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Restoring sensitivity to apoptosis in cancer cells therefore represents a potential opportunity to overcome this wall of resistance.

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Cancer cells learn how to evade apoptosis and thus develop resistance to the “killing” effect of chemo or radiotherapy, contributing to disease recurrence.

Apoptosis plays a critical role in development and the body’s normal function, eliminating any unnecessary or unwanted cells in a highly regulated process. There is much more research going on in this field to deepen our understanding of cancer vulnerabilities, escape mechanisms and synergies between various DNA damage pathways to improve the therapeutic impact of this new class of drugs.īehind cancer’s wall of resistance to treatment is an escape mechanism allowing it to evade cell death, or apoptosis. We already use information about the DNA repair enzymes that can predict clinical success of DDR inhibitors, yet we know are probably only scratching the surface due to a complex interplay between the targets, the mechanisms of DNA damage and the combination approaches. We believe our diverse pipeline of selective and potent DDR inhibitors has the potential to deliver on the promise of this class of agents, transforming cancer care and tipping treatment balance towards cancer cell death.

1 Targeting DDR defects in cancer cells represents a unique opportunity to eliminate cancer cells that can be explored in variety of clinical settings.Īt Merck, we are exploring three targets that are implicated in several DNA repair mechanisms: ataxia telangiectasia RAD3 related (ATR), ataxia telangiectasia mutated (ATM), and DNA-dependent protein kinases (DNA-PK). Cells with defects in their DNA repair machinery fail to preserve their genetic integrity, and the accumulation of mutations and genetic instability, which represent an important cancer vulnerability, is well-recognized as a hallmark of cancer. The inhibition of DNA damage response is among many exciting cancer treatment approaches being investigated today, taking us directly to the core of cancer-its faulty and unrepaired DNA. Targeting a Potential Vulnerability of Cancer Some of these combinations include our current standard of care treatments, and in potential combinations with our pipeline molecules. This extends into targeting specific vulnerabilities in some cancers, inhibiting certain escape mechanisms that help cancer cells survive, as well as exploiting synergies between combinations of treatments that may be beneficial to certain patients. Collectively, we have made significant progress in understanding the biology of cancer, which is helping us uncover and exploit increasingly precise ways-precision medicine approaches-to defeat cancer cells. It relies on identifying the right patients likely to benefit from therapy based on their unique tumor biology. The ability to hit cancer at its core takes more than developing new treatments. With synergistic approaches in our pipeline that target key pathways involved in cancer cell survival, we are deploying mechanisms that hit cancer at its core-its DNA. And as we also look to pioneer novel medicines and accelerate the development of new therapeutic approaches, we direct our scientific expertise and research efforts to the unmet needs where we can deliver the greatest impact for patients. We focus every day on expanding the impact our therapies can have for patients, from maximizing the reach of our established standard-of-care medicines to investigating new ways to improve outcomes for people living with cancer. Accelerating the Science of Cancer at Merck

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