Publications by authors named "K Todoerti"
Purpose: In multiple myeloma (MM), tumor cells reprogram metabolic pathways to sustain growth and monoclonal immunoglobulin production. This study examines acetyl-CoA carboxylase 1 (ACC1), the enzyme driving the rate-limiting step in de novo lipogenesis (DNL), in MM metabolic reprogramming, particularly in c-MYC (MYC)-driven subtypes.
Experimental Design: ACC1 expression was evaluated across MM genetic subgroups, focusing on MYC translocations.
Background: In resectable gastric/gastroesophageal junction adenocarcinoma, microsatellite instability-high (MSI-H) confers improved survival, but limited benefit from chemotherapy. Immunotherapy may eliminate the need for chemotherapy or surgery.
Patients And Methods: INFINITY is a multicenter, multicohort phase II trial (NCT04817826) investigating in cohort 1 the activity and safety of tremelimumab + durvalumab (T300/D) as neoadjuvant treatment of mismatch repair deficient/MSI-H, resectable gastric/gastroesophageal junction adenocarcinoma.
Article Synopsis
- - The DIS3 gene is mutated in about 10% of multiple myeloma (MM) patients, and its expression is influenced by chromosomal abnormalities found in around 40% of cases, but its exact role in MM is still unclear.
- - Research shows that reducing DIS3 levels in MM cell lines slows down cell growth and disrupts the normal cell cycle, particularly increasing the number of cells in the early phase and reducing those in the later phases.
- - DIS3 also plays a key role in centrosome duplication, and its absence can lead to abnormal centrosome numbers, potentially causing genomic instability, which is common in MM and may contribute to the disease's progression.
Cancer cells fuel growth and energy demands by increasing their NAD biosynthesis dependency, which therefore represents an exploitable vulnerability for anti-cancer strategies. CD38 is a NAD-degrading enzyme that has become crucial for anti-MM therapies since anti-CD38 monoclonal antibodies represent the backbone for treatment of newly diagnosed and relapsed multiple myeloma patients. Nevertheless, further steps are needed to enable a full exploitation of these strategies, including deeper insights of the mechanisms by which CD38 promotes tumorigenesis and its metabolic additions that could be selectively targeted by therapeutic strategies.
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