Publications by authors named "Eti Sinha"

Article Synopsis
  • Cancer patients, particularly those with melanoma and non-small cell lung cancer (NSCLC), show higher rates of clonal hematopoiesis, which could influence their treatment and outcomes.
  • The study examines how immune checkpoint blockade (ICB) therapy impacts the hematopoietic clonal architecture and whether changes in clonal expansion affect hematopoietic health in these patients.
  • Findings suggest that mutations within the hematopoietic system increase with extended ICB therapy, raising questions about the potential for clonal hematopoiesis to predict therapy responses and the long-term risks of developing myeloid malignancies.
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Clonal hematopoiesis of indeterminate potential (CHIP) is defined by the presence of a cancer-associated somatic mutation in white blood cells in the absence of overt hematological malignancy. It arises most commonly from loss-of-function mutations in the epigenetic regulators DNMT3A and TET2. CHIP predisposes to both hematological malignancies and atherosclerotic cardiovascular disease in humans.

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Clonal hematopoiesis (CH) represents clonal expansion of mutated hematopoietic stem cells detectable in the peripheral blood or bone marrow through next generation sequencing. The current prevailing model posits that CH mutations detected in the peripheral blood mirror bone marrow mutations with clones widely disseminated across hematopoietic compartments. We sought to test the hypothesis that all clones are disseminated throughout hematopoietic tissues by comparing CH in hip vs peripheral blood specimens collected at the time of hip replacement surgery.

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Purpose: Hematologic toxic effects of peptide receptor radionuclide therapy (PRRT) can be permanent. Patients with underlying clonal hematopoiesis (CH) may be more inclined to develop hematologic toxicity after PRRT. However, this association remains understudied.

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