Endocrine oncology (Bristol, England)最新文献_第3页

The evolution in pituitary tumour classification: a clinical perspective. 垂体瘤分类的演变：临床视角。

Endocrine oncology (Bristol, England) Pub Date : 2023-04-21 eCollection Date: 2023-01-01 DOI: 10.1530/EO-22-0079

Nele F Lenders, Peter E Earls, Warrick J Inder, Ann I McCormack

{"title":"The evolution in pituitary tumour classification: a clinical perspective.","authors":"Nele F Lenders, Peter E Earls, Warrick J Inder, Ann I McCormack","doi":"10.1530/EO-22-0079","DOIUrl":"10.1530/EO-22-0079","url":null,"abstract":"Objective: Pituitary tumours comprise a pathologically and clinically diverse group of neoplasms. Classification frameworks have changed dramatically in the past two decades, reflecting improving understanding of tumour biology. This narrative review examines the evolution of pituitary tumour classification, from a clinical perspective.Results: In 2004, pituitary tumours were classified as 'typical' or 'atypical', based on the presence of markers of proliferation, Ki67, mitotic count and p53. In 2017, the new WHO marked a major paradigm shift, with a new focus on lineage-based classification, determined by transcription factor and hormonal immunohistochemistry. The terms 'typical' and 'atypical' were omitted, though the importance of proliferative markers Ki67 and mitotic count was acknowledged. The recent WHO 2022 classification incorporates further refinements, specifically recognising some less common types that may represent less well-differentiated tumours. Whilst 'high risk' tumour types have been identified, further work is still required to improve prognostication.Conclusions: Recent WHO classifications have marked significant progress in the diagnostic evaluation of pituitary tumours, though shortcomings and challenges remain for both clinicians and pathologists in managing these tumours.","PeriodicalId":72907,"journal":{"name":"Endocrine oncology (Bristol, England)","volume":"3 1","pages":"e220079"},"PeriodicalIF":0.0,"publicationDate":"2023-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2c/1f/EO-22-0079.PMC10305559.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9869873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of 11-oxygenated androgens in prostate cancer. 11-氧化雄激素在前列腺癌症中的作用。

Endocrine oncology (Bristol, England) Pub Date : 2023-03-13 eCollection Date: 2023-01-01 DOI: 10.1530/EO-22-0072

Gido Snaterse, Johannes Hofland, Bruno Lapauw

{"title":"The role of 11-oxygenated androgens in prostate cancer.","authors":"Gido Snaterse, Johannes Hofland, Bruno Lapauw","doi":"10.1530/EO-22-0072","DOIUrl":"10.1530/EO-22-0072","url":null,"abstract":"11-oxygenated androgens are a class of steroids capable of activating the androgen receptor (AR) at physiologically relevant concentrations. In view of the AR as a key driver of prostate cancer (PC), these steroids are potential drivers of disease and progression. The 11-oxygenated androgens are adrenal-derived, and persist after androgen deprivation therapy (ADT), the mainstay treatment for advanced PC. Consequently, these steroids are of particular interest in the castration-resistant prostate cancer (CRPC) setting. The principal androgen of the pathway, 11-ketotestosterone (11KT), is a potent AR agonist and the predominant circulating active androgen in CRPC patients. Additionally, several precursor steroids are present in the circulation which can be converted into active androgens by steroidogenic enzymes present in PC cells. In vitro evidence suggests that adaptations frequently observed in CRPC favour the intratumoral accumulation of 11-oxygenated androgens in particular. Still, apparent gaps in our understanding of the physiology and role of the 11-oxygenated androgens remain. In particular, in vivo and clinical evidence supporting these in vitro findings is limited. Despite recent advances, a comprehensive assessment of intratumoral concentrations has not yet been performed. The exact contribution of the 11-oxygenated androgens to CRPC progression therefore remains unclear. This review will focus on the current evidence linking the 11-oxygenated androgens to PC, will highlight current gaps in our knowledge, and will provide insight into the potential clinical importance of the 11-oxygenated androgens in the CRPC setting based on the current evidence.","PeriodicalId":72907,"journal":{"name":"Endocrine oncology (Bristol, England)","volume":"3 1","pages":"e220072"},"PeriodicalIF":0.0,"publicationDate":"2023-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/00/17/EO-22-0072.PMC10305623.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9869872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Kinase inhibitors in thyroid cancers. 甲状腺癌中的激酶抑制剂。

Endocrine oncology (Bristol, England) Pub Date : 2023-01-13 eCollection Date: 2023-01-01 DOI: 10.1530/EO-22-0062

Vineeth Sukrithan, Prachi Jain, Manisha H Shah, Bhavana Konda

{"title":"Kinase inhibitors in thyroid cancers.","authors":"Vineeth Sukrithan, Prachi Jain, Manisha H Shah, Bhavana Konda","doi":"10.1530/EO-22-0062","DOIUrl":"10.1530/EO-22-0062","url":null,"abstract":"Objective: The treatment landscape for thyroid cancers has changed rapidly with the availability of kinase inhibitors against VEGFR, BRAF, MEK, NTRK, and RET. We provide an up-to-date review of the role of kinase inhibitors in thyroid cancer and discuss upcoming trials.Design & methods: A comprehensive review of the available literature describing kinase inhibitors in thyroid cancer was performed.Results and conclusions: Kinase inhibitors have become the standard of care for patients with metastatic radioactive iodine-refractory thyroid cancer. Short-term treatment can re-sensitize differentiated thyroid cancer to radioactive iodine, thereby potentially improving outcomes and sparing toxicities associated with the long-term use of kinase inhibitors. The approval of cabozantinib as salvage therapy for progressive radioactive iodine-refractory differentiated thyroid cancer following failure with sorafenib or lenvatinib adds to the available armamentarium of active agents. Vandetanib and cabozantinib have become mainstay treatments for metastatic medullary thyroid cancer regardless of RET mutation status. Selpercatinib and pralsetinib, potent and selective receptor kinase inhibitors with activity against RET, have revolutionized the treatment paradigm for medullary thyroid cancers and other cancers with driver mutations in RET. Dabrafenib plus trametinib for BRAF mutated anaplastic thyroid cancer provides an effective treatment option for this aggressive cancer with a dismal prognosis. In order to design the next generation of agents for thyroid cancer, future efforts will need to focus on developing a better understanding of the mechanisms of resistance to kinase inhibition including bypass signaling and escape mutations.","PeriodicalId":72907,"journal":{"name":"Endocrine oncology (Bristol, England)","volume":"3 1","pages":"e220062"},"PeriodicalIF":0.0,"publicationDate":"2023-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10171999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Thrombotic microangiopathy associated with lenvatinib therapy. 与lenvatinib治疗相关的血栓性微血管病。

Endocrine oncology (Bristol, England) Pub Date : 2023-01-01 DOI: 10.1530/EO-22-0078

Macarena Contreras Angulo, Belén García Izquierdo, Laura Armengod Grao, Nuria Palacios García

{"title":"Thrombotic microangiopathy associated with lenvatinib therapy.","authors":"Macarena Contreras Angulo, Belén García Izquierdo, Laura Armengod Grao, Nuria Palacios García","doi":"10.1530/EO-22-0078","DOIUrl":"https://doi.org/10.1530/EO-22-0078","url":null,"abstract":"Summary: Systemic thrombotic microangiopathy (TMA) is a serious condition whose early treatment is essential to reduce morbidity and mortality. TMA with only renal involvement has been associated with tyrosine kinase inhibitors, including lenvatinib, a drug used for certain advanced neoplasms. To date, TMA with systemic involvement associated with this drug has not been described. We present the case of a patient with progressive metastatic thyroid cancer who developed this complication after starting treatment with lenvatinib. We describe the signs and symptoms that led to the diagnosis and the treatment required for her recovery.Learning points: Thrombotic microangiopathy (TMA) is a group of disorders characterized by thrombosis in capillaries and arterioles due to an endothelial injury. Both, localized and systemic forms have been described.TMA with systemic involvement is characterized by hemolytic anemia, low platelets, and organ damage.Vascular endothelial growth factor signaling inhibitors have been associated with TMA, either restricted to the kidney or with systemic involvement.Lenvatinib has been rarely associated with TMA. Although only forms with isolated or predominantly renal involvement had been described so far, a predominantly systemic form can occur.Lenvatinib-induced systemic TMA must be distinguished from primary forms by measuring ADAMTS-13. Treatment includes discontinuation of the drug and supportive measures.When anemia and thrombocytopenia coexist in a patient receiving treatment with lenvatinib, a peripheral blood smear to exclude TMA is recommended.","PeriodicalId":72907,"journal":{"name":"Endocrine oncology (Bristol, England)","volume":"3 1","pages":"e220078"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10171994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ectopic ACTH Cushing's syndrome caused by a large-cell neuroendocrine lung carcinoma responding to desmopressin. 去氨加压素所致大细胞神经内分泌肺癌所致异位ACTH库欣综合征。

Endocrine oncology (Bristol, England) Pub Date : 2023-01-01 DOI: 10.1530/EO-23-0002

Stéphanie Larose, Dany Rioux, Roula Albadine, André Lacroix

{"title":"Ectopic ACTH Cushing's syndrome caused by a large-cell neuroendocrine lung carcinoma responding to desmopressin.","authors":"Stéphanie Larose, Dany Rioux, Roula Albadine, André Lacroix","doi":"10.1530/EO-23-0002","DOIUrl":"https://doi.org/10.1530/EO-23-0002","url":null,"abstract":"Ectopic adrenocorticotrophic hormone (ACTH) secretion (EAS) is a rare cause of ACTH-dependent Cushing's syndrome (CS), most often caused by a thoracic neuroendocrine tumor (NET). Large-cell neuroendocrine carcinomas (LCNEC) with EAS are rare and usually present a more severe ACTH secretion and hypercortisolism. We report a 44-year-old non-smoker man, who presented clinical and biochemical evidence of ACTH-dependent CS. Desmopressin 10 μg i.v. produced a 157% increase in ACTH and a 25% increase in cortisol from baseline; there was no stimulation of ACTH or cortisol during the corticotropin-releasing hormone (CRH) test and no suppression with high dose dexamethasone. Pituitary MRI identified a 5 mm lesion, but inferior petrosal venous sinus sampling under desmopressin did not identify a central ACTH source. Thorax and abdominal imaging identified a left lung micronodule. Surgery confirmed a lung LCNEC with strongly positive ACTH immunohistochemistry (IHC) in the primary and lymph node metastasis. The patient was in CS remission after surgery and adjuvant chemotherapy but developed a recurrence 9.5 years later, with LCNEC pulmonary left hilar metastases, ectopic CS, and positive ACTH IHC. This is the first report of LCNEC, with morphologic feature of carcinoid tumor of the lung with ectopic ACTH stimulated by desmopressin. Long delay prior to metastatic recurrence indicates relatively indolent NET. This case report indicates that response to desmopressin, which usually occurs in Cushing's disease or benign NETs, can occur in malignant LCNEC.","PeriodicalId":72907,"journal":{"name":"Endocrine oncology (Bristol, England)","volume":"3 1","pages":"e230002"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4b/5a/EO-23-0002.PMC10305561.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10171997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Curcumin effects on Leydig cell functions and potential therapeutic uses. 姜黄素对间质细胞功能的影响及其潜在的治疗用途。

Endocrine oncology (Bristol, England) Pub Date : 2023-01-01 DOI: 10.1530/EO-22-0075

Trinidad Raices, María Luisa Varela, Adriana María Belén Abiuso, Elba N Pereyra, Carolina Mondillo, Omar P Pignataro, María Fernanda Riera

{"title":"Curcumin effects on Leydig cell functions and potential therapeutic uses.","authors":"Trinidad Raices, María Luisa Varela, Adriana María Belén Abiuso, Elba N Pereyra, Carolina Mondillo, Omar P Pignataro, María Fernanda Riera","doi":"10.1530/EO-22-0075","DOIUrl":"https://doi.org/10.1530/EO-22-0075","url":null,"abstract":"Curcumin has been ascribed with countless therapeutic effects, but its impact on testicular function has been scarcely researched. Leydig cells comprise the androgen-secreting population of the testis and may give rise to Leydig cell tumours (LCTs). Due to their steroid-secreting nature, LCTs entail endocrine, reproductive, and psychological disorders. Approximately 10% are malignant and do not respond to chemotherapy and radiotherapy. The aim of this study was to assess curcumin's impact on Leydig cells' functions and its potential effect on LCT growth. In vitro assays on MA-10 Leydig cells showed that curcumin (20-80 µmol/L) stimulates acute steroidogenesis, both in the presence and absence of db-cAMP. This effect is accompanied by an increase in StAR expression. Regarding curcumin's in vitro cytostatic capacity, we show that 40-80 µmol/L curcumin reduces MA-10 Leydig cells' proliferative capacity, which could be explained by the arrest in G2/M and the reduced viability due to the activation of the apoptotic pathway. Finally, CB6F1 mice were inoculated with MA-10 cells to generate ectopic LCT in both flanks. They received i.p. injections of 20 mg/kg curcumin or vehicle every other day for 15 days. We unveiled curcumin's capacity to inhibit LCT growth as evidenced by reduced tumour volume, weight, and area under the growth curves. No detrimental effects on general health parameters or testicular integrity were observed. These results provide novel evidence of curcumin's effects on the endocrine cell population of the testis and propose this natural compound as a therapeutic agent for LCT.","PeriodicalId":72907,"journal":{"name":"Endocrine oncology (Bristol, England)","volume":"3 1","pages":"e220075"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10172000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exploring genetic loci of type 2 diabetes and cancer: a review. 2型糖尿病和癌症基因位点的研究进展

Endocrine oncology (Bristol, England) Pub Date : 2023-01-01 DOI: 10.1530/EO-22-0094

Molly Endicott, Chrissie Thirlwell, Amy P Webster

{"title":"Exploring genetic loci of type 2 diabetes and cancer: a review.","authors":"Molly Endicott, Chrissie Thirlwell, Amy P Webster","doi":"10.1530/EO-22-0094","DOIUrl":"https://doi.org/10.1530/EO-22-0094","url":null,"abstract":"Diabetes and cancer are two heterogenous diseases which are rapidly increasing in prevalence globally. A link between these two non-communicable diseases was first identified over 100 years ago; however, recent epidemiological studies and advances in genomic research have provided greater insight into the association between diabetes and cancer. Epidemiological studies have suggested that individuals with diabetes have an increased risk of several types of cancer (including liver, pancreas, colorectal, breast, and endometrial) and an increased risk of cancer mortality. However, this increased risk is not observed in all cancers, for example, there is a reduced risk of prostate cancer in individuals with diabetes. It has also been observed that cancer patients have an increased risk of developing diabetes, highlighting that the relationship between these diseases is not straightforward. Evidence of a shared genetic aetiology along with numerous lifestyle and clinical factors have made it challenging to establish if the relationship between the two diseases is causal or a result of confounding factors. This review takes a pan-cancer approach to highlight the complexities of the interactions between type 2 diabetes and cancer development, indicating where advances in genomic research have enabled a greater insight into these two diseases.","PeriodicalId":72907,"journal":{"name":"Endocrine oncology (Bristol, England)","volume":"3 1","pages":"e220094"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1f/09/EO-22-0094.PMC10388678.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10283674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of DNA methylation in human pancreatic neuroendocrine tumours. DNA甲基化在人类胰腺神经内分泌肿瘤中的作用。

Endocrine oncology (Bristol, England) Pub Date : 2023-01-01 DOI: 10.1530/EO-23-0003

Katherine A English, Rajesh V Thakker, Kate E Lines

{"title":"The role of DNA methylation in human pancreatic neuroendocrine tumours.","authors":"Katherine A English, Rajesh V Thakker, Kate E Lines","doi":"10.1530/EO-23-0003","DOIUrl":"https://doi.org/10.1530/EO-23-0003","url":null,"abstract":"Pancreatic neuroendocrine tumours (PNETs) are the second most common pancreatic tumour. However, relatively little is known about their tumourigenic drivers, other than mutations involving the multiple endocrine neoplasia 1 (MEN1), ATRX chromatin remodeler, and death domain-associated protein genes, which are found in ~40% of sporadic PNETs. PNETs have a low mutational burden, thereby suggesting that other factors likely contribute to their development, including epigenetic regulators. One such epigenetic process, DNA methylation, silences gene transcription via 5'methylcytosine (5mC), and this is usually facilitated by DNA methyltransferase enzymes at CpG-rich areas around gene promoters. However, 5'hydroxymethylcytosine, which is the first epigenetic mark during cytosine demethylation, and opposes the function of 5mC, is associated with gene transcription, although the significance of this remains unknown, as it is indistinguishable from 5mC when conventional bisulfite conversion techniques are solely used. Advances in array-based technologies have facilitated the investigation of PNET methylomes and enabled PNETs to be clustered by methylome signatures, which has assisted in prognosis and discovery of new aberrantly regulated genes contributing to tumourigenesis. This review will discuss the biology of DNA methylation, its role in PNET development, and impact on prognostication and discovery of epigenome-targeted therapies.","PeriodicalId":72907,"journal":{"name":"Endocrine oncology (Bristol, England)","volume":"3 1","pages":"e230003"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10171998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acknowledgement to reviewers 审稿人致谢

Endocrine oncology (Bristol, England) Pub Date : 2023-01-01 DOI: 10.1530/eo-3-a1

Tahsin Ogùuz

引用次数: 0

Clinical presentation of sporadic and hereditary pheochromocytoma/paraganglioma. 散发性遗传性嗜铬细胞瘤/副神经节瘤的临床表现。

Endocrine oncology (Bristol, England) Pub Date : 2023-01-01 DOI: 10.1530/EO-22-0040

Sofia Maria Lider Burciulescu, Caren Randon, Frederic Duprez, Wouter Huvenne, David Creytens, Kathleen B M Claes, Robin de Putter, Guy T'Sjoen, Corin Badiu, Bruno Lapauw

{"title":"Clinical presentation of sporadic and hereditary pheochromocytoma/paraganglioma.","authors":"Sofia Maria Lider Burciulescu, Caren Randon, Frederic Duprez, Wouter Huvenne, David Creytens, Kathleen B M Claes, Robin de Putter, Guy T'Sjoen, Corin Badiu, Bruno Lapauw","doi":"10.1530/EO-22-0040","DOIUrl":"https://doi.org/10.1530/EO-22-0040","url":null,"abstract":"Pheochromocytomas (PHEO) and paragangliomas (PGL) can occur sporadic or within genetic predisposition syndromes. Despite shared embryology, there are important differences between PHEO and PGL. The aim of this study was to describe the clinical presentation and disease characteristics of PHEO/PGL. A retrospective analysis of consecutively registered patients diagnosed with or treated for PHEO/PGL in a tertiary care centre was performed. Patients were compared according to anatomic location (PHEO vs PGL) and genetic status (sporadic vs hereditary). In total, we identified 38 women and 29 men, aged 50 ± 19 years. Of these, 42 (63%) had PHEO, and 25 (37%) had PGL. Patients with PHEO presented more frequently with sporadic than hereditary disease (45 years vs 27 (77%) vs 8 (23%)) than patients with PGL (9 (36%) vs 16 (64%), respectively) and were older at diagnosis (55 ± 17 vs 40 ± 18 years, P = 0.001), respectively). About half of the cases in both PHEO and PGL were diagnosed due to disease-related symptoms. In patients with PHEO, tumour diameter was larger (P = 0.001), metanephrine levels higher (P = 0.02), and there was more frequently a history of cardiovascular events than in patients with PGL. In conclusion, we found that patients with PGL more frequently have a hereditary predisposition than those with PHEO, contributing to the fact that diagnosis is generally made earlier in PGL. Although diagnosis in both PHEO and PGL was mostly due to related symptoms, patients with PHEO more often presented with cardiovascular comorbidities than those with PGL which might relate to a higher number of functionally active tumours in the former.","PeriodicalId":72907,"journal":{"name":"Endocrine oncology (Bristol, England)","volume":"3 1","pages":"e220040"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9869871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0