Publications by authors named "F Gandini"

In chronic lymphocytic leukemia, the reliability of next-generation sequencing (NGS) to detect variants ≤10% allelic frequency (low-VAF) is debated. We tested the ability to detect 23 such variants in 41 different laboratories using their NGS method of choice. The sensitivity was 85.

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Men who have sex with men (MSM) and people with HIV are at increased risk of anal HPV infection and cancer. This study aimed to assess the prevalence of anal HPV among MSM with HIV (MWH) and without HIV (MWoH), as well as among MSM under and over 35 years. Factors associated with infection from high-risk (HR) HPV were investigated.

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The NFKBIE gene, which encodes the NF-κB inhibitor IκBε, is mutated in 3-7% of patients with chronic lymphocytic leukemia (CLL). The most recurrent alteration is a 4-bp frameshift deletion associated with NF-κB activation in leukemic B cells and poor clinical outcome. To study the functional consequences of NFKBIE gene inactivation, both in vitro and in vivo, we engineered CLL B cells and CLL-prone mice to stably down-regulate NFKBIE expression and investigated its role in controlling NF-κB activity and disease expansion.

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The work discusses the results of hair and urine testing performed in 51 cases of suspected in utero drug exposure handled at the University Hospital of Verona from 2016 to 2022. On the day of birth or the day after birth, urine from mother and newborn (UM and UN) and hair from mother (HM), newborn (HN) and father (HF), if possible, were collected. Urine underwent immunoassay and GC-MS analysis, whereas hair underwent LC-MS/MS and GC-MS/MS analysis.

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Article Synopsis
  • Patients with chronic lymphocytic leukemia (CLL) on ibrutinib treatment often develop resistance due to mutations in the BTK and PLCG2 genes, with varying frequencies impacting patient outcomes.
  • A study of 98 CLL patients revealed that 65% of those who relapsed exhibited at least one mutation in BTK or PLCG2, while 12% of responding patients also had mutations, indicating a potential for progression.
  • The findings suggest that other genetic mutations may contribute to resistance, with BTK mutation profiles differing between relapsing patients, but no significant impact on TP53 mutations was observed, highlighting the complexity of treatment resistance.
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