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Search for other papers by Zaid Al-Qurayshi in
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Department of Head and Neck Surgical Oncology, NCI, Cairo University, Cairo, Egypt
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Differentiated thyroid cancer (DTC) with minimal extrathyroidal extension (MEE) is classified as stage III regardless of the tumor size. In this study, we aim to examine the effect of MEE on the overall survival and management of this population. A retrospective cohort study was performed, which utilized the National Cancer Database (NCDB), 2004–2012. The study population included patients, aged ≥ 45 years, who underwent surgery for DTC (pT3N0M0) with MEE compared to that in patients with pT2N0M0. A total of 9556 patients were included. These were divided into four groups, 4410 patients with pT2N0M0 (Group 1: T ≤ 4 cm without MEE), 3274 with pT3N0M0 (Group 2: T ≤ 4 cm with MEE), 447 with pT3N0M0 (Group 3: T > 4 cm with MEE) and 1430 patients with pT3N0M0 without MEE (Group 4: T > 4 cm without MEE). Median follow-up time was 46.7 months (interquartile range: 27.8–72.1). Patients in Group 2 (T ≤ 4 cm with MEE) had no significant worse survival compared to patients in Group 1 (T ≤ 4 cm without MEE) (P = 0.85), whereas Groups 3 and 4 (T > 4 cm), both had significantly lower survival (P < 0.001) with no difference between the two groups. Total thyroidectomy was associated with improved overall survival compared to that in lobectomy in Group 4 (T > 4 cm without MEE). Radioiodine utilization was associated with improved survival only with tumors larger than 4 cm with or without MEE. In DTC patients aged older than 45 years of age with tumor size less than 4 cm, MEE has no survival significance. Tumor size is an independent prognostic marker regardless of MEE status. Our data support re-evaluation of the current staging system.
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Search for other papers by M Trybula in
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The classification and management of neuroendocrine neoplasms (NENs) arising in the tubular gastrointestinal (GI) tract and pancreas have significantly evolved over the last decades. In the latest WHO classification published in 2022, NENs are separated regardless of their primary origin into two main groups: well-differentiated neuroendocrine tumors (NETs) and poorly differentiated neuroendocrine carcinomas (NECs). The substantial changes in the grading system changed the definition of grade 3 to include high-grade well-differentiated NETs (G3-NETs), and poorly differentiated NECs (-NECs). Although these two subgroups are considered high grades with Ki-67 >20%, they have different genomic profiles, prognosis, and clinical behavior, which critically influence their treatment strategies. The available clinical trial data to guide therapy of these high-grade subgroups are extremely limited, which impacts their management. In this review, we will summarize the current advances in the multidisciplinary approach for the management of high-grade gastroenteropancreatic NENs (GEP-NENs) including G3-NETs and NECs.
Search for other papers by Adrian F Daly in
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Search for other papers by Philippe A Lysy in
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Department of Endocrinology, Department of Human Genetics, Pediatric Endocrinology Unit, Cliniques Universitaires Saint Luc and Department of Pathology, Laboratory of Molecular Biology, Aix Marseille Université, Section on Endocrinology and Genetics, Laboratoire d'Hormonologie – CBPE, Université Catholique de Louvain, Department of Neurosurgery, Centre Hospitalier Universitaire de Liège, University of Liège, Domaine Universitaire du Sart‐Tilman, 4000 Liège, Belgium
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Department of Endocrinology, Department of Human Genetics, Pediatric Endocrinology Unit, Cliniques Universitaires Saint Luc and Department of Pathology, Laboratory of Molecular Biology, Aix Marseille Université, Section on Endocrinology and Genetics, Laboratoire d'Hormonologie – CBPE, Université Catholique de Louvain, Department of Neurosurgery, Centre Hospitalier Universitaire de Liège, University of Liège, Domaine Universitaire du Sart‐Tilman, 4000 Liège, Belgium
Search for other papers by Amira Mohamed in
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Search for other papers by Veronique Beauloye in
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Department of Endocrinology, Department of Human Genetics, Pediatric Endocrinology Unit, Cliniques Universitaires Saint Luc and Department of Pathology, Laboratory of Molecular Biology, Aix Marseille Université, Section on Endocrinology and Genetics, Laboratoire d'Hormonologie – CBPE, Université Catholique de Louvain, Department of Neurosurgery, Centre Hospitalier Universitaire de Liège, University of Liège, Domaine Universitaire du Sart‐Tilman, 4000 Liège, Belgium
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X-linked acrogigantism (X-LAG) syndrome is a newly described form of inheritable pituitary gigantism that begins in early childhood and is usually associated with markedly elevated GH and prolactin secretion by mixed pituitary adenomas/hyperplasia. Microduplications on chromosome Xq26.3 including the GPR101 gene cause X-LAG syndrome. In individual cases random GHRH levels have been elevated. We performed a series of hormonal profiles in a young female sporadic X-LAG syndrome patient and subsequently undertook in vitro studies of primary pituitary tumor culture following neurosurgical resection. The patient demonstrated consistently elevated circulating GHRH levels throughout preoperative testing, which was accompanied by marked GH and prolactin hypersecretion; GH demonstrated a paradoxical increase following TRH administration. In vitro, the pituitary cells showed baseline GH and prolactin release that was further stimulated by GHRH administration. Co-incubation with GHRH and the GHRH receptor antagonist, acetyl-(d-Arg2)-GHRH (1-29) amide, blocked the GHRH-induced GH stimulation; the GHRH receptor antagonist alone significantly reduced GH release. Pasireotide, but not octreotide, inhibited GH secretion. A ghrelin receptor agonist and an inverse agonist led to modest, statistically significant increases and decreases in GH secretion, respectively. GHRH hypersecretion can accompany the pituitary abnormalities seen in X-LAG syndrome. These data suggest that the pathology of X-LAG syndrome may include hypothalamic dysregulation of GHRH secretion, which is in keeping with localization of GPR101 in the hypothalamus. Therapeutic blockade of GHRH secretion could represent a way to target the marked hormonal hypersecretion and overgrowth that characterizes X-LAG syndrome.
