Within the past year, three similar peptides with specific growth hormone (GH) releasing effects have been extracted from human tissue, identified, and synthesized. Human pancreatic tumor GH releasing factor (I-40)-OH (hpGRF-40) was the sole hpGRF isolated from the pancreatic tumor of a patient in Charlottesville and was the predominant peptide isolated from the pancreatic tumor of a patient in Lyon. The Lyon tumor also contained hpGRF(1-37)-OH and hpGRF(1-44)-NH2. Both immunological and biochemical data suggest that hpGRF-40 and hpGRF-44 are present in the human hypothalamus and may be the human GH releasing hormone(s) (GHRH). In cultures of rat pituitary cells, hpGRF stimulates GH but affects neither basal and dopamine-inhibited prolactin release nor basal and gonadotropin releasing hormone (GnRH)-stimulated luteinizing hormone (LH) release. hpGRF stimulates cyclic AMP production within seconds, an effect which is blocked by somatostatin. In contrast, while hpGRF stimulates phosphatidylinositol turnover in the pituitary, the effect is not inhibited by somatostatin. In the human, hpGRF-40 (1 microgram/kg) given intravenously (i.v.) stimulates GH release within 5 minutes. hpGRF-40 does not elevate serum prolactin levels, thyrotropin (TSH), LH, or corticotropin (measured indirectly through plasma cortisol), or blood glucose or plasma concentrations of insulin, glucagon, pancreatic polypeptide, cholecystokinin, gastrin, gastric inhibitory peptide, motilin, or somatostatin. When graded doses of hpGRF (0.1-10 micrograms/kg) are given i.v., no differences are noted in the maximal levels of serum GH achieved.(ABSTRACT TRUNCATED AT 250 WORDS)
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http://dx.doi.org/10.1007/BF01406325 | DOI Listing |
Theranostics
January 2025
Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
The tumor microenvironment (TME) is involved in cancer initiation and progression. With advances in the TME field, numerous therapeutic approaches, such as antiangiogenic treatment and immune checkpoint inhibitors, have been inspired and developed. Nevertheless, the sophisticated regulatory effects on the biological balance of the TME remain unclear.
View Article and Find Full Text PDFClin Transl Oncol
January 2025
UPMC Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA, USA.
Background: Small extracellular vesicles (sEV) released by tumor cells (tumor-derived sEV; TEX) mediate intercellular communication between tumor and non-malignant cells and were shown to impact disease progression. This study investigates the relationship between the expression levels of the vesiculation-related genes linked to sEV production and the tumor microenvironment (TME).
Methods: Two independent gene sets were analyzed, both previously linked to sEV production in various non-malignant or malignant cells.
Abdom Radiol (NY)
January 2025
Mayo Clinic Rochester, Rochester, MN, USA.
Purpose: To determine whether renal cell carcinoma metastases (RCC-Mets) to the pancreas can be differentiated from pancreatic neuroendocrine tumors (PNETs) in patients with RCC on CT or MRI at presentation.
Methods: This retrospective study included patients with biopsy-proven RCC-Mets (n = 102) or PNETs (n = 32) at diagnosis or after nephrectomy for RCC. Inter-observer agreement (Cohen kappa) was assessed in 95 patients with independent reads by two radiologists, with discrepancies resolved by consensus for final analysis.
Purpose: As the pancreas is a low contrast visibility organ, pancreatic ductal adenocarcinoma detection is challenging due to subtle attenuation differences between tumor and pancreatic parenchyma. Photon counting CT (PCCT) has superior iodine contrast-to-noise ratio than conventional CT and also affords the creation of low keV virtual monoenergetic images, both of which increase adenocarcinoma conspicuity. The purpose therefore was to identify the optimal virtual monoenergy for visualizing PDAC during the pancreatic parenchymal phase of enhancement at PCCT using both quantitative and qualitative analyses.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Life Sciences, School of Natural Sciences (SONS), Shiv Nadar Institution of Eminence, Delhi NCR, India.
Inhibin, β, which is also known as INHBA, encodes a protein that belongs to the Transforming Growth factor-β (TGF-β) superfamily, which plays a pivotal role in cancer. Gastrointestinal tract (GI tract) cancer refers to the cancers that develop in the colon, liver, esophagus, stomach, rectum, pancreas, and bile ducts of the digestive system. The role of INHBA in all GI tract cancers remains understudied.
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