivity and resistance. The molecular determinants of sensitivity and primary or acquired resistance have traditionally been identified through characterization of the malignant target cells. Well-established markers of drug sensitivity, already clinically implemented, include estrogen receptors, amplified human epidermal growth factor receptor 2 (HER2) and mutated epidermal growth factor receptor (EGFR) or BRAF, which guides the use of endocrine treatment and targeted therapies1,2,3. Other markers identify resistance to treatment, such as RAS mutations that define a group of patients with colorectal cancer not susceptible to treatment with EGFR-targeting antibodies4. However, in spite of this progress it is clear that many aspects of drug sensitivity remain unknown.

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Figure 1: Tumor microenvironment regulates drug sensitivity.

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  1. Arne Östman is in the Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.,

    Arne Östman

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Correspondence to Arne Östman.

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Östman, A. The tumor microenvironment controls drug sensitivity. Nat Med 18, 1332–1334 (2012). https://doi.org/10.1038/nm.2938

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