Overview of Chronic Lymphocytic Leukemia

Transcript:

Lori A. Leslie, MD: Hello, and welcome to CURE Expert Connections®. I’m Dr Lori Leslie from the John Theurer Cancer Center in Hackensack, New Jersey, where I direct the indolent lymphoma and CLL [chronic lymphocytic leukemia] programs. I would like to welcome my fellow expert panelist, Mr Iida, to introduce himself.

Hoshiyuki Iida, APN: Hello. My name is Hoshiyuki Iida, I’m a nurse practitioner at Hackensack University Medical Center in New Jersey. I have 17 years of experience, starting as a bedside nurse and oncology nurse in giving chemotherapy, and then proceeding to an outpatient clinic as a nurse practitioner collaborating with Dr Leslie and our other practitioners. I’m also a facilitator for the North Bergen and upstate New York CLL support group. We meet once a month since COVID-19 began, and we are celebrating our 17th year.

Lori A. Leslie, MD: Today we’re going to discuss the management of chronic lymphocytic leukemia, or CLL, and address BTKi [Bruton tyrosine kinase inhibitor] treatment options for both newly diagnosed treatment naive and relapsed/refractory patients in CLL. First, I’ll start by providing an overview of CLL. CLL is a blood cancer of a type of white blood cell called a lymphocyte. It’s a B lymphocyte and CLL is a spectrum of disorders. Sometimes it’s referred to as chronic lymphocytic leukemia or small lymphocytic lymphoma [SLL], and this can be confusing. I’m a lymphoma specialist, but I’m also an expert in CLL, and sometimes patients will come to me and say, “Do I have leukemia or do I have lymphoma?” The answer to that is, it depends on how you present. If patients have an elevated white blood cell count over a certain degree, then we call that chronic lymphocytic leukemia regardless of whether they have enlarged lymph nodes or an enlarged spleen. About 15% of patients don’t have an elevated white blood cell count but present with enlarged lymph nodes or an enlarged spleen; we call that entity small lymphocytic lymphoma. It’s important to know that these 2 things are considered the same disease, and the treatment landscape is similar for both.

As we go through the discussion today, we’ll be referring to the CLL/SLL entity as CLL. In terms of incidence, there are about 20,000 new cases of CLL in the United States each year, but there are over 200,000 people living with CLL because it’s a chronic disease. It’s something that we think of as [requiring] long-term management, so once people have a diagnosis, usually when they meet their providers, it becomes a long-term relationship as they manage this disease process together over many years.

Over the past few years, we’ve learned a lot about the biology of CLL and what mistake happens in the lymphocyte to cause this abnormal growth. There are a few different things we do to help risk stratify patients who have CLL or help identify patients who might have a slow course and others who might progress more rapidly after they’re diagnosed. Most of this is done by a variety of tests that are standard of care that can be done in the blood work, that look at different genetic, chromosome, or molecular changes that happen in the cancer cells themselves. Not genetic changes that a patient is born with, but things that happen accidentally later that lead to this abnormal cell growth and a clinical presentation that we call chronic lymphocytic leukemia. Some of those tests include something called FISH [fluorescence in situ hybridization] testing or molecular testing for a certain abnormality called TP53.

TP53 is the spell checker of the cell. As you have a cell and it’s growing and dividing to make a new cell, in all of your normal cells in the body, there’s a spell check mechanism that goes through and makes sure there are no genetic mistakes. If there are, then the spell check mechanism corrects that so the new cell is an exact copy of the old cell. In cancers, including CLL, that process can be abnormal or missing. That process is controlled by this protein called TP53. One higher risk marker in CLL, and the one that helps us stratify patients in the guidelines as well, is this abnormality of 17p or TP53, which is the spell checker of your cell. As one could imagine, if I turn spell check off when I’m typing a document, by the time I get to the 20th copy, it would be unrecognizable from when I started. That’s the same thing that happens in the cancer cell. That genetic instability allows the cell to make mistakes and get these abnormal signals that they should be growing, when they really shouldn’t. It’s these molecular changes, these protein changes, that help us risk stratify patients with CLL in our treatment landscape and help us pick what types of treatment to use when someone needs to start a therapy.

Transcript edited for clarity.