Reducing the Impact of Chemotherapy-Induced Myelosuppression
EP: 1.Chemotherapy Use & Chemotherapy-Induced Myelosuppression
EP: 2.Management of Chemo-Induced Myelosuppression
EP: 3.Chemotherapy-Induced Myelosuppression & COVID-19
EP: 4.CDK4/6 Inhibitors and Myelopreservation
EP: 5.Analyses of CDK4/6 Inhibitors for Myelopreservation
EP: 6.Chemotherapy-Induced Myelosuppression in SCLC: CDK4/6 Inhibition
EP: 7.CDK4/6 Inhibitors for SCLC: Trials of Interest
EP: 8.CDK4/6 Inhibitors & Myelopreservation in Other Cancers
EP: 9.Reducing the Impact of Chemotherapy-Induced Myelosuppression
Gary H. Lyman, MD, MPH, FASCO, FRCP: As we’ve seen, myelosuppression remains a part of our management of patients with systemic cytotoxic chemotherapy. It’s probably here for the long term. Even targeted therapies or checkpoint inhibitors are often given along with, or in sequence with, myelosuppressive chemotherapy. It will remain the backbone of many cancer therapy regimens.
Particularly in the time of a pandemic, we’re trying to reduce exposure to the health care system, infectious complications, and the need for transfusions, given the limited resources in blood banks. Any strategy that may preserve marrow function in patients with a pending need for cytotoxic therapy for the cancer—which will not wait and needs to be treated—is imperative. This is clearly the time for exploring these new agents, such as trilaciclib.
Beyond the pandemic, as we resume more traditional care of patients, any strategies that reduce the impact of the cancer or treatment on the patient—their functioning, fatigue, the need to be seen in the hospital—or anything that reduces the cost of managing these complications needs to be given very serious consideration. Our goal to reduce the hematopoietic toxicities due to myelosuppression has to remain paramount in our treatment planning and our shared decision-making with patients. We need to do everything we can to maintain and improve their quality of life as they go through this very difficult time in battling cancer, in some cases the pandemic, and the toxicities of the treatments that they need to receive.
Paul Bunn, MD: Obviously, trilaciclib is early in its clinical development. It’s been primarily studied in small cell lung cancer to date. I would say that in small cell lung cancer, the major data we’re missing are related to cost. It’s probably cost-effective by preventing the most frequent adverse effects. Then there’s quality of life. Because the most frequent adverse effect that bothers patients is fatigue, we need more data on the quality-of-life implications of myelopreservation. Outside small cell lung cancer, we need information on the antitumor effects of trilaciclib in other cancers. Besides the antitumor effects, we need the myelopreservation effects in other tumors. Chemotherapy administration is different in different therapies. For example, in small cell lung cancer, etoposide is given for 3 days in a row and topotecan for 5 days in a row, whereas in non–small cell cancer, almost all treatments are administered on 1 day. We need data for many types of chemotherapy administration. It’s highly likely that this would have myelopreservation effects irrespective of the schedule, but we need to study it appropriately for different schedules. There are many unanswered questions, and we all look forward to the results of clinical trials to answer these questions.
The unanswered questions in small cell lung cancer, which are being addressed in some ongoing trials, other than cost and quality-of-life benefits, are related to the immune benefits. As immunotherapy becomes more prevalent, we need to understand the potential beneficial effects of trilaciclib on immunotherapy, both by itself and in combination with other immunotherapies.
Transcript edited for clarity.
