Browsing by Author "Piyade, Betul"

Now showing 1 - 4 of 4

Endoscopic ultrasound-guided hepatogastrostomy to treat a biliocutaneous fistula
(GEORG THIEME VERLAG KG, 2020-01-01) Saka, Didem; Barbur, Erol; Boynukara, Can; Piyade, Betul; Sisman, Gurhan
EUS-guided transgastric pancreatic necrosectomy in a patient with sleeve gastrectomy (with video)
(WOLTERS KLUWER MEDKNOW PUBLICATIONS, 2021-01-01) Sisman, Gurhan; Barbur, Erol; Saka, Didem; Piyade, Betul; Boynukara, Can
Intramural Component of Venous, Lymphatic, and Perineural Invasion in Colon Cancer: A Threat or an Illusion?
(GALENOS PUBL HOUSE, 2022-01-01) Ozer, Leyla; Tasci, Elif Senocak; Mutlu, Arda Ulas; Piyade, Betul; Ramoglu, Nur; Ajredini, Mirac; Gurleyik, Damla; Cecen, Recep; Dincer, Sena Nur; Musevitoglu, Turan; Goksel, Suha; Ince, Umit; Kayhan, Cavit Kerem; Erdamar, Sibel; Yildiz, Ibrahim; Aytac, Erman
Background: Extramural venous invasion is an independent predictor of poor outcome in colorectal cancer, whereas the significance of the intramural component of venous and lymphatic and perineural invasion is unclear. Aims: To evaluate the prognostic impact of intramural components for venous, lymphatic, and perineural invasions and the relation of these invasion patterns with clinicopathological features in patients with colon cancer. Study Design: A retrospective cross-sectional study. Methods: The analysis included 626 patients with colon cancer in stages II and III. All patients were divided into four categories (no invasion, intramural invasion only, extramural invasion only, or both intramural and extramural invasions) for vascular invasion, lymphatic invasion and perineural invasion. The primary outcomes were 5-year disease-free and overall survival. Results: Right-sided (for vascular invasion, 24.7\% vs. 33.9\%, p = 0.007
Mechanisms of T-Cell Exhaustion in Pancreatic Cancer
(MDPI, 2020-01-01) Saka, Didem; Gokalp, Muazzez; Piyade, Betul; Cevik, Nedim Can; Sever, Elif Arik; Unutmaz, Derya; Ceyhan, Guralp O.; Demir, Ihsan Ekin; Asimgil, Hande
T-cell exhaustion is a phenomenon that represents the dysfunctional state of T cells in chronic infections and cancer and is closely associated with poor prognosis in many cancers. The endogenous T-cell immunity and genetically edited cell therapies (CAR-T) failed to prevent tumor immune evasion. The effector T-cell activity is perturbed by an imbalance between inhibitory and stimulatory signals causing a reprogramming in metabolism and the high levels of multiple inhibitory receptors like programmed cell death protein-1 (PD-1), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), T cell immunoglobulin and mucin domain-containing protein 3 (TIM-3), and Lymphocyte-activation gene 3 (Lag-3). Despite the efforts to neutralize inhibitory receptors by a single agent or combinatorial immune checkpoint inhibitors to boost effector function, PDAC remains unresponsive to these therapies, suggesting that multiple molecular mechanisms play a role in stimulating the exhaustion state of tumor-infiltrating T cells. Recent studies utilizing transcriptomics, mass cytometry, and epigenomics revealed a critical role of Thymocyte selection-associated high mobility group box protein (TOX) genes and TOX-associated pathways, driving T-cell exhaustion in chronic infection and cancer. Here, we will review recently defined molecular, genetic, and cellular factors that drive T-cell exhaustion in PDAC. We will also discuss the effects of available immune checkpoint inhibitors and the latest clinical trials targeting various molecular factors mediating T-cell exhaustion in PDAC.