TRAIL receptor signaling: From the basics of canonical signal transduction toward its entanglement with ER stress and the unfolded protein response.
TRAIL receptor signaling: From the basics of canonical signal transduction toward its entanglement with ER stress and the unfolded protein response. Int Rev Cell Mol Biol. 2020;351:57-99 Authors: Stöhr D, Jeltsch A, Rehm M Abstract The cytokine tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the large TNF superfamily that can trigger apoptosis in transformed or infected cells by binding and activating two receptors, TRAIL receptor 1 (TRAILR1) and TRAIL receptor 2 (TRAILR2). Compared to other death ligands of the same family, TRAIL induces apoptosis preferentially in malignant cells while sparing normal tissue and has therefore been extensively investigated for its suitability as an anti-cancer agent. Recently, it was noticed that TRAIL receptor signaling is also linked to endoplasmic reticulum (ER) stress and the unfolded protein response (UPR). The role of TRAIL receptors in regulating cellular apoptosis susceptibility therefore is broader than previously thought. Here, we provide an overview of TRAIL-induced signaling, covering the core signal transduction during extrinsic apoptosis as well as its link to alternative outcomes, such as necroptosis or NF-κB activation. We discuss how environmental factors, transcriptional regulators, and genetic or epigenetic alterations regulate TRAIL receptors and thus alter cellular TRAIL susceptibility. Finally, we provide insight into the role of TRAIL receptors in sig...
ConclusionsUnlike [18F]FDG, [18F]BODIPY 1 showed prominent accumulation in BAT under both inactive and stimulated status. [18F]BODIPY 1 may serve as a valuable BAT PET agent to possibly assess BAT mitochondria density, thus BAT thermogenic capacity after further evaluation.
ConclusionsHypoxia modulation may play a role in nal-IRI ’s mechanism of action. Nal-IRI demonstrated greater anti-tumor activity in the more aggressive and hypoxic tumor model. Furthermore, hypoxia imaging provided early prediction of treatment response.
AbstractPurposeTo investigate and validate the potential role of a radiomics signature in predicting the side-specific probability of extracapsular extension (ECE) of prostate cancer (PCa).ProceduresThe preoperative magnetic resonance imaging data of 238 prostatic samples from 119 enrolled PCa patients were retrospectively assessed. The samples with were randomized in a two-to-one ratio into training (n = 74) and validation (n = 45) datasets. The radiomics features were derived from T2-weighted images (T2WIs). The optimal radiomics features were identified from the least absolute shrinkage and s...
ConclusionsIntegrated [68Ga]PSMA-11 PET/MRI provides a similarly high diagnostic performance for localization of recurrent PC as PET/CT. For the detection of local recurrences [68Ga]PSMA-11 PET/MRI is superior compared with [68Ga]PSMA-11 PET/CT.
Publication date: Available online 25 May 2020Source: Life SciencesAuthor(s): Serena L'Abbate, Ilaria Russo, Claudia Kusmic
Dear colleagues, please advise concerning this patient: 40 yo male, high PS, diagnosed a couple of years ago of colic cancer that was locally treated. Aug 2020: he was diagnosed of left parietal (at the level of the motor strip) solitary brain lesion. octobre 2020: he underwent a complete resection , followed by cavity SRS 18Gy /1 fr April 2020: refractory seizures MRI showed a relapsing left parietal cavity lesion, whose epicenter was next to the trolard vein. he was re-resected quasi... re-irradiation after single fraction cavity SRS? What dose?
Publication date: Available online 12 May 2020Source: The Journal of Molecular DiagnosticsAuthor(s): Manny D. Bacolod, Aashiq H. Mirza, Jianmin Huang, Sarah F. Giardina, Philip B. Feinberg, Steven A. Soper, Francis Barany
To observe the surgical index at the different learning stages of thoraco-laparoscopic esophagectomy in the prone position for esophageal cancer and to investigate the learning curve of this surgical procedure.
We report that the loss of 4.1N correlated with progress in clinical stage, as well as poor survival in EOC patients. The loss of 4.1N induces EMT in adherent EOC cells and its expression inhibits anoikis resistance and EMT by directly binding and accelerating the degradation of 14-3-3 in suspension EOC cells. Furthermore, the loss of 4.1N could increase the rate of entosis, which aggravates cell death resistance in suspension EOC cells. Moreover, xenograft tumors in nude mice also show that the loss of 4.1N can aggravate peritoneal dissemination of EOC cells. Single-agent and combination therapy with a ROCK inhibitor and ...
Publication date: Available online 26 May 2020Source: Oral Surgery, Oral Medicine, Oral Pathology and Oral RadiologyAuthor(s): Radosław Mlak, Tomasz Powrózek, Anna Brzozowska, Iwona Homa-Mlak, Marcin Mazurek, Paweł Gołębiowski, Dorota Korzeb, Mansur Rahnama-Hezavah, Teresa Małecka-Massalska