Consequences of Chemotherapy-Induced Neutropenia

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EP: 1.Consequences of Chemotherapy-Induced Neutropenia

EP: 2.Guideline Recommendations for CIN Prophylaxis

EP: 3.CIN Prophylaxis: When to Intervene

EP: 4.G-CSFs for Chemotherapy-Induced Neutropenia

EP: 5.CIN Prophylaxis: Treating With G-CSFs

EP: 6.Managing Chemotherapy-Induced Neutropenia With G-CSFs

EP: 7.Managing CIN in Patients With Breast Cancer

EP: 8.Anticancer Therapy: Safety vs Efficacy

EP: 9.CIN Prophylaxis and Bone Pain

EP: 10.Potential Dosing Strategies to Mitigate CIN

EP: 11.CIN Treatment Advances: SIMBA Therapy

EP: 12.CIN: Takeaways From the PROTECTIVE-1 Study

EP: 13.CIN: Implications of the PROTECTIVE-2 Study

EP: 14.Novel Chemoprotective Therapies Under Investigation

EP: 15.CIN: Adopting SIMBA Therapy Into Clinical Practice

EP: 16.Therapeutic Advances in Prophylaxis Against CIN

Hope S. Rugo, MD, FASCO: Hello, and welcome to this OncLive® Peer Exchange titled “Advances in the Management of Chemotherapy-Induced Neutropenia.” I’m Dr Hope Rugo from the University of California San Francisco [Helen Diller] Comprehensive Cancer Center. Joining me in this discussion about chemotherapy-induced neutropenia, specifically in breast cancer, are my colleagues: William Gradishar from Northwestern University [Feinberg School of Medicine], Rita Nanda from the University of Chicago, and Tiffany Traina from Memorial Sloan Kettering Cancer Center.

We’re going to discuss a number of topics pertaining to chemotherapy-induced neutropenia, and we’ll discuss the latest research in the field as well as the impact of recent clinical trials on making decisions around treatment selection and some new directions that you might not have heard about. Without further ado, we’ll get started on our first topic, and we’ll talk about these various issues as we go along and get comments from our panel members.

We’re going to first talk a little about what chemotherapy-induced neutropenia is. We tend to think of this as something we already know about, so why are we learning about it again. But it’s important to review what we know and how we define chemotherapy-induced neutropenia. Rita, do you want to share with us what you think about when you think chemotherapy-induced neutropenia or CIN?

Rita Nanda, MD: Practically, I think about white blood cell count and absolute neutrophil count, which would preclude me from providing treatments, as I would like to. Generally, I use an ANC [absolute neutrophil count] of about 1000 per µL as a cut point for determining whether it’s safe for me to proceed with chemotherapy as planned for patients. As you can imagine, this comes up for us in the clinic as we’re treating patients, with both early and advanced-stage cancer, predominantly with ongoing chemotherapy. It can certainly impact our ability to keep their chemotherapy on schedule. It can lead to dose reductions that can potentially impact the efficacy of the therapies that patients are given. It can be quite challenging in clinics to manage, prevent, anticipate and then keep patients on track in terms of their curative chemotherapy or therapy that’s helping to extend life and keep their symptoms under control.

Hope S. Rugo, MD, FASCO: Bill, are there specific agents or regimens that you mostly worry about? Do you see febrile neutropenia much?

William J. Gradishar, MD: We try not to see much of it, but we still do, and it’s not always entirely predictable whom it is going to occur in. Even among patients getting the same regimen, there can be some variability in the propensity of a given patient who develops neutropenia of severity that causes some issues escalating to hospitalization. As Rita pointed out, there are different settings. Obviously in the adjuvant setting—I’m speaking as a breast cancer doctor—we try to keep patients on schedule. We try to abide by the regimen optimally. The reason we all appreciate this is because by giving the intended dose we end up with the greatest efficacy in terms of reducing the risk of recurrence.

Those regimens have been dated and were generated decades ago from some of the early trials. With the kind of regimens we see in the adjuvant or curative setting, we try to keep the patients on schedule. In some cases, to do that we have to support them with growth factors so that their counts don’t bottom out.

In the metastatic disease setting or advanced disease setting, we’re a little more liberal about spreading things out or dose reducing, because it’s more of a palliative setting. But certainly, in the curative setting, it’s critically important. That said, there are certain agents—for instance, if 1 is using an anthracycline-based regimen and giving it densely, we often have to support that with a growth factor. In the absence of that, patients can develop significant neutropenia. Certainly with agents such as docetaxel, when we use them as part of a regimen—say, even in a HER2 [human epidermal growth factor receptor 2]–positive patient where we’re combining HER2-directed therapy with additional chemotherapy. In addition to the taxane, we will often give a growth factor.

The intention for all this is to get the dose in so that you can realize the curative intent of that regimen without compromising the dose or schedule that you’re utilizing.

Transcript edited for clarity.