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Objective: To construct a CT-based diagnostic nomogram for distinguishing grade 3 pancreatic neuroendocrine tumors (G3 PNETs) from pancreatic ductal adenocarcinomas (PDACs) and assess their respective survival outcomes. Methods: Patients diagnosed with G3 PNETs (n = 30) and PDACs (n = 78) through surgery or biopsy from two medical centers were retrospectively identified. Demographic and radiological information, including age, gender, tumor diameter, shape, margin, dilatation of pancreatic duct, and invasive behavior, were carefully collected. A nomogram was established after univariate and multivariate logistic regression analyses. The Kaplan-Meier survival was performed to analyze their survival outcomes. Results: Factors with a p-value <0.05, including age, CA 19-9, pancreatic duct dilatation, irregular shape, ill-defined margin, pancreatic atrophy, combined pancreatitis, arterial/portal enhancement ratio, were included in the multivariate logistic analysis. The independent predictive factors, including age (OR, 0.91; 95% CI, 0.85-0.98), pancreatic duct dilatation (OR, 0.064; 95% CI, 0.01-0.32), and portal enhancement ratio (OR, 1,178.08; 95% CI, 5.96-232,681.2) were determined to develop a nomogram. The internal calibration curve and decision curve analysis demonstrate that the nomogram exhibits good consistency and discriminative capacity in distinguishing G3 PNETs from PDACs. Patients diagnosed with G3 PNETs exhibited considerably better overall survival outcomes compared to those diagnosed with PDACs (median survival months, 42 vs. 9 months, p < 0.001). Conclusions: The nomogram model based on age, pancreatic duct dilatation, and portal enhancement ratio demonstrates good accuracy and discriminative ability effectively predicting the probability of G3 PNETs from PDACs. Furthermore, patients with G3 PNETs exhibit better prognosis than PDACs.

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Introduction: Insulinomas are rare, usually sporadic, and typically benign pancreatic neuroendocrine tumours. Pre-operative localization is challenging and evidence on comparative analysis of anatomic and scintigraphic modalities for pre-operative tumour localization is limited, even in contemporary series. Methods: The current study was designed to study the clinical features and management challenges of insulinomas managed at a tertiary care centre. Clinical features, diagnosis, imaging techniques, surgical procedures, and outcomes details were collated. Pre-operative imaging techniques (CT/MRI, nuclear scintigraphy) were compared with intraoperative and histopathological findings to assess their accuracy of localization. Results: Thirty-seven patients (15 females [42%]; median age 36 years [IQR 28-49]) were included in the study. In four patients (10.8%), the tumour occurred in the setting of multiple endocrine neoplasia type 1 (MEN 1) while the remaining were sporadic. The sensitivity of pre-operative localization was 61.5% (multiphasic CT), 66.6% (multiphasic MRI), 100% (68Ga Exendin-4 PET-CT), and 91.6% (EUS). Three patients with normal multiphasic CT had localization on 68Ga Exendin-4 PET-CT. The positive predictive value (PPV) of both Exendin-PET-CT and EUS was similar at 91.6% and 91.6%, respectively. All patients (except one with nesidioblastosis), who underwent enucleation or partial pancreatic resection, were cured. Conclusion: 68Ga Exendin-4 PET-CT based is a non-invasive imaging modality that has high sensitivity and PPV and can be used as a first-line imaging modality. The overall prognosis of these tumours is good with high cure rates attained following surgical resection.

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PURPOSE: Accurate identification of lymph node (LN) metastases is pivotal for surgical planning of pancreatic neuroendocrine tumours (PanNETs); however, current imaging techniques have sub-optimal diagnostic sensitivity. Aim of this study is to investigate whether [68Ga]Ga-DOTATOC PET radiomics might improve the identification of LN metastases in patients with non-functioning PanNET (NF-PanNET) referred to surgical intervention. METHODS: Seventy-two patients who performed preoperative [68Ga]Ga-DOTATOC PET between December 2017 and March 2022 for NF-PanNET. [68Ga]Ga-DOTATOC PET qualitative assessment of LN metastases was measured using diagnostic balanced accuracy (bACC), sensitivity (SN), specificity (SP), positive and negative predictive values (PPV, NPV). SUVmax, SUVmean, Somatostatin receptor density (SRD), total lesion SRD (TLSRD) and IBSI-compliant radiomic features (RFs) were obtained from the primary tumours. To predict LN involvement, these parameters were engineered, selected and used to train different machine learning models. Models were validated using tenfold repeated cross-validation and control models were developed. Models' bACC, SN, SP, PPV and NPV were collected and compared (Kruskal-Wallis, Mann-Whitney). RESULTS: LN metastases were detected in 29/72 patients at histology. [68Ga]Ga-DOTATOC PET qualitative examination of LN involvement provided bACC = 60%, SN = 24%, SP = 95%, PPV = 78% and NPV = 65%. The best-performing radiomic model provided a bACC = 70%, SN = 77%, SP = 61%, PPV = 60% and NPV = 83% (outperforming the control model, p < 0.05*). CONCLUSION: In this study, [68Ga]Ga-DOTATOC PET radiomics allowed to increase diagnostic sensitivity in detecting LN metastases from 24 to 77% in NF-PanNET patients candidate to surgery. Especially in case of micrometastatic involvement, this approach might assist clinicians in a better patients' stratification.

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BACKGROUND: While many pancreatic neuroendocrine tumours (PanNET) show indolent behaviour, predicting the biological behaviour of small nonfunctional PanNETs remains a challenge. Nonfunctional PanNETs with an epigenome and transcriptome that resemble islet alpha cells (ARX-positive) are more aggressive than neoplasms that resemble islet beta cells (PDX1-positive). In this study, we explore the ability of immunohistochemistry for ARX and PDX1 and telomere-specific fluorescence in situ hybridisation (FISH) for alternative lengthening of telomeres (ALT) to predict recurrence. METHODS: Two hundred fifty-six patients with PanNETs were identified, and immunohistochemistry for ARX and PDX1 was performed. Positive staining was defined as strong nuclear staining in >5% of tumour cells. FISH for ALT was performed in a subset of cases. RESULTS: ARX reactivity correlated with worse disease-free survival (DFS) (P = 0.011), while there was no correlation between PDX1 reactivity and DFS (P = 0.52). ALT-positive tumours (n = 63, 31.8%) showed a significantly lower DFS (P < 0.0001) than ALT-negative tumours (n = 135, 68.2%). ARX reactivity correlated with ALT positivity (P < 0.0001). Among nonfunctional tumours, recurrence was noted in 18.5% (30/162) of ARX-positive tumours and 7.5% (5/67) of ARX-negative tumours. Among WHO grade 1 and 2 PanNETs with ≤2 cm tumour size, 14% (6/43) of ARX-positive tumours recurred compared to 0 of 33 ARX-negative tumours and 33.3% (3/9) ALT-positive tumours showed recurrence versus 4.4% (2/45) ALT-negative tumours. CONCLUSION: Immunohistochemistry for ARX and ALT FISH status may aid in distinguishing biologically indolent cases from aggressive small low-grade PanNETs, and help to identify patients who may preferentially benefit from surgical intervention.

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Ectopic adrenocorticotropic hormone secretion (EAS) from the pancreatic neuroendocrine tumour (PNET) is rare, aggressive, and challenging to treat. We hereby present a rare case of EAS from PNET presenting with Cushing syndrome diagnosed with endoscopic ultrasound-guided fine-needle aspiration cytology. This case highlights the advanced presentation of EAS from PNET with poor clinical correlation of hypercortisolism and the grade of PNET.

A secreção ectópica de hormona adrenocorticotrópica (SEA) por tumores neuroendócrinos pancreáticos (TNE-P) é rara, agressiva e difícil de tratar. Apresentamos um caso raro de SEA por TNE-P apresentando-se com síndroma de Cushing, diagnosticado através de ecoendoscopia com punção aspirativa com agulha fina. Este caso enfatiza a apresentação avançada dos TNE-P com SEA e a correlação baixa com o grau de hipercortisolismo e o grau do TNE-P.

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Background: Insulinoma is a rare type of pancreatic neuroendocrine tumor with low incidence and low-malignant features. While very few insulinomas present with malignant behaviours, such as lymph node and liver metastasis, only a few studies have focused on this field owing to the limitation of samples. Existing evidence suggests that metastatic insulinoma largely derive from non-functional pancreatic neuroendocrine tumor. However, we found a portion of metastatic insulinomas may derive from non-metastatic insulinomas and explored their clinicopathological signatures and genetic characteristics. Methods: Four metastatic insulinoma patients with synchronous liver metastasis or lymph node metastasis at the Peking Union Medical College Hospital between October 2016 and December 2018 were enrolled, and whole exon and genome sequencing were performed on fresh frozen tissues and peripheral blood samples. Clinicopathological information and genomic sequencing results were collected and matched to explore the characteristics of the metastatic insulinomas. Results: These four metastatic insulinoma patients underwent surgery or interventional therapy, and their blood glucose levels immediately increased and maintained within standard range after treatment. For these four patients, the proinsulin/insulin molar ratio <1 and primary tumors were all present as PDX1+, ARX-, and insulin+, which were similar to non-metastatic insulinomas. However, the liver metastasis showed PDX1+ and ARX+, insulin+. Meanwhile, genomic sequencing data showed no recurrently mutations and typical CNV patterns. However, one patient harboured the YY1 T372R mutation, a recurrently mutated gene in non-metastatic insulinomas. Conclusions: A portion of metastatic insulinomas were largely derived from non-metastatic insulinomas in hormone secretion and ARX/PDX1 expression patterns. Meanwhile, the accumulation of ARX expression may be involved in the progression of metastatic insulinomas.

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Background: Splanchnic vein thrombosis due to co-existing metastatic pancreatic neuroendocrine tumour (pNET) and JAK2V617F mutation is a rare condition. Case report: Here we present a case of a young woman with complete remission of a non-functioning grade 2 pNET with unresectable liver metastases, coexisting with JAK2V617F mutation. Splenectomy and distal pancreatectomy were performed. Neither surgical removal, nor radiofrequency ablation of the liver metastases was possible. Therefore, somatostatin analogue (SSA) and enoxaparine were started. Peptide receptor radionuclide therapy (PRRT) was given in 3 cycles 6-8 weeks apart. Genetic testing revealed no multiple endocrine neoplasia type 1 (MEN-1) gene mutations. After shared decision making with the patient, she gave birth to two healthy children, currently 2 and 4 years old. On pregnancy confirmation, SSA treatment was interrupted and resumed after each delivery. Ten years after the diagnosis of pNET, no tumour is detectable by MRI or somatostatin receptor scintigraphy. PRRT followed by continuous SSA therapy, interrupted only during pregnancies, resulted in complete remission and enabled the patient to complete two successful pregnancies.

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Non-functioning pancreatic neuroendocrine tumours (NF-pNETs) are potentially malignant neoplasms that are detected with increasing frequency. The management of small (≤ 2 cm) asymptomatic NF-pNETs remains an area of controversy and clinical dilemma. Follow-up seems to be a reasonable strategy because of the relatively limited metastatic potential of these tumours, the good clinical prognosis, and considering the high complication rate associated with surgery. However, some studies show metastatic potential of these tumours, fuelling an ongoing debate in the literature regarding their management. Making the decision to observe or perform surgery is thus not an easy task. New, promising therapeutic methods involving ablation under endoscopic ultrasound (EUS) guidance with ethanol or radiofrequency ablation have been applied for these lesions with good clinical outcomes but only with short-term follow-up data. In this review, we address the emerging question of when to follow-up and when to perform surgery for small asymptomatic pancreatic tumours, with consideration of the potential of ablative therapies.

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ATRX is a chromatin remodeller that maintains telomere homeostasis. Loss of ATRX is described in approximately 10% of pancreatic neuroendocrine tumours (PanNETs) and associated with poorer prognostic features. Here, we present a genetically engineered mouse model (GEMM) addressing the role of Atrx loss (AtrxKO) in pancreatic ß cells, evaluating a large cohort of ageing mice (for up to 24 months (mo.)). Atrx loss did not cause PanNET formation but rather resulted in worsening of ageing-related pancreatic inflammation and endocrine dysfunction in the first year of life. Histopathological evaluation highlighted an exacerbated prevalence and intensity of pancreatic inflammation, ageing features, and hepatic steatosis in AtrxKO mice. Homozygous floxed mice presented hyperglycaemia, increased weights, and glucose intolerance after 6 months, but alterations in insulinaemia were not detected. Floxed individuals presented an improper growth of their pancreatic endocrine fraction that may explain such an endocrine imbalance. A pilot study of BRACO-19 administration to AtrxKO mice resulted in telomere instability, reinforcing the involvement of Atrx in the maintenance of ß cell telomere homeostasis. Thereby, a non-obese dysglycaemic GEMM of disrupted Atrx is here presented as potentially useful for metabolic studies and putative candidate for inserting additional tumourigenic genetic events.

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Pancreatic neuroendocrine tumours (NETs) are currently graded using the World Health Organization (WHO) 2019 system, which is based solely on mitotic count and Ki-67 proliferative index. Although necrosis is a well recognised adverse prognostic feature that is included in the grading systems of NETs of certain types such as pulmonary carcinoid and medullary thyroid carcinoma, there is currently insufficient evidence to support its inclusion in the grading of pancreatic NETs. Therefore, we sought to investigate the prognostic significance of tumour necrosis in our cohort of resected pancreatic NETs, with a view to providing evidence to support its incorporation into the WHO grading scheme. Under our proposal, pancreatic NETs without necrosis would continue to be graded based solely on mitotic count and Ki-67 index using the established WHO cut-offs, while NETs with tumour necrosis would be classified as grade 3, irrespective of proliferative activity. Using this system in our cohort of 110 resected pancreatic NETs, overall survival (OS) was 250, 198, and 151 months (p=0.039) and disease-free survival (DFS) was 180 months, 117 months, and 38 months (p<0.0001) for grades 1, 2, and 3, respectively. In contrast, there was no significant difference in OS (p=0.231) or DFS (p=0.058) between low grade (grade 1) and intermediate-high grade (grade 2/3) tumours using the current WHO system which does not consider necrosis. Interobserver concordance for assessment of necrosis was excellent. In conclusion, necrosis is an independent predictor of OS and DFS for pancreatic NETs, and our findings strongly support its addition to the grading scheme for this tumour.

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BACKGROUND: Nonfunctional pancreatic neuroendocrine tumours are difficult to diagnose in the early stage of disease due to a lack of clinical symptoms, but they can rarely manifest as autoimmune pancreatitis. Autoimmune pancreatitis is an uncommon disease that may cause recurrent acute pancreatitis and is therefore often regarded as a special type of chronic pancreatitis. CASE SUMMARY: We report a case of a 42-year-old female who had nonspecific upper abdominal pain for 4 years and radiological abnormalities of the pancreas that mimicked autoimmune pancreatitis. The symptoms and pancreatic imaging did not improve following 1 year of steroid therapy. Finally, pancreatic biopsy was performed through endoscopic ultrasonography-guided fine-needle aspiration biopsy, and nonfunctional pancreatic neuroendocrine tumours were ultimately diagnosed. Pancreatectomy has resolved her symptoms. CONCLUSION: Therefore, the differentiation of nonfunctional pancreatic neuroendocrine tumours from autoimmune pancreatitis is very important, although it is rare. We propose that endoscopic ultrasonography-guided fine-needle aspiration biopsy should be performed if imaging characteristics are equivocal or the diagnosis is in question.

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BACKGROUND: The optimal duration of capecitabine combined with temozolomide (CapTem) for metastatic pancreatic neuroendocrine tumours (PanNETs) remains controversial. The present study aimed to assess the activity and safety of prolonged CapTem and Cap maintenance therapy in patients with metastatic PanNETs. METHODS: Retrospective real-world data of 94 patients with metastatic PanNETs were obtained from one cancer centre. Fifteen patients were treated with Cap maintenance therapy after fixed 12-13 cycles of CapTem (group I), 44 patients were treated with prolonged CapTem until disease progression (group II), and 35 patients were treated with fixed 12-13 cycles of CapTem (group III). RESULTS: The mean ± SE follow-up period was 41.79 ± 26.31 months. The median CapTem treatment duration was 12 months in group I and 14 months in group II. The median time to best partial response was 12 months both in groups I and group II. The objective response rates of groups I and II were significantly higher than those of group III (73.3%, 41.9%, and 20%, respectively, p = .002). The median progression-free survival (mPFS) of group I and group II was significantly higher than that of group III (35 months, 26 months vs. 19 months, p < .001). Safety analysis of the three groups indicated rare events of grade 3-4 toxicities, with nausea, vomiting, fatigue, and anaemia being the most common adverse effects. CONCLUSIONS: Patients with PanNETs who responded well to CapTem treatment may benefit from prolonged CapTem and Cap maintenance therapy after fixed cycles. Prospective studies are encouraged to further explore the prolonged CapTem treatment and maintenance therapy.

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Pancreatic neuroendocrine neoplasms (PanNENs) are the neuroendocrine neoplasms with greatest rate of increase in incidence. Approximately 10% of PanNENs arise as inherited tumour syndromes which include multiple endocrine neoplasia type 1, multiple endocrine neoplasia type 4, von Hippel-Lindau syndrome, neurofibromatosis type1, tuberous sclerosis complex 1/2, Cowden syndrome, and Glucagon cell hyperplasia and neoplasia as well as familial insulinomatosis. In sporadic PanNENs, driver mutations in MEN1, DAXX/ATRX and mTOR pathway genes are associated with development and progression in pancreatic neuroendocrine tumours. The other changes are in VEGF pathway, Notch pathway, germline mutations in MUTYH, CHEK2, BRCA2, PHLDA3 as well as other genetic alterations. On the other hand, pancreatic neuroendocrine carcinomas share similar genetic alterations with ductal adenocarcinomas, e.g., TP53, RB1 or KRAS. In addition, microRNA and changes in immune microenvironment were noted in PanNENs. Updates on these genetic knowledges contribute to the development of management strategies for patients with PanNENs.

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Pancreatic neuroendocrine tumours (panNET) are heterogeneous neoplasms usually characterised by slow growth and secretion of hormones, which often cause symptoms. The effect of these symptoms on quality of life (QoL) has not previously been examined in detail. EORTC (European Organisation for Research and Treatment of Cancer) guidelines were followed in phases 1-3 to produce a potential module of questions usable for trials in panNET, focusing on three common types of panNET. For two less common types, a list of symptoms was constructed. Following an extensive literature search and phase 1a interviews with patients and healthcare workers, a long list of potential issues (169) was obtained. This list was shown to 12 patients from three countries in phase 1b interviews to check that no items were missed. The list was reduced to 57 issues. The list of issues was converted to questions, mainly from existing validated questions within the EORTC item library. The list of questions was then used in a phase 3 international study in eight countries using seven languages. A provisional module of 24 items is presented for use in nonfunctioning panNET, gastrinoma and insulinoma. This module increases knowledge concerning QoL in this condition and may be a useful adjunct in clinical trials. A phase 4 trial is being considered for validation of this questionnaire.

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INTRODUCTION: Neuroendocrine tumours (NETs) are rare tumours with an increasing incidence. While low- and intermediate-grade pancreatic NET (PanNET) and small intestinal NET (siNET) are slow growing, they have a relatively high rate of metastasizing to the liver, leading to substantially worse outcomes. In many solid tumours, the outcome is determined by the quality of the antitumour immune response. However, the quality and significance of antitumour responses in NETs are incompletely understood. This study provides clinico-pathological analyses of the tumour immune microenvironment in PanNET and siNETs. METHODS: Formalin-fixed paraffin-embedded tissue from consecutive resected PanNETs (61) and siNETs (131) was used to construct tissue microarrays (TMAs); 1-mm cores were taken from the tumour centre, stroma, tumour edge, and adjacent healthy tissue. TMAs were stained with antibodies against CD8, CD4, CD68, FoxP3, CD20, and NCR1. T-cell counts were compared with counts from lung cancers. RESULTS: For PanNET, median counts were CD8+ 35.4 cells/mm2, CD4+ 7.6 cells/mm2, and CD68+ macrophages 117.7 cells/mm2. For siNET, there were CD8+ 39.2 cells/mm2, CD4+ 24.1 cells/mm2, and CD68+ 139.2 cells/mm2. The CD8+ cell density in the tumour and liver metastases were significantly lower than in the adjacent normal tissues, without evidence of a cell-rich area at the tumour edge that might have suggested immune exclusion. T-cell counts in lung cancer were significantly higher than those in PanNET and siNETs: CD8+ 541 cells/mm2 and CD4+ 861 cells/mm2 (p ≤ 0.0001). CONCLUSION: PanNETs and siNETs are immune cold with no evidence of T cell exclusion; the low density of immune infiltrates indicates poor antitumour immune responses.

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BACKGROUND: To analysed the short- and long-term outcomes of patients who underwent surgical resection for non-functioning pancreatic neuroendocrine tumours (NF-PNETs) to gain insights into treatment approaches for this rare and heterogeneous entity. METHODS: All patients who underwent surgical resection for NF-PNETs at The Second Affiliated Hospital of Guangzhou Medical University, and West China Hospital, Sichuan University, from 2009 to 2019 were retrospectively reviewed. The data of patients was including perioperative management, pathologic analysis and follow-up. RESULTS: A total of 119 cases with histologically or cytologically confirmed NF-PNETs, The mean age of the patients was 52, and 56.3% were female. Twenty-three patients received post-operative adjuvant therapy, and five of nine (55.6%) patients with distant metastasis showed recurrence 14(60.9%) G2/G3 patients without distant metastasis received post-operative therapy with octreotide. Of these 14 patients, 3 (21.4%) revealed recurrence. Univariate analysis indicated that symptoms (P = 0.03), tumour size >4 cm (P = 0.029), ENETS stages III-IV (P < 0.001), positive lymph nodes (P < 0.001), vascular/perineural invasion (P < 0.001), and pathology grade G2 were associated with significantly higher risks of recurrence; age, gender, surgery type, and tumour location were not. Multivariate analysis revealed that positive lymph nodes (P < 0.001), vascular/peripheral invasion (P < 0.001), and pathology grade G3 (P = 0.03) are significant prognostic factors of tumour recurrence. CONCLUSION: Positive lymph nodes, vascular/peripheral invasion and pathology grade G3 were related to recurrence of NF-PNETs. Lymph node resection is recommend when FNA biopsy indicates pathology grade G3 for patients with NF-PNETs.

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BACKGROUND: The pathological classification of well-differentiated pancreatic neuroendocrine tumour (pNET) is based largely upon Ki-67 index. However, current controversies abound about the classification of pNETG1/pNETG2. PATIENTS AND METHODS: Clinicopathological data were retrospectively analysed for 153 pNETG1/pNETG2 patients hospitalized at China-Japan Friendship Hospital. The critical values of pNETG1/pNETG2 were examined by using the area under the receiver operating characteristic curve and survival analysis was used to compare the clinical prognosis of pNETG1/G2. RESULTS: Among them, 52.3% were males. The median age was 49 (18-81) years and the clinical types were pNETG1 (n = 38) and pNETG2 (n = 115). According to the receiver operating characteristic curve, the optimal cut-off value was 5.5% for classifying pNETG1/pNETG2. Significant differences between pNETG1 (n = 101) and pNETG2 (n = 52) existed in overall survival (P = 0.001) and disease-free survival (P = 0.013) when Ki-67 index was 5%. Yet no significant differences existed in overall survival (P = 0.378) or disease-free survival (P = 0.091) between pNETG1 and pNETG2 when Ki-67 index was 3%. Furthermore, multivariate analysis indicated that the revised pathological grade was an independent risk factor for mortality and post-operative recurrence of pNET patients (P = 0.003 and 0.014; hazard ratio (HR) = 4.005 and 2.553). CONCLUSION: Thus, differentiating pNETG1/pNETG2 with Ki-67 index (5%) is proposed as the cut-off value and a new Ki-67 index (5%) is a better predictor of pNET mortality and post-operative recurrence than Ki-67 index (3%).

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Predicting grade 1 (G1) and 2 (G2) primary pancreatic neuroendocrine tumour (panNET) is crucial to foresee panNET clinical behaviour. Fifty-one patients with G1-G2 primary panNET demonstrated by pre-surgical [68Ga]Ga-DOTANOC PET/CT and diagnostic conventional imaging were grouped according to the tumour grade assessment method: histology on the whole excised primary lesion (HS) or biopsy (BS). First-order and second-order radiomic features (RFs) were computed from SUV maps for the whole tumour volume on HS. The RFs showing the lowest p-values and the highest area under the curve (AUC) were selected. Three radiomic models were assessed: A (trained on HS, validated on BS), B (trained on BS, validated on HS), and C (using the cross-validation on the whole dataset). The second-order normalized homogeneity and entropy was the most effective RFs couple predicting G2 and G1. The best performance was achieved by model A (test AUC = 0.90, sensitivity = 0.88, specificity = 0.89), followed by model C (median test AUC = 0.87, sensitivity = 0.83, specificity = 0.82). Model B performed worse. Using HS to train a radiomic model leads to the best prediction, although a "hybrid" (HS+BS) population performs better than biopsy-only. The non-invasive prediction of panNET grading may be especially useful in lesions not amenable to biopsy while [68Ga]Ga-DOTANOC heterogeneity might recommend FDG PET/CT.

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Focal pancreatic lesions include a heterogeneous group of solid and cystic lesions, with different natures and variable clinical, imagiological, and pathological characteristics. Several endoscopic ultrasound (EUS)-guided ablative techniques have been tested during the last decade for the treatment of these pancreatic lesions, mostly consisting of the injection of ablative agents and, more recently, radiofrequency ablation. The most encouraging EUS-guided ablation outcomes are being reached in the treatment of some pancreatic cystic neoplasms and small (≤2 cm) pancreatic neuroendocrine tumours (pNETs). Data supporting a potential role of ablative therapies in the treatment of pancreatic ductal adenocarcinoma is still lacking. In this article, GRUPUGE presents an updated perspective of the potential role of EUS-guided ablation for the treatment of pancreatic cystic neoplasms and pNETs, addressing the selection criteria and technical issues of different techniques and analysing recent data on their safety and efficacy.

As lesões focais do pâncreas integram grupos heterogéneos de lesões sólidas e quísticas, de diferentes naturezas e com características clínicas, imagiológicas e patológicas variáveis. Na última década foram avaliadas diversas técnicas ablativas guiadas por ecoendoscopia para o tratamento destas lesões pancreáticas focais, consistindo maioritariamente na injeção de agentes ablativos e, mais recentemente, na ablação por radiofrequência. Os resultados mais promissores das técnicas ablativas guiadas por ecoendoscopia têm surgido no tratamento de algumas lesões quísticas do pâncreas e pequenos tumores neuro-endócrinos pancreáticos (≤2 cm). Ainda existem poucos dados a suportar um potencial papel das terapêuticas ablativas no tratamento do adenocarcinoma ductal do pancreas. No presente artigo o GRUPUGE apresentada uma perspectiva atual do potencial papel da ablação guiada por ecoendoscopia no tratamento de neoplasias quísticas do pâncreas e de tumores neuro-endócrinos pancreáticos, focando aspectos relativos à seleção dos doentes, questões técnicas dos vários procedimentos disponíveis e analisando dados recentes relativos à sua segurança e eficácia.