How to Reduce the No-Show Rate in the Psychiatric Oncology Clinic: Clinical Safety and Effectiveness Project.

Mental health stability among patients with cancer improves adherence to oncology treatment, contributing to better outcomes. In a comprehensive cancer center, the no-show rate for the psychiatric oncology clinic was higher than that of any other clinic at the center. A quality improvement project was designed to enhance patients' engagement in their mental health visits to emotionally equip them for their oncology treatments.

Esophageal cancer as initial presentation of Fanconi anemia in patients with a hypomorphic variant.

Fanconi anemia (FA) is a clinically heterogenous and genetically diverse disease with 22 known complementation groups (FA-A to FA-W), resulting from the inability to repair DNA interstrand cross-links. This rare disorder is characterized by congenital defects, bone marrow failure, and cancer predisposition. is the most commonly mutated gene in FA and a variety of mostly private mutations have been documented, including small and large indels and point and splicing variants.

Distinct roles of BRCA2 in replication fork protection in response to hydroxyurea and DNA interstrand cross-links.

DNA interstrand cross-links (ICLs) are a form of DNA damage that requires the interplay of a number of repair proteins including those of the Fanconi anemia (FA) and the homologous recombination (HR) pathways. Pathogenic variants in the essential gene when monoallelic, predispose to breast and ovarian cancer, and when biallelic, result in a severe subtype of Fanconi anemia. BRCA2 function in the FA pathway is attributed to its role as a mediator of the RAD51 recombinase in HR repair of programmed DNA double-strand breaks (DSB).

Advances in understanding DNA processing and protection at stalled replication forks.

The replisome, the molecular machine dedicated to copying DNA, encounters a variety of obstacles during S phase. Without a proper response to this replication stress, the genome becomes unstable, leading to disease, including cancer. The immediate response is localized to the stalled replisome and includes protection of the nascent DNA.