I think this is a very good question. Just one thing I’d say, I’d argue actually changes management is to pay attention to both lesion types in patients with clonal cytopenia, not explained by other etiologies. That is, you know, to pay attention to both clonal hematopoiesis with the somatic lesions and also the mosaic chromosome alterations together. And here’s why that is different...
I think this is a very good question. Just one thing I’d say, I’d argue actually changes management is to pay attention to both lesion types in patients with clonal cytopenia, not explained by other etiologies. That is, you know, to pay attention to both clonal hematopoiesis with the somatic lesions and also the mosaic chromosome alterations together. And here’s why that is different. Because in the recent work, it was found that the mosaic chromosome alteration is about three times more common than CHIP in cancer-free individuals. And the biologic hit at the same locus significantly increases the risk for hematologic disorders. And the risk isn’t just additive, it is synergistic. With a hazard ratio about 5.5 for CHIP alone, 3 for mosaic chromosome alteration alone, and 80 when they overlap. And also for the blood count abnormalities go from about 23% with either lesion alone to 50% when they overlap. So I think this is a management change. Let’s say a patient’s come to us with a lower risk on either test in isolation, but it can be generally high risk on both. And each test alone may just falsely reassure us. However, if we look at both, you know, it actually changes, you know, the risk actually changes. I think it changes who I bring back in three months instead of one year, who I counsel differently and who I see who’s going to be benefited from a clinical trial perspective. So this is how I see it. Thank you.
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