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Peptide Receptor Radionuclide Therapy for Neuroendocrine Tumours
Published in Michael Ljungberg, Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
Anna Sundlöv, Katarina Sjögreen Gleisner
In summary, neuroendocrine tumours are defined by their organ of origin, the proliferation rate, and their hormonal activity. All these factors, together with the stage of the disease (local tumour growth only, regional spread or distant metastases), need to be kept in mind when deciding which treatment the patient should receive.
Endocrine Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Neuroendocrine tumors (NETs) arise from cells of the nervous and hormonal (i.e., endocrine) systems. They are thought to originate in cells whose normal function is at the neuroendocrine interface (e.g., Kulchitsky or similar enterochromaffin-like cells). Such cells are found not only in endocrine glands themselves, but also in a number of other organs and body tissues that respond to hormones (e.g., GI and pulmonary systems). Many neuroendocrine tumors are benign, but some are malignant and can arise in different areas of the body, although they are most often located in the GI tract (i.e., intestine) or lungs. However, they can also occur in the pancreas, thymus, thyroid, parathyroid, pituitary, adrenomedullary glands, liver, gallbladder, breast, genitourinary tract, and skin (e.g., Merkel cell skin carcinoma).
The respiratory system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Carcinoid tumours are low-grade malignant neuroendocrine tumours similar to those seen, for example, in the gut. They are divided into typical carcinoid (TC) and atypical carcinoid (AC). The division is based on the mitotic rate, TC having fewer than two mitoses per 2 mm2, and no necrosis, AC having two to ten mitoses per 2 mm2, and/or foci of necrosis. TCs have a good prognosis if surgically excised but 10%–15% of cases show lymph node metastases at presentation. In approximately 10% of cases, tumour cells release bioactive molecules such as serotonin. These patients develop carcinoid syndrome characterized clinically by intermittent diarrhoea, cyanosis, and flushing.
Piflufolastat F-18 (18F-DCFPyL) for PSMA PET imaging in prostate cancer
Published in Expert Review of Anticancer Therapy, 2022
Andrew F. Voter, Rudolf A. Werner, Kenneth J. Pienta, Michael A. Gorin, Martin G. Pomper, Lilja B. Solnes, Steven P. Rowe
The power of molecular imaging, including PSMA-PET, derives from the exquisite precision of the agents in combination with their modularity. While 18F-DCFPyL is exclusively an imaging agent, different warheads can be loaded onto the PSMA inhibitor delivery vehicle to address a range of clinical scenarios. This approach has been validated in neuroendocrine tumors. Somatostatin receptor PET/CT with 68Ga-labelled somatostatin analogues rapidly replaced 111In-based somatostatin receptor scintigraphy scans for imaging and staging of neuroendocrine tumors [108]. However, replacement of the gallium-68 PET imaging radionuclide with a lutetium-177 warhead yielded a therapeutic agent that has revolutionized the treatment of carcinoid tumors [109]. Similar efforts are underway for the PSMA agents, with initial trials showing favorable results for the treatment of metastatic castration-resistant prostate cancer [110–112]. The VISION trial, a prospective, phase III randomized trial, demonstrated that men with metastatic castration-resistant, PSMA-positive prostate cancer who were treated with 177Lu-PSMA-617 in addition to standard of care therapies had a significantly increased overall survival. This led to the FDA approval of 177Lu-PSMA-617 for use in this population in 2022 [113]. Further trials to explore the potential role of this agent earlier in the disease course are currently underway.
Early esophageal neuroendocrine tumor
Published in Baylor University Medical Center Proceedings, 2022
Heather Branstetter, Atin Agarwal, Scott Paulson, Anh D. Nguyen, Vani Konda
The histology from the EMR specimen demonstrated a 1 mm tumor with cells in both nest and rosette pattern extending into the muscularis mucosa (Figure 2). The cells were positive for chromogranin, synaptophysin, and cytokeratin on immunohistochemical staining. Additionally, Ki-67 was <2%. These histologic findings were consistent with a well-differentiated neuroendocrine tumor. There were negative margins on the resected specimen, and a computed tomography scan showed no evidence of metastatic disease. Oncology concluded that the tumor was a primary distal esophageal neuroendocrine tumor that was completely resected by EMR with negative margins. The rest of the biopsy specimens obtained with a mapping protocol were consistent with Barrett’s esophagus, with focal low-grade dysplasia but no evidence of high-grade dysplasia or esophageal adenocarcinoma. The patient completed endotherapy and is in her second year of surveillance without evidence of recurrence of either dysplasia or tumor.
Somatostatin-derived amyloidosis: a novel type of amyloidosis associated with well-differentiated somatostatin-producing neuroendocrine tumours
Published in Amyloid, 2022
Benjamin J. Van Treeck, Surendra Dasari, Paul J. Kurtin, Jason D. Theis, Samih H. Nasr, Lizhi Zhang, Saba Yasir, Rondell P. Graham, Ellen D. McPhail, Samar Said
Gastroenteropancreatic well-differentiated neuroendocrine tumours are uncommon, with an incidence of 6.98 cases per 100,000 individuals per year [7]. These neuroendocrine tumours are derived from neuroendocrine cells in the pancreatic islets of Langerhans, intestine mucosal Kulchitsky cells, and enterochromaffin cells of the stomach [8]. Because neuroendocrine tumours are derived from neuroendocrine cells that normally secrete hormones, a minority of neuroendocrine tumours continue to secrete hormones, such as insulin, glucagon, and somatostatin, after neoplastic transformation and are termed functional. Functional neuroendocrine tumours commonly produce syndromes related to the secreted hormones, such as hypoglycaemia resulting from insulin secretion and somatostatin syndrome resulting from somatostatin secretion. However, most neuroendocrine tumours are non-functional. Here, we report a new type of amyloidosis (somatostatin-associated amyloidosis) in the setting of non-functional, well-differentiated, somatostatin-producing neuroendocrine tumours (somatostatinomas). To our knowledge, this type of amyloidosis has not been previously reported in humans.