The ACE Environmental Advisory may be the first of a series of papers designed to provide useful information on current sector topics faced by risk managers. ‘With this environmental risk practice's vast scope of products, services and expertise, we are committed to providing practical info on a variety of relevant issues,’ said William P. Hazelton, Executive Vice President, ACE Environmental Risk. ‘This advisory addresses a matter of important importance to those associated with healthcare facility structure projects. Our goal is to assist them in creating a comprehensive approach to the management of potential pollutant dangers and exposures.’ Related StoriesAddressing quality of life needs in prostate malignancy: an interview with Professor Louis DenisUsing integrated molecular pathology to control incidental pancreatic cysts: an interview with Dr Ananya DasOJ Bio at Medica 2015 – Point of Care diagnostics' part in reducing antibiotics prescribing The ACE Environmental Advisory was co-authored by Jack Frost, Assistant Vice President, ACE Environmental Risk, Steve Piatkowski, Vice President, ACE Environmental Frank and Risk Westfall, Vice President, ESIS Health, Safety and Environmental Services.However, it is not clear why stem cells from sufferers with chronic-stage CML and polycythemia vera are prone to accumulate DNA damage.29 Regular cells undergo many DNA strand breaks per genome per cell division, and adequate DNA repair mechanisms, combined with the removal of damaged cells by apoptosis, are therefore needed for homeostasis.31 Inhibition of the Bcl-xL deamidation pathway in chronic-phase CML and polycythemia vera provides a mechanism for circumventing the apoptotic response and permitting accumulation of DNA harm within the malignant clone. It has been reported that cells expressing oncogenic tyrosine kinases, including BCR-ABL, are resistant to DNA harm.32-34 Level of resistance to DNA-damaging brokers depends on BCR-ABL catalytic activity.32 In keeping with this finding, the combination of antileukemic chemotherapy with the tyrosine kinase inhibitor imatinib produces synergistic or increased apoptosis.35-38 Our results reveal the molecular basis for the potency of such combination therapies.