Publications by authors named "G Bodanapu"

Individuals with hematologic malignancy have increased risk of latent tuberculosis infection (LTBI) reactivation and (SS) dissemination. However, screening prior to chemotherapy or corticosteroids is not routine. We conducted a LTBI and SS screening intervention amongst patients with hematologic malignancies.

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Article Synopsis
  • - The study analyzed the effects of cytogenetic abnormalities in 283 AL amyloidosis patients treated with daratumumab-based therapies, focusing on abnormalities like t(11;14), deletion(13q), and gain/amp(1q).
  • - Among various subgroups, only +1q showed a significant lower rate of very good partial response and was linked to worse hematologic event-free survival, while t(11;14) did not negatively impact overall survival.
  • - The findings suggest that patients with the +1q abnormality may benefit from targeted clinical trials with novel immunotherapies to improve their treatment outcomes.
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Activated Notch signaling is highly prevalent in T-cell acute lymphoblastic leukemia (T-ALL), but pan-Notch inhibitors showed excessive toxicity in clinical trials. To find alternative ways to target Notch signals, we investigated cell division cycle 73 (Cdc73), which is a Notch cofactor and key component of the RNA polymerase-associated transcriptional machinery, an emerging target in T-ALL. Although we confirmed previous work that CDC73 interacts with NOTCH1, we also found that the interaction in T-ALL was context-dependent and facilitated by the transcription factor ETS1.

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Activated Notch signaling is highly prevalent in T-cell acute lymphoblastic leukemia (T-ALL) but pan-Notch inhibitors were toxic in clinical trials. To find alternative ways to target Notch signals, we investigated Cell division cycle 73 (Cdc73), which is a Notch cofactor and component of transcriptional machinery, a potential target in T-ALL. While we confirmed previous work that CDC73 interacts with NOTCH1, we also found that the interaction in T-ALL was context-dependent and facilitated by the lymphoid transcription factor ETS1.

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