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MicroRNAs as regulators of tumor metabolism. MicroRNAs作为肿瘤代谢的调节因子。
IF 3.9 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-08-01 DOI: 10.1530/ERC-22-0267
Francesca Ruggieri, Katharina Jonas, Manuela Ferracin, Michael Dengler, Vanessa Jӓger, Martin Pichler

Cancer cells reprogram their metabolism to support their growth. Since the discovery of the Warburg effect, several other metabolic alterations and metabolites have been described in cancer cells, including lactate, glutamine, and lipid metabolism reprogramming. Together these alterations provide rapidly dividing tumor cells with metabolic intermediates needed for nucleotide, protein, and fatty acid biosynthesis. MicroRNAs are a class of small non-coding RNAs involved in the regulation of virtually all biological pathways. Altered microRNA expression patterns are associated with the onset and development of several diseases, including cancer. Tumor suppressor microRNAs targeting molecules involved in tumor metabolism are frequently downregulated in cancers. Therefore, microRNAs can serve as potential tumor biomarkers and also represent interesting therapeutic targets. This review summarizes recent findings about microRNAs involved in the regulation of tumor metabolism.

癌细胞重新编程它们的新陈代谢来支持它们的生长。自Warburg效应发现以来,在癌细胞中已经描述了其他几种代谢改变和代谢物,包括乳酸、谷氨酰胺和脂质代谢重编程。这些改变共同为快速分裂的肿瘤细胞提供了核苷酸、蛋白质和脂肪酸生物合成所需的代谢中间体。MicroRNAs是一类小的非编码rna,参与几乎所有生物途径的调控。microRNA表达模式的改变与包括癌症在内的几种疾病的发生和发展有关。靶向肿瘤代谢分子的肿瘤抑制microrna在癌症中经常下调。因此,microRNAs可以作为潜在的肿瘤生物标志物,也代表了有趣的治疗靶点。本文综述了近年来参与肿瘤代谢调控的microrna的研究进展。
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引用次数: 0
Autophagic blockade potentiates anlotinib-mediated ferroptosis in anaplastic thyroid cancer. 自噬阻断增强了间变性甲状腺癌症中安洛替尼介导的脱铁性贫血。
IF 3.9 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-08-01 Print Date: 2023-09-01 DOI: 10.1530/ERC-23-0036
Jiajun Wu, Juyong Liang, Ruiqi Liu, Tian Lv, Kangyin Fu, Liehao Jiang, Wenli Ma, Yan Pan, Zhuo Tan, Qing Liu, Weihua Qiu, Minghua Ge, Jiafeng Wang

Anlotinib-mediated angiogenic remodeling was delineated in various tumors. Meanwhile, we previously showed that anlotinib inhibited tumor angiogenesis in anaplastic thyroid cancer (ATC). However, the potential role of anlotinib on cell lethality in ATC remains an enigma. Herein, we found that anlotinib inhibited the viability, proliferation, and migration of KHM-5M, C643, and 8505C cells in a dose-dependently manner. Under anlotinib treatment, PANoptosis (pyroptosis, apoptosis, and necroptosis) markers were not changed; however, ferroptosis targets (transferrin, HO-1, FTH1, FTL, and GPX4) were significantly downregulated. ROS levels also increased in a concentration-dependent manner after anlotinib treatment in KHM-5M, C643, and 8505C cells. In addition, protective autophagy was activated in response to anlotinib, and autophagic blockade potentiated anlotinib-mediated ferroptosis and antitumor effects in vitro and in vivo. Our new discovery identified autophagy-ferroptosis signaling pathway which provides mechanistic insight into anlotinib-mediated cell death, and synergistic combination therapy may help develop new ATC treatment strategies.

安洛替尼介导的血管生成重塑在各种肿瘤中被描述。同时,我们先前发现安洛替尼抑制间变性甲状腺癌症(ATC)中的肿瘤血管生成。然而,安洛替尼对ATC细胞致死性的潜在作用仍然是个谜。在此,我们发现安洛替尼以剂量依赖性的方式抑制KHM-5M、C643和8505C细胞的活力、增殖和迁移。在安洛替尼治疗下,PANoptosis(焦下垂、细胞凋亡和坏死)标志物没有改变;然而,脱铁靶点(转铁蛋白、HO-1、FTH1、FTL和GPX4)显著下调。安洛替尼处理KHM-5M、C643和8505C细胞后,ROS水平也以浓度依赖性方式增加。此外,对安洛替尼的反应激活了保护性自噬,自噬阻断增强了安洛替尼介导的脱铁作用和体内外抗肿瘤作用。我们的新发现确定了自噬脱铁信号通路,该通路为安洛替尼介导的细胞死亡提供了机制见解,协同联合治疗可能有助于开发新的ATC治疗策略。
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引用次数: 0
A phase II study of bevacizumab and temsirolimus in advanced extra-pancreatic neuroendocrine tumors. 贝伐单抗和替西莫司治疗晚期胰腺外神经内分泌肿瘤的II期研究。
IF 3.9 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-08-01 DOI: 10.1530/ERC-22-0301
Sonia M Abuzakhm, Vineeth Sukrithan, Briant Fruth, Rui Qin, Jonathan Strosberg, Timothy J Hobday, Thomas Semrad, Diane Reidy Lagunes, Hedy Lee Kindler, George P Kim, Jennifer J Knox, Andreas Kaubisch, Miguel Villalona-Calero, Helen Chen, Charles Erlichman, Manisha H Shah

We assessed the efficacy and safety of combining bevacizumab with temsirolimus in patients with advanced extra-pancreatic neuroendocrine tumors. This NCI-sponsored multicenter, open-label, phase II study (NCT01010126) enrolled patients with advanced, recurrent, or metastatic extra-pancreatic neuroendocrine tumors. All patients were treated with temsirolimus and bevacizumab until disease progression or unacceptable toxicity. Temsirolimus 25 mg was administered intravenously on days 1, 8, 15, and 22, and bevacizumab 10 mg/kg intravenously on days 1 and 15 of a 4-week cycle. Discontinuation of temsirolimus or bevacizumab did not require discontinuation of the other agent. The primary endpoints were objective response rate and 6-month progression-free survival rate. Fifty-nine patients were enrolled in this study, and 54 were evaluable for efficacy and adverse events. While median progression-free survival was 7.1 months, median duration of treatment with temsirolimus was 3.9 months, and with bevacizumab was 3.5 months. The objective response rate of combination therapy was 2%, and 6-month progression-free survival was 48%. The most frequently reported grade 3-4 adverse events included fatigue (13%), hypertension (13%), and bleeding (13%). Close to 54% of patients discontinued treatment due to adverse events, refusal of further treatment, or treatment delays. Three deaths occurred on study, with 2 treatment-related fatal bowel perforations. Given the minimal efficacy and increased toxicity seen with the combination of bevacizumab and temsirolimus, we do not recommend the use of this regimen in patients with advanced extra-pancreatic neuroendocrine tumors.

我们评估了贝伐单抗联合替西莫司治疗晚期胰腺外神经内分泌肿瘤患者的疗效和安全性。这项nci赞助的多中心、开放标签、II期研究(NCT01010126)招募了晚期、复发或转移性胰腺外神经内分泌肿瘤患者。所有患者均接受替西莫司和贝伐单抗治疗,直到疾病进展或不可接受的毒性。替西莫司25mg在第1、8、15和22天静脉注射,贝伐单抗10mg /kg在4周周期的第1和15天静脉注射。停用替西莫司或贝伐单抗不需要停用另一种药物。主要终点为客观缓解率和6个月无进展生存率。59名患者参加了这项研究,其中54名患者的疗效和不良事件可评估。中位无进展生存期为7.1个月,替西莫司治疗的中位持续时间为3.9个月,贝伐单抗治疗的中位持续时间为3.5个月。联合治疗的客观有效率为2%,6个月无进展生存率为48%。最常见的3-4级不良事件包括疲劳(13%)、高血压(13%)和出血(13%)。近54%的患者因不良事件、拒绝进一步治疗或治疗延误而停止治疗。研究中发生3例死亡,2例与治疗相关的致命性肠穿孔。考虑到贝伐单抗和替西莫司联合使用的最小疗效和增加的毒性,我们不推荐在晚期胰腺外神经内分泌肿瘤患者中使用该方案。
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引用次数: 0
Papillary thyroid cancer immune phenotypes via tumor-infiltrating lymphocyte spatial analysis. 通过肿瘤浸润淋巴细胞空间分析的乳头状甲状腺癌症免疫表型。
IF 3.9 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-07-28 Print Date: 2023-09-01 DOI: 10.1530/ERC-23-0110
Myungwoo Nam, Woojung Yang, Hye Sung Kim, Jewel Park, Gahee Park, Sukjun Kim, Sanghoon Song, Chan-Young Ock, Victor G Wang, Jeffrey H Chuang, Young Kwang Chae

Standard-of-care treatment options provide an excellent prognosis for papillary thyroid cancers (PTCs); however, approximately 10% of cases are advanced PTCs, resulting in less than 50% 5-year survival rates. Understanding the tumor microenvironment is essential for understanding cancer progression and investigating potential biomarkers for treatment, such as immunotherapy. Our study focused on tumor-infiltrating lymphocytes (TILs), which are the main effectors of antitumor immunity and related to the mechanism of immunotherapy. Using an artificial intelligence model, we analyzed the density of intratumoral and peritumoral TILs in the pathologic slides of The Cancer Genome Atlas PTC cohort. Tumors were classified into three immune phenotypes (IPs) based on the spatial distribution of TILs: immune-desert (48%), immune-excluded (34%), and inflamed (18%). Immune-desert IP was mostly characterized by RAS mutations, high thyroid differentiation score, and low antitumor immune response. Immune-excluded IP predominantly consisted of BRAF V600E-mutated tumors and had a higher rate of lymph node metastasis. Inflamed IP was characterized by a high antitumor immune response, as demonstrated by a high cytolytic score, immune-related cell infiltrations, expression of immunomodulatory molecules (including immunotherapy target molecules), and enrichment of immune-related pathways. This study is the first to investigate IP classification using TILs in PTC through a tissue-based approach. Each IP had unique immune and genomic profiles. Further studies are warranted to assess the predictive value of IP classification in advanced PTC patients treated with immunotherapy.

标准护理治疗方案为甲状腺乳头状癌(PTC)提供了良好的预后;然而,大约10%的病例是晚期PTC,导致5年生存率低于50%。了解肿瘤微环境对于了解癌症进展和研究潜在的治疗生物标志物(如免疫疗法)至关重要。我们的研究重点是肿瘤浸润淋巴细胞(TILs),它是抗肿瘤免疫的主要效应物,并与免疫治疗机制有关。使用人工智能模型,我们分析了癌症基因组图谱PTC队列病理切片中肿瘤内和肿瘤周围TIL的密度。根据TIL的空间分布,肿瘤被分为三种免疫表型(IP):免疫沙漠(48%)、免疫排斥(34%)和炎症(18%)。免疫沙漠IP的主要特征是RAS突变、甲状腺分化评分高和抗肿瘤免疫反应低。免疫排斥性IP主要由BRAF V600E突变肿瘤组成,淋巴结转移率较高。炎症IP的特征是高抗肿瘤免疫反应,表现为高细胞溶解评分、免疫相关细胞浸润、免疫调节分子(包括免疫治疗靶分子)的表达和免疫相关途径的富集。本研究首次通过基于组织的方法研究PTC中使用TIL的IP分类。每个IP都有独特的免疫和基因组图谱。需要进一步的研究来评估IP分类对接受免疫治疗的晚期PTC患者的预测价值。
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引用次数: 0
Deregulated kinase action in prostate cancer: molecular basis and therapeutic implications. 前列腺癌症中激酶作用的失调:分子基础和治疗意义。
IF 4.1 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-07-26 Print Date: 2023-09-01 DOI: 10.1530/ERC-23-0011
Nidhi Singh, Hannelore V Heemers

Prostate cancer (CaP) remains the second leading cause of cancer-related mortality in American men. Systemic treatments for metastatic CaP, which causes the majority of deaths, include androgen deprivation therapy and chemotherapy. These treatments induce remissions but do not cure CaP. Novel and functionally diverse therapeutic targets that control the cell biology that drives aggressive CaP progression are needed to overcome treatment resistance. Because signal transduction that mediates CaP cell behavior is tightly regulated by phosphorylation, kinases have attracted interest as alternative targets for CaP treatments. Here, we examine emerging evidence from recent NextGen sequencing and (phospho) proteomics analyses on clinical CaP specimens that were obtained during lethal disease progression to determine the role of deregulated kinase action in CaP growth, treatment resistance, and recurrence. We provide an overview of kinases that are impacted by gene amplification, gene deletion or somatic mutations during the progression from localized treatment-naïve CaP to metastatic castration-resistant CaP or neuroendocrine CaP, and the potential impact of such alterations on aggressive CaP behavior and treatment efficacy. Furthermore, we review knowledge on alterations in the phosphoproteome that occur during the progression to treatment-resistant CaP, the molecular mechanisms in the control of these changes, and the signal transduction associated with them. Finally, we discuss kinase inhibitors under evaluation in CaP clinical trials and the potential, challenges, and limitations to moving knowledge on the CaP kinome forward to new therapeutic strategies.

癌症(CaP)仍然是美国男性癌症相关死亡率的第二大原因。导致大多数死亡的转移性前列腺癌的系统治疗包括雄激素剥夺治疗和化疗。这些治疗可诱导缓解,但不能治愈CaP。需要新的、功能多样的治疗靶点来控制驱动CaP侵袭性进展的细胞生物学,以克服治疗耐药性。由于介导CaP细胞行为的信号转导受到磷酸化的严格调节,激酶作为CaP治疗的替代靶点引起了人们的兴趣。在这里,我们检查了最近对致命疾病进展过程中获得的临床CaP样本进行的NextGen测序和(磷酸)蛋白质组学分析的新证据,以确定失调激酶作用在CaP生长、治疗耐药性和复发中的作用。我们概述了在从局部治疗幼稚型前列腺癌进展为转移性去势抵抗型前列腺癌或神经内分泌型前列腺癌的过程中,受基因扩增、基因缺失或体细胞突变影响的激酶,以及这种改变对侵袭性前列腺癌行为和治疗效果的潜在影响。此外,我们还回顾了在向耐治疗CaP发展过程中发生的磷酸蛋白质组改变、控制这些变化的分子机制以及与之相关的信号转导的知识。最后,我们讨论了CaP临床试验中正在评估的激酶抑制剂,以及将CaP激酶组知识推向新的治疗策略的潜力、挑战和局限性。
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引用次数: 0
Pathological features in non-neoplastic congenital and adult hyperinsulinism: from nesidioblastosis to current terminology and understanding. 非肿瘤性先天性和成人高胰岛素血症的病理特征:从无细胞母细胞增生到目前的术语和理解。
IF 3.9 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-07-26 Print Date: 2023-09-01 DOI: 10.1530/ERC-23-0034
Christine Sempoux, Gunter Klöppel

Nesidioblastoma and nesidioblastosis were terms given to neoplastic and non-neoplastic lesions of the pancreas associated with pancreatogenous hyperinsulinaemic hypoglycaemia. While nesidioblastoma was rapidly replaced by islet cell tumour, nesidioblastosis, defined as the proliferation of islet cells budding off from pancreatic ducts, was the diagnostic term associated with congenital hyperinsulinism of infancy (CHI) and adult non-neoplastic hyperinsulinaemic hypoglycaemia (ANHH). When it was shown that nesidioblastosis was not specific for CHI or ANHH, it was no longer applied to CHI but kept for the morphological diagnosis of ANHH. In severe CHI cases, a diffuse form with hypertrophic ß-cells in all islets can be distinguished from a focal form with hyperactive ß-cells changes in a limited adenomatoid hyperplastic area. Genetically, mutations were identified in several ß-cell genes involved in insulin secretion. Most common are mutations in the ABCC8 or KCNJ11 genes, solely affected in the diffuse form and associated with a focal maternal allelic loss on 11p15.5 in the focal form. Focal CHI can be localized by 18F-DOPA-PET and is thus curable by targeted resection. Diffuse CHI that fails medical treatment requires subtotal pancreatectomy. In ANHH, an idiopathic form can be distinguished from a form associated with gastric bypass, in whom GLP1-induced stimulation of the ß-cells is discussed. While the ß-cells in idiopathic ANHH are diffusely affected and are either hypertrophic or show only little changes, it is controversial whether there is a ß-cell increase or ß-cell hyperactivity in patients with gastric bypass. Recognizing morphological signs of ß-cell hyperactivity needs a good knowledge of the non-neoplastic endocrine pancreas across all ages.

nesidioblastomas和nesidiobastosis是指与胰源性高胰岛素血症低血糖相关的胰腺肿瘤性和非肿瘤性病变。虽然神经母细胞瘤很快被胰岛细胞瘤所取代,但神经母细胞增多症(定义为从胰管出芽的胰岛细胞增殖)是与婴儿期先天性高胰岛素血症(CHI)和成人非肿瘤性高胰岛素低血糖症(ANHH)相关的诊断术语。当发现无胚母细胞增生对CHI或ANHH没有特异性时,它不再适用于CHI,而是保留用于ANHH的形态学诊断。在严重的CHI病例中,所有胰岛中弥漫性肥大的ß细胞可以与局限性腺瘤样增生区域中过度活跃的223细胞变化的局灶性形式区分开来。从遗传学角度来看,在参与胰岛素分泌的几个ß细胞基因中发现了突变。最常见的是ABCC8或KCNJ11基因的突变,仅以弥漫形式受到影响,并与局灶形式11p15.5的局灶性母体等位基因缺失有关。局灶性CHI可通过18F-DOPA-PET定位,因此可通过靶向切除治愈。药物治疗失败的弥漫性CHI需要进行胰次全切除术。在ANHH中,特发性形式可以与胃旁路相关的形式区分开来,在胃旁路中讨论了GLP1诱导的对ß-细胞的刺激。虽然特发性ANHH中的ß-细胞受到广泛影响,要么肥大,要么变化很小,但胃旁路移植患者中是否存在ß;细胞增加或ß-细胞过度活跃仍存在争议。识别ß-细胞过度活跃的形态学迹象需要对所有年龄段的非肿瘤内分泌胰腺有很好的了解。
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引用次数: 1
Interleukin-6 promotes the dedifferentiation of papillary thyroid cancer cells. 白细胞介素-6促进甲状腺乳头状癌症细胞的去分化。
IF 3.9 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-07-25 Print Date: 2023-09-01 DOI: 10.1530/ERC-23-0130
Guo-Qiang Zhang, Chuang Xi, Chen-Tian Shen, Hong-Jun Song, Quan-Yong Luo, Zhong-Ling Qiu

Radioiodine treatment is a fundamental therapy for patients with papillary thyroid cancer (PTC). Sodium/iodide symporter (NIS)-mediated iodine uptake is a prerequisite for the efficacy of radioiodine therapy. Interleukin-6 (IL-6) is a pro-tumor cytokine, but its regulation of NIS expression in PTC has not been elucidated. In this study, we found that IL-6 enhanced the proliferation ability of PTC cells. Moreover, the negative association between IL-6 and NIS expression in thyroid cancer tissues was demonstrated. IL-6 downregulated thyroid-specific genes such as NIS, thyroid peroxidase, and thyroid-stimulating hormone receptor and thyroid-specific transcription factors including thyroid transcription factor-1 (TTF-1) and paired box protein-8 (PAX-8). The inhibitory effects of IL-6 on NIS expression were alleviated by mitogen-activated protein kinase and Janus kinase inhibitors. Depletion of c-Jun or STAT3 also rescued IL-6-induced NIS downregulation, with STAT3 depletion exerting a stronger effect. TTF-1 protein expression was also restored by depleting c-Jun or STAT3. STAT3 depletion, but not c-Jun depletion, alleviated the inhibitory effect of IL-6 on PAX-8 expression. Moreover, the downregulation of NIS by IL-6 was rescued by overexpressing TTF-1 and PAX-8. Tocilizumab, an IL-6 receptor blocker, did not have any cytostatic activity in PTC cells, and it also failed to induce redifferentiation in vitro. However, we found that the drug blocked the inhibitory effect of IL-6 on NIS expression. In summary, IL-6 inhibits NIS transcription in PTC cells by activating mitogen-activated protein kinase and Janus kinase signaling.

放射性碘治疗是癌症(PTC)患者的基本治疗方法。钠/碘转运体(NIS)介导的碘摄取是放射性碘治疗效果的先决条件。白细胞介素-6(IL-6)是一种促肿瘤细胞因子,但其对PTC中NIS表达的调节尚未阐明。在本研究中,我们发现IL-6增强了PTC细胞的增殖能力。此外,在甲状腺癌症组织中,IL-6和NIS表达之间的负相关性被证明。IL-6下调甲状腺特异性基因,如NIS、甲状腺过氧化物酶和促甲状腺激素受体,以及甲状腺特异性转录因子,包括甲状腺转录因子-1(TTF-1)和配对盒蛋白-8(PAX-8)。丝裂原活化蛋白激酶和Janus激酶抑制剂减轻了IL-6对NIS表达的抑制作用。c-Jun或STAT3的耗竭也挽救了IL-6诱导的NIS下调,STAT3耗竭发挥了更强的作用。TTF-1蛋白表达也通过消耗c-Jun或STAT3而恢复。STAT3缺失,而不是c-Jun缺失,减轻了IL-6对PAX-8表达的抑制作用。此外,IL-6对NIS的下调通过过表达TTF-1和PAX-8而得到挽救。托奇利珠单抗是一种IL-6受体阻滞剂,在PTC细胞中没有任何细胞抑制活性,在体外也未能诱导再分化。然而,我们发现该药物阻断了IL-6对NIS表达的抑制作用。总之,IL-6通过激活丝裂原活化蛋白激酶和Janus激酶信号传导来抑制PTC细胞中的NIS转录。
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引用次数: 0
Prostate cancer and bone: clinical presentation and molecular mechanisms. 前列腺癌与骨:临床表现和分子机制。
IF 3.9 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-07-25 Print Date: 2023-09-01 DOI: 10.1530/ERC-22-0360
Kristina V Wells, Margaret L Krackeler, Maitreyee K Jathal, Mamta Parikh, Paramita M Ghosh, J Kent Leach, Damian C Genetos

Prostate cancer (PCa) is an increasingly prevalent health problem in the developed world. Effective treatment options exist for localized PCa, but metastatic PCa has fewer treatment options and shorter patient survival. PCa and bone health are strongly entwined, as PCa commonly metastasizes to the skeleton. Since androgen receptor signaling drives PCa growth, androgen-deprivation therapy whose sequelae reduce bone strength constitutes the foundation of advanced PCa treatment. The homeostatic process of bone remodeling - produced by concerted actions of bone-building osteoblasts, bone-resorbing osteoclasts, and regulatory osteocytes - may also be subverted by PCa to promote metastatic growth. Mechanisms driving skeletal development and homeostasis, such as regional hypoxia or matrix-embedded growth factors, may be subjugated by bone metastatic PCa. In this way, the biology that sustains bone is integrated into adaptive mechanisms for the growth and survival of PCa in bone. Skeletally metastatic PCa is difficult to investigate due to the entwined nature of bone biology and cancer biology. Herein, we survey PCa from origin, presentation, and clinical treatment to bone composition and structure and molecular mediators of PCa metastasis to bone. Our intent is to quickly yet effectively reduce barriers to team science across multiple disciplines that focuses on PCa and metastatic bone disease. We also introduce concepts of tissue engineering as a novel perspective to model, capture, and study complex cancer-microenvironment interactions.

前列腺癌(PCa)是发达国家日益普遍的健康问题。局部前列腺癌有有效的治疗方案,但转移性前列腺癌的治疗方案较少,患者生存期较短。前列腺癌与骨骼健康紧密相连,因为前列腺癌通常转移到骨骼。由于雄激素受体信号驱动前列腺癌的生长,雄激素剥夺疗法(其后遗症是降低骨强度)是晚期前列腺癌治疗的基础。骨重塑的稳态过程——由造骨成骨细胞、骨吸收破骨细胞和调节性骨细胞协同作用产生——也可能被PCa破坏,促进转移性生长。驱动骨骼发育和体内平衡的机制,如局部缺氧或基质嵌入生长因子,可能被骨转移性前列腺癌所抑制。通过这种方式,维持骨骼的生物学被整合到骨骼中PCa生长和存活的适应机制中。由于骨生物学和癌症生物学的相互交织,骨转移性前列腺癌很难研究。在此,我们从PCa的起源、表现、临床治疗到骨组成和结构以及PCa转移到骨的分子介质进行了调查。我们的目的是快速而有效地减少跨多学科的团队科学障碍,专注于PCa和转移性骨病。我们还介绍了组织工程的概念,作为一个新的视角来建模,捕获和研究复杂的癌症微环境相互作用。
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引用次数: 0
Glucagon cell hyperplasia and neoplasia: a recently recognized endocrine receptor disease. 胰高血糖素细胞增生和肿瘤:一种最近发现的内分泌受体疾病。
IF 3.9 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-07-18 Print Date: 2023-08-01 DOI: 10.1530/ERC-23-0032
Bence Sipos, Gunter Klöppel

Glucagon cell hyperplasia and neoplasia (GCHN) is the name of an endocrine receptor disease, whose morphology was first described in 2006. Three years later, this rare disease was found to be to be caused by an inactivating mutation of the glucagon receptor (GCGR) gene. Functionally, the genetic defect mainly affects glucagon signaling in the liver with changes in the metabolism of glycogen, fatty acids and amino acids. Recent results of several studies in GCGR knockout mice suggested that elevated serum amino acid levels probably stimulate glucagon cell hyperplasia with subsequent transformation into glucagon cell neoplasia. This process leads over time to numerous small and some large pancreatic neuroendocrine tumors which are potentially malignant. Despite high glucagon serum levels, the patients develop no glucagonoma syndrome. In 2015, GCHN was identified as an autosomal recessive hereditary disorder.

胰高血糖素细胞增生和肿瘤(GCHN)是一种内分泌受体疾病的名称,其形态学于2006年首次被描述。三年后,这种罕见的疾病被发现是由胰高血糖素受体(GCGR)基因的失活突变引起的。从功能上讲,遗传缺陷主要影响肝脏中的胰高血糖素信号传导,并改变糖原、脂肪酸和氨基酸的代谢。最近对GCGR敲除小鼠的几项研究结果表明,血清氨基酸水平升高可能刺激胰高血糖素细胞增生,随后转化为胰高血糖蛋白细胞瘤变。随着时间的推移,这个过程会导致许多小的和一些大的胰腺神经内分泌肿瘤,这些肿瘤具有潜在的恶性。尽管胰高血糖素血清水平较高,但患者未出现胰高血糖素瘤综合征。2015年,GCHN被鉴定为一种常染色体隐性遗传性疾病。
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引用次数: 0
Expert Consensus Practice Recommendations of the North American Neuroendocrine Tumor Society for the management of high grade gastroenteropancreatic and gynecologic neuroendocrine neoplasms. 北美神经内分泌肿瘤学会关于治疗高级别胃肠胰腺和妇科神经内分泌肿瘤的专家共识实践建议。
IF 4.1 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-07-11 Print Date: 2023-08-01 DOI: 10.1530/ERC-22-0206
Jennifer R Eads, Thorvardur R Halfdanarson, Tim Asmis, Andrew M Bellizzi, Emily K Bergsland, Arvind Dasari, Ghassan El-Haddad, Michael Frumovitz, Joshua Meyer, Erik Mittra, Sten Myrehaug, Eric Nakakura, Nitya Raj, Heloisa P Soares, Brian Untch, Namrata Vijayvergia, Jennifer A Chan

High-grade neuroendocrine neoplasms are a rare disease entity and account for approximately 10% of all neuroendocrine neoplasms. Because of their rarity, there is an overall lack of prospectively collected data available to advise practitioners as to how best to manage these patients. As a result, best practices are largely based on expert opinion. Recently, a distinction was made between well-differentiated high-grade (G3) neuroendocrine tumors and poorly differentiated neuroendocrine carcinomas, and with this, pathologic details, appropriate imaging practices and treatment have become more complex. In an effort to provide practitioners with the best guidance for the management of patients with high-grade neuroendocrine neoplasms of the gastrointestinal tract, pancreas, and gynecologic system, the North American Neuroendocrine Tumor Society convened a panel of experts to develop a set of recommendations and a treatment algorithm that may be used by practitioners for the care of these patients. Here, we provide consensus recommendations from the panel on pathology, imaging practices, management of localized disease, management of metastatic disease and surveillance and draw key distinctions as to the approach that should be utilized in patients with well-differentiated G3 neuroendocrine tumors vs poorly differentiated neuroendocrine carcinomas.

高级别神经内分泌肿瘤是一种罕见疾病,约占所有神经内分泌肿瘤的 10%。由于其罕见性,目前总体上缺乏前瞻性收集的数据,无法就如何最好地管理这些患者向从业人员提供建议。因此,最佳治疗方法主要基于专家意见。最近,分化良好的高级别(G3)神经内分泌肿瘤和分化不良的神经内分泌癌被区分开来,病理细节、适当的影像学检查和治疗方法也随之变得更加复杂。为了给从业人员提供治疗胃肠道、胰腺和妇科系统高级别神经内分泌肿瘤患者的最佳指导,北美神经内分泌肿瘤学会召集了一个专家小组,以制定一套建议和治疗算法,供从业人员用于这些患者的治疗。在此,我们就病理学、影像学实践、局部疾病的治疗、转移性疾病的治疗和监测等方面提出了专家小组的共识建议,并就分化良好的 G3 神经内分泌肿瘤患者与分化不良的神经内分泌癌患者应采用的治疗方法进行了重点区分。
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Endocrine-related cancer
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