The gastrointestinal stromal tumor (GIST) is a rare mesenchymal tumor. One should pay special attention when the GIST comes in obese patients during surgery. The laparoscopic resections with standard techniques, such as gastric bypass, have been described with good results. However, GIST resection associated sleeve gastrectomy for the treatment of obesity is rare, but can be done safely, depending on the location of the tumor.
Gastrointestinal stromal tumors (GIST) are rare in the rectum. These usually present with symptoms produced by compression of pelvic organs or bleeding. Surgery is the treatment of choice, however, at times the surgery can be mutilating and organ preservation may not be possible.
Objective: Tacrolimus, a calcineurin inhibitor (CNI), is the first-line treatment for chronic myeloid leukemia (CML) and advanced gastrointestinal stromal tumors (GIST). Imatinib and tacrolimus are both substrates of the hepatic enzymes CYP3A4/5 and efflux transporter P-gp, so drug-drug interactions may occur during their co-administration treatment. Therefore, this study aimed to evaluate the pharmacokinetic interaction between imatinib and tacrolimus in rats.
Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, 1300 York Ave, New York, NY 10065, USA; Englander Institute for Precision Medicine, Weill Cornell Medicine, 413 East 69th Street, New York, NY 10021, USA. Electronic address:
Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasm of the digestive tract. Despite multiple therapeutic advances, patients with advanced disease frequently develop resistance to tyrosine kinase inhibitors (TKIs), and therefore represent a therapeutic challenge. We employed whole genome sequencing (WGS) on three metastatic GISTs refractory to various TKIs and explored a publicly available cohort of 499 GISTs.
Synovial sarcoma is an aggressive soft-tissue cancer that shows limited responses to current immunotherapeutic approaches using immune checkpoint blockade or adoptive cell therapy. To improve immunotherapy for this cancer, understanding how the immune cells in the tumor microenvironment associate with histological subtype, disease progression and current therapies is vital. To evaluate the immune infiltrate in synovial sarcoma in relation to histological subtype, disease progression and in response to cytotoxic treatment, we performed immunodetection of T cells, CD68 myeloid cells, endothelial cells and keratin on a series of 41 synovial sarcoma patients at various stages of disease.
