Publications by authors named "Monica Nair"

Article Synopsis
  • - Immune effector cell-associated hematotoxicity (ICAHT) is a common toxicity linked to CAR T-cell therapy, notably affecting patients with various lymphomas and multiple myeloma, but has not been previously studied in B-cell acute lymphoblastic leukemia (B-ALL).
  • - In a study involving 156 young patients with relapsed/refractory B-ALL, severe neutropenia was observed for a median of 13 days, with over half experiencing significant ICAHT, which indicated the need for better predictive models for this condition.
  • - The researchers developed the ALL-Hematotox (ALL-HT) score, improving on existing models by incorporating bone marrow disease burden, which accurately predicted severe neutrop
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Background: Cribriform (CF) and/or intraductal carcinoma (IDC) are associated with more aggressive prostate cancer (CaP) and worse outcomes.

Objective: The transcriptomic features that typify CF/IDC are not well described and the capacity for clinically utilized genomic classifiers to improve risk modeling for CF/IDC remains undefined.

Design, Setting, And Participants: We performed a retrospective review of CaP patients who had Decipher testing at a single high-volume institution.

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Interrogation of cell-free DNA (cfDNA) represents an emerging approach to non-invasively estimate disease burden in multiple myeloma (MM). Here, we examined low-pass whole genome sequencing (LPWGS) of cfDNA for its predictive value in relapsed/ refractory MM (RRMM). We observed that cfDNA positivity, defined as ≥10% tumor fraction by LPWGS, was associated with significantly shorter progression-free survival (PFS) in an exploratory test cohort of 16 patients who were actively treated on diverse regimens.

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Article Synopsis
  • The study highlights how cancer cells, particularly in multiple myeloma, adapt to treatment through cellular plasticity and genetic variation, enabling them to resist therapies.
  • Researchers utilized single-cell analysis to identify different transcriptional states within cancer cells, revealing how these cells can change their gene expression patterns and enhancer usage for survival.
  • The findings suggest that the treatment process creates new opportunities for immunotherapy by identifying specific targets like CXCR4, which could help overcome the challenges of treatment resistance.
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Purpose: Although remarkably effective in some patients, precision medicine typically induces only transient responses despite initial absence of resistance-conferring mutations. Using -mutated myeloma as a model for resistance to precision medicine we investigated if mutated cancer cells have the ability to ensure their survival by rapidly adapting to BRAF inhibitor treatment.

Experimental Design: Full-length single-cell RNA (scRNA) sequencing (scRNA-seq) was conducted on 3 patients with -mutated myeloma and 1 healthy donor.

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Lineage plasticity and stemness have been invoked as causes of therapy resistance in cancer, because these flexible states allow cancer cells to dedifferentiate and alter their dependencies. We investigated such resistance mechanisms in relapsed/refractory early T-cell progenitor acute lymphoblastic leukemia (ETP-ALL) carrying activating NOTCH1 mutations via full-length single-cell RNA sequencing (scRNA-seq) of malignant and microenvironmental cells. We identified 2 highly distinct stem-like states that critically differed with regard to cell cycle and oncogenic signaling.

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