Splanchnic vein thrombosis (SpVT) is an uncommon site of venous thrombosis that is associated with complications including portal hypertension and hepatic dysfunction. The evaluation and management of this patient population has evolved in recent years, but there are limited data from clinical trials to guide management. Given the various acquired and biologic risk factors leading to the development of SpVT and the potential complications that can arise from it, input from a multidisciplinary team can be valuable in managing such patients, including thrombosis specialists or hematologists, gastroenterologists or hepatologists, interventional radiologists, and surgeons.
View Article and Find Full Text PDFMalignancy is a risk factor for splanchnic vein thrombosis (SpVT). Data on the natural history of cancer-associated SpVT are limited. This was a single-center, retrospective cohort study of 581 adult patients with cancer and SpVT.
View Article and Find Full Text PDFBackground: Optimal anticoagulation management in patients with myeloproliferative neoplasms (MPN) experiencing splanchnic vein thrombosis (SpVT) requires balancing risks of bleeding and recurrent thrombosis.
Objectives: We conducted a systematic review and meta-analysis to assess the incidence of bleeding and thrombosis recurrence in patients with MPN-SpVT.
Methods: We included retrospective or prospective studies in English with ≥10 adult patients with MPN-SpVT.
Metastatic lesions are largely responsible for cancer-related deaths and are synonymous with a poor prognosis. However, this is not always true for patients with oligometastases whose disease may be amenable to curative-intent local therapies. It has been proposed that an "intermediate state" (oligometastasis) exists in between locoregional and advanced disease states; however, the clinical definition of oligometastasis varies, and there is limited understanding of how tumor biology differs between oligometastases and polymetastases.
View Article and Find Full Text PDFdsDNA breaks (DSBs) are resected in a 5'→3' direction, generating single-stranded DNA (ssDNA). This promotes DNA repair by homologous recombination and also assembly of signaling complexes that activate the DNA damage checkpoint effector kinase Chk1. In fission yeast (), genetic screens have previously uncovered a family of three xeroderma pigmentosum G (XPG)-related nucleases (XRNs), known as Ast1, Exo1, and Rad2.
View Article and Find Full Text PDFRecurrent somatic mutations of in aggressive pediatric high-grade gliomas generate K27M or G34R/V mutant histone H3.3. H3.
View Article and Find Full Text PDFDNA is subject to a wide variety of damage. In order to maintain genomic integrity, cells must respond to this damage by activating repair and cell cycle checkpoint pathways. The initiating events in the DNA damage response entail recognition of the lesion and the assembly of DNA damage response complexes at the DNA.
View Article and Find Full Text PDFCell cycle checkpoints are surveillance mechanisms that monitor the order, integrity, and fidelity of the major events of the cell cycle. These include growth to the appropriate cell size, the replication and integrity of the chromosomes, and their accurate segregation at mitosis. Many of these mechanisms are ancient in origin and highly conserved, and hence have been heavily informed by studies in simple organisms such as the yeasts.
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