Pub Date : 2024-02-09DOI: 10.1097/jp9.0000000000000173
Gayathri Swaminathan, Toshie Saito, S. Husain
The ‘omics’ revolution has transformed the biomedical research landscape by equipping scientists with the ability to interrogate complex biological phenomenon and disease processes at an unprecedented level. The volume of ‘big’ data generated by the different omics studies such as genomics, transcriptomics, proteomics, and metabolomics has led to the concurrent development of computational tools to enable in silico analysis and aid data deconvolution. Considering the intensive resources and high costs required to generate and analyze big data, there has been centralized, collaborative efforts to make the data and analysis tools freely available as ‘Open Source’, to benefit the wider research community. Pancreatology research studies have contributed to this ‘big data rush’ and have additionally benefitted from utilizing the open source data as evidenced by the increasing number of new research findings and publications that stem from such data. In this review, we briefly introduce the evolution of open source omics data, data types, the ‘FAIR’ guiding principles for data management and reuse, and centralized platforms that enable free and fair data accessibility, availability, and provide tools for omics data analysis. We illustrate, through the case study of our own experience in mining pancreatitis omics data, the power of repurposing open source data to answer translationally relevant questions in pancreas research.
{"title":"Exploiting Open Source Omics Data to Advance Pancreas Research","authors":"Gayathri Swaminathan, Toshie Saito, S. Husain","doi":"10.1097/jp9.0000000000000173","DOIUrl":"https://doi.org/10.1097/jp9.0000000000000173","url":null,"abstract":"The ‘omics’ revolution has transformed the biomedical research landscape by equipping scientists with the ability to interrogate complex biological phenomenon and disease processes at an unprecedented level. The volume of ‘big’ data generated by the different omics studies such as genomics, transcriptomics, proteomics, and metabolomics has led to the concurrent development of computational tools to enable in silico analysis and aid data deconvolution. Considering the intensive resources and high costs required to generate and analyze big data, there has been centralized, collaborative efforts to make the data and analysis tools freely available as ‘Open Source’, to benefit the wider research community. Pancreatology research studies have contributed to this ‘big data rush’ and have additionally benefitted from utilizing the open source data as evidenced by the increasing number of new research findings and publications that stem from such data. In this review, we briefly introduce the evolution of open source omics data, data types, the ‘FAIR’ guiding principles for data management and reuse, and centralized platforms that enable free and fair data accessibility, availability, and provide tools for omics data analysis. We illustrate, through the case study of our own experience in mining pancreatitis omics data, the power of repurposing open source data to answer translationally relevant questions in pancreas research.","PeriodicalId":92925,"journal":{"name":"Journal of pancreatology","volume":" 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139789517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-09DOI: 10.1097/jp9.0000000000000173
Gayathri Swaminathan, Toshie Saito, S. Husain
The ‘omics’ revolution has transformed the biomedical research landscape by equipping scientists with the ability to interrogate complex biological phenomenon and disease processes at an unprecedented level. The volume of ‘big’ data generated by the different omics studies such as genomics, transcriptomics, proteomics, and metabolomics has led to the concurrent development of computational tools to enable in silico analysis and aid data deconvolution. Considering the intensive resources and high costs required to generate and analyze big data, there has been centralized, collaborative efforts to make the data and analysis tools freely available as ‘Open Source’, to benefit the wider research community. Pancreatology research studies have contributed to this ‘big data rush’ and have additionally benefitted from utilizing the open source data as evidenced by the increasing number of new research findings and publications that stem from such data. In this review, we briefly introduce the evolution of open source omics data, data types, the ‘FAIR’ guiding principles for data management and reuse, and centralized platforms that enable free and fair data accessibility, availability, and provide tools for omics data analysis. We illustrate, through the case study of our own experience in mining pancreatitis omics data, the power of repurposing open source data to answer translationally relevant questions in pancreas research.
{"title":"Exploiting Open Source Omics Data to Advance Pancreas Research","authors":"Gayathri Swaminathan, Toshie Saito, S. Husain","doi":"10.1097/jp9.0000000000000173","DOIUrl":"https://doi.org/10.1097/jp9.0000000000000173","url":null,"abstract":"The ‘omics’ revolution has transformed the biomedical research landscape by equipping scientists with the ability to interrogate complex biological phenomenon and disease processes at an unprecedented level. The volume of ‘big’ data generated by the different omics studies such as genomics, transcriptomics, proteomics, and metabolomics has led to the concurrent development of computational tools to enable in silico analysis and aid data deconvolution. Considering the intensive resources and high costs required to generate and analyze big data, there has been centralized, collaborative efforts to make the data and analysis tools freely available as ‘Open Source’, to benefit the wider research community. Pancreatology research studies have contributed to this ‘big data rush’ and have additionally benefitted from utilizing the open source data as evidenced by the increasing number of new research findings and publications that stem from such data. In this review, we briefly introduce the evolution of open source omics data, data types, the ‘FAIR’ guiding principles for data management and reuse, and centralized platforms that enable free and fair data accessibility, availability, and provide tools for omics data analysis. We illustrate, through the case study of our own experience in mining pancreatitis omics data, the power of repurposing open source data to answer translationally relevant questions in pancreas research.","PeriodicalId":92925,"journal":{"name":"Journal of pancreatology","volume":"45 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139849408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-06DOI: 10.1097/jp9.0000000000000172
Sen Yang, Yuze Hua, Qiaofei Liu, Quan Liao
Patients with peritoneal metastatic pancreatic ductal adenocarcinoma (pmPDAC) with high-level serum carbohydrate antigens (CAs) always suffer extremely dismal prognosis, with a median survival of several months. Herein, we reported a case of pmPDAC with high serum CAs who had long-term clinical remission with normalization of CAs after chemoradiation. In November 2019, a 64-year-old male patient was admitted to our center with a solid mass measuring 2.8×2.5×2.0cm in the body of the pancreas near the celiac trunk. Positron emission tomography-computed tomography (PET-CT) revealed an SUVmax of 4.2. The serum CA 242 level exceeded 150.0 U/ml (normal range: 0-20 U/ml), and CA 19-9 was elevated at 975.2 U/ml (normal range: 0-34 U/ml). During laparotomy, the tumor was found to encircle the celiac trunk over 180 degrees, with several small peritoneal nodules in the lesser omental cavity. Pathological examination confirmed the diagnosis of pmPDAC. Next-generation sequencing revealed RAS G12V, EGFR mutation (-), low TMB (tumor mutation burden), and MSS (microsatellite stability). The patient underwent six cycles of the AG regimen (gemcitabine plus nab-paclitaxel), resulting in significant tumor shrinkage and a sharp decline in CAs. Partial remission was achieved. However, due to intolerant neurotoxicity, the AG regimen was discontinued. Subsequently, synchronous oral fluorouracil (S1) and radiation therapy were administered. Five months after radiation treatment, all CAs normalized. Oral S1 was continued for an additional three months. Eventually, all anti-cancer drugs were stopped. Computed tomography scans indicated that the tumor still surrounded the celiac trunk and common hepatic artery. After a thorough discussion, a wait-and-see strategy was adopted. Remarkably, 32 months after stopping anti-cancer medication, the patient remains in good health, with sustained normalization of CAs. At the last follow-up, he had lived for 50 months, and the normalization of the CAs was sustained for 36 months. Although he still suffers the risk of disease progression, it is a successful case of state-of-the-art chemoradiation for a dismal pmPDAC patient.
{"title":"Long-term Sustained Clinical Remission of Peritoneal Metastatic Pancreatic Ductal Adenocarcinoma After Sequential Chemoradiation Therapy: A Case Report","authors":"Sen Yang, Yuze Hua, Qiaofei Liu, Quan Liao","doi":"10.1097/jp9.0000000000000172","DOIUrl":"https://doi.org/10.1097/jp9.0000000000000172","url":null,"abstract":"Patients with peritoneal metastatic pancreatic ductal adenocarcinoma (pmPDAC) with high-level serum carbohydrate antigens (CAs) always suffer extremely dismal prognosis, with a median survival of several months. Herein, we reported a case of pmPDAC with high serum CAs who had long-term clinical remission with normalization of CAs after chemoradiation. In November 2019, a 64-year-old male patient was admitted to our center with a solid mass measuring 2.8×2.5×2.0cm in the body of the pancreas near the celiac trunk. Positron emission tomography-computed tomography (PET-CT) revealed an SUVmax of 4.2. The serum CA 242 level exceeded 150.0 U/ml (normal range: 0-20 U/ml), and CA 19-9 was elevated at 975.2 U/ml (normal range: 0-34 U/ml). During laparotomy, the tumor was found to encircle the celiac trunk over 180 degrees, with several small peritoneal nodules in the lesser omental cavity. Pathological examination confirmed the diagnosis of pmPDAC. Next-generation sequencing revealed RAS G12V, EGFR mutation (-), low TMB (tumor mutation burden), and MSS (microsatellite stability). The patient underwent six cycles of the AG regimen (gemcitabine plus nab-paclitaxel), resulting in significant tumor shrinkage and a sharp decline in CAs. Partial remission was achieved. However, due to intolerant neurotoxicity, the AG regimen was discontinued. Subsequently, synchronous oral fluorouracil (S1) and radiation therapy were administered. Five months after radiation treatment, all CAs normalized. Oral S1 was continued for an additional three months. Eventually, all anti-cancer drugs were stopped. Computed tomography scans indicated that the tumor still surrounded the celiac trunk and common hepatic artery. After a thorough discussion, a wait-and-see strategy was adopted. Remarkably, 32 months after stopping anti-cancer medication, the patient remains in good health, with sustained normalization of CAs.\u0000 At the last follow-up, he had lived for 50 months, and the normalization of the CAs was sustained for 36 months. Although he still suffers the risk of disease progression, it is a successful case of state-of-the-art chemoradiation for a dismal pmPDAC patient.","PeriodicalId":92925,"journal":{"name":"Journal of pancreatology","volume":"253 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139858459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-06DOI: 10.1097/jp9.0000000000000172
Sen Yang, Yuze Hua, Qiaofei Liu, Quan Liao
Patients with peritoneal metastatic pancreatic ductal adenocarcinoma (pmPDAC) with high-level serum carbohydrate antigens (CAs) always suffer extremely dismal prognosis, with a median survival of several months. Herein, we reported a case of pmPDAC with high serum CAs who had long-term clinical remission with normalization of CAs after chemoradiation. In November 2019, a 64-year-old male patient was admitted to our center with a solid mass measuring 2.8×2.5×2.0cm in the body of the pancreas near the celiac trunk. Positron emission tomography-computed tomography (PET-CT) revealed an SUVmax of 4.2. The serum CA 242 level exceeded 150.0 U/ml (normal range: 0-20 U/ml), and CA 19-9 was elevated at 975.2 U/ml (normal range: 0-34 U/ml). During laparotomy, the tumor was found to encircle the celiac trunk over 180 degrees, with several small peritoneal nodules in the lesser omental cavity. Pathological examination confirmed the diagnosis of pmPDAC. Next-generation sequencing revealed RAS G12V, EGFR mutation (-), low TMB (tumor mutation burden), and MSS (microsatellite stability). The patient underwent six cycles of the AG regimen (gemcitabine plus nab-paclitaxel), resulting in significant tumor shrinkage and a sharp decline in CAs. Partial remission was achieved. However, due to intolerant neurotoxicity, the AG regimen was discontinued. Subsequently, synchronous oral fluorouracil (S1) and radiation therapy were administered. Five months after radiation treatment, all CAs normalized. Oral S1 was continued for an additional three months. Eventually, all anti-cancer drugs were stopped. Computed tomography scans indicated that the tumor still surrounded the celiac trunk and common hepatic artery. After a thorough discussion, a wait-and-see strategy was adopted. Remarkably, 32 months after stopping anti-cancer medication, the patient remains in good health, with sustained normalization of CAs. At the last follow-up, he had lived for 50 months, and the normalization of the CAs was sustained for 36 months. Although he still suffers the risk of disease progression, it is a successful case of state-of-the-art chemoradiation for a dismal pmPDAC patient.
{"title":"Long-term Sustained Clinical Remission of Peritoneal Metastatic Pancreatic Ductal Adenocarcinoma After Sequential Chemoradiation Therapy: A Case Report","authors":"Sen Yang, Yuze Hua, Qiaofei Liu, Quan Liao","doi":"10.1097/jp9.0000000000000172","DOIUrl":"https://doi.org/10.1097/jp9.0000000000000172","url":null,"abstract":"Patients with peritoneal metastatic pancreatic ductal adenocarcinoma (pmPDAC) with high-level serum carbohydrate antigens (CAs) always suffer extremely dismal prognosis, with a median survival of several months. Herein, we reported a case of pmPDAC with high serum CAs who had long-term clinical remission with normalization of CAs after chemoradiation. In November 2019, a 64-year-old male patient was admitted to our center with a solid mass measuring 2.8×2.5×2.0cm in the body of the pancreas near the celiac trunk. Positron emission tomography-computed tomography (PET-CT) revealed an SUVmax of 4.2. The serum CA 242 level exceeded 150.0 U/ml (normal range: 0-20 U/ml), and CA 19-9 was elevated at 975.2 U/ml (normal range: 0-34 U/ml). During laparotomy, the tumor was found to encircle the celiac trunk over 180 degrees, with several small peritoneal nodules in the lesser omental cavity. Pathological examination confirmed the diagnosis of pmPDAC. Next-generation sequencing revealed RAS G12V, EGFR mutation (-), low TMB (tumor mutation burden), and MSS (microsatellite stability). The patient underwent six cycles of the AG regimen (gemcitabine plus nab-paclitaxel), resulting in significant tumor shrinkage and a sharp decline in CAs. Partial remission was achieved. However, due to intolerant neurotoxicity, the AG regimen was discontinued. Subsequently, synchronous oral fluorouracil (S1) and radiation therapy were administered. Five months after radiation treatment, all CAs normalized. Oral S1 was continued for an additional three months. Eventually, all anti-cancer drugs were stopped. Computed tomography scans indicated that the tumor still surrounded the celiac trunk and common hepatic artery. After a thorough discussion, a wait-and-see strategy was adopted. Remarkably, 32 months after stopping anti-cancer medication, the patient remains in good health, with sustained normalization of CAs.\u0000 At the last follow-up, he had lived for 50 months, and the normalization of the CAs was sustained for 36 months. Although he still suffers the risk of disease progression, it is a successful case of state-of-the-art chemoradiation for a dismal pmPDAC patient.","PeriodicalId":92925,"journal":{"name":"Journal of pancreatology","volume":"6 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139798693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-14DOI: 10.1097/jp9.0000000000000165
Parth S Patel, V. Akshintala
Endoscopic retrograde cholangiopancreatography (ERCP) has continued to develop over recent decades with regards to both indications for its use and improvements in technique. The most common complication is post- endoscopic retrograde cholangiopancreatography pancreatitis (PEP) with incidence rates being reported at ~10%. The exact mechanism of PEP is unknown but is likely multi-factorial with papillary edema contributing to the activation of the inflammatory cascade playing an important role. Selected risk factors include patient-related factors (female, sex, younger age, sphincter of Oddi dysfunction, and history of PEP) and procedure-related factors (difficult cannulation, multiple pancreatic duct guidewire passes, pancreatic acinarization, multiple pancreatic duct contrast injections and precut sphincterotomy). Several preventative prophylactic strategies have been posited; however, current guidelines recommend the use of rectal NSAIDs, aggressive IV fluid hydration and pancreatic duct stents. Appropriate patient selection and the use of non-invasive imaging modalities for diagnosis of pancreaticobiliary abnormalities is a key aspect in prevention. Future studies continue to explore various pharmacologic, procedure-related and combination strategies for prevention and will be important as the use of ERCP continues to grow.
{"title":"Post-Endoscopic Retrograde Cholangiopancreatography Pancreatitis – A Review","authors":"Parth S Patel, V. Akshintala","doi":"10.1097/jp9.0000000000000165","DOIUrl":"https://doi.org/10.1097/jp9.0000000000000165","url":null,"abstract":"Endoscopic retrograde cholangiopancreatography (ERCP) has continued to develop over recent decades with regards to both indications for its use and improvements in technique. The most common complication is post- endoscopic retrograde cholangiopancreatography pancreatitis (PEP) with incidence rates being reported at ~10%. The exact mechanism of PEP is unknown but is likely multi-factorial with papillary edema contributing to the activation of the inflammatory cascade playing an important role. Selected risk factors include patient-related factors (female, sex, younger age, sphincter of Oddi dysfunction, and history of PEP) and procedure-related factors (difficult cannulation, multiple pancreatic duct guidewire passes, pancreatic acinarization, multiple pancreatic duct contrast injections and precut sphincterotomy). Several preventative prophylactic strategies have been posited; however, current guidelines recommend the use of rectal NSAIDs, aggressive IV fluid hydration and pancreatic duct stents. Appropriate patient selection and the use of non-invasive imaging modalities for diagnosis of pancreaticobiliary abnormalities is a key aspect in prevention. Future studies continue to explore various pharmacologic, procedure-related and combination strategies for prevention and will be important as the use of ERCP continues to grow.","PeriodicalId":92925,"journal":{"name":"Journal of pancreatology","volume":"18 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139002829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-14DOI: 10.1097/jp9.0000000000000162
M. Bachand, Mohamed-Anas Chennouf, Mandy Malick, Annie Beaudoin
Long term surveillance of branch-duct intraductal papillary mucinous neoplasms (BD-IPMN) remains controversial, particularly regarding cysts follow up > 5 years. The primary endpoint of this study was to assess the risk of malignant transformation of presumed BD-IPMN during follow-up and identify clinical and morphological predictors of malignancy. We performed a retrospective analysis of data from all patients with a presumed BD-IPMN diagnosis at the CIUSSS de l’Estrie CHUS, from 2004-2018. The final database included 380 patients with presumed BD-IPMN with a median follow up of 43,9 months (IQR 28,6-73,3 months). Mean age at diagnosis was 65,5 years [27-90], 159 patients (42,8%) were male and 17 patients (4,5%) underwent resection of their lesion during their surveillance period. In our cohort, 132 patients (34,7%) had a follow-up > 5 years. Overall risk of malignancy was 2.1% [0.9%-4.1%]. During follow-up, neoplastic transformation was observed in 2/132 patients (1,5%) surveilled > 5 years. Malignancy was significantly associated with cyst growth > 2,5 mm/year (57,1% vs 5,8% p < 0,001) dilated MPD (71,4% vs 4,9% p<0,001), solid component (71,4% vs 1,3% p<0,001), positive cytology (37,5% vs 0,5% p<0,001), development of high-risk stigmatas (87,5% vs 1,9% p <0,001) or worrisome features (87,5% vs 23,9% p<0,001) during follow up and symptoms of jaundice (25% vs 0,5% p=0,002) and abdominal pain (50% vs 9,4% p=0,005). While overall malignancy risk remains low in presumed BD-IPMN, continuous surveillance should be pursued after 5 years in surgically fit individuals, particularly in patients who develop our identified risk factors.
对分支导管内乳头状粘液瘤（BD-IPMN）的长期监测仍存在争议，尤其是对随访时间超过 5 年的囊肿。本研究的主要终点是评估随访期间假定的 BD-IPMN 恶性转化的风险，并确定恶变的临床和形态学预测因素。 我们对CIUSSS de l'Estrie CHUS在2004-2018年间诊断出的所有假定BD-IPMN患者的数据进行了回顾性分析。 最终数据库包括380名推测为BD-IPMN的患者，中位随访时间为43.9个月（IQR为28.6-73.3个月）。诊断时的平均年龄为 65.5 岁 [27-90]，159 名患者（42.8%）为男性，17 名患者（4.5%）在监测期间接受了病灶切除术。在我们的队列中，132 名患者（34.7%）的随访时间超过 5 年。恶性肿瘤的总体风险为 2.1% [0.9%-4.1%]。在随访期间，2/132 名（1.5%）随访时间超过 5 年的患者出现了肿瘤变。恶性肿瘤与囊肿生长速度大于 2.5 毫米/年（57.1% vs 5.8% p < 0.001）、MPD 扩张（71.4% vs 4.9% p < 0.001）、实性成分（71.4% vs 1.3% p < 0.001）、细胞学阳性（37.5% vs 0.5% p < 0、001）、随访期间出现高风险烙印（87.5% vs 1.9% p<0.001）或令人担忧的特征（87.5% vs 23.9% p<0.001）以及黄疸（25% vs 0.5% p=0.002）和腹痛（50% vs 9.4% p=0.005）症状。 虽然假定的 BD-IPMN 的总体恶性肿瘤风险仍然很低，但对于适合手术的患者，尤其是出现我们所确定的风险因素的患者，应在 5 年后继续进行监测。
{"title":"Branch-duct intraductal papillary mucinous neoplasm (BD-IPMN): a retrospective study on neoplastic risk after 5 years surveillance","authors":"M. Bachand, Mohamed-Anas Chennouf, Mandy Malick, Annie Beaudoin","doi":"10.1097/jp9.0000000000000162","DOIUrl":"https://doi.org/10.1097/jp9.0000000000000162","url":null,"abstract":"\u0000 \u0000 Long term surveillance of branch-duct intraductal papillary mucinous neoplasms (BD-IPMN) remains controversial, particularly regarding cysts follow up > 5 years. The primary endpoint of this study was to assess the risk of malignant transformation of presumed BD-IPMN during follow-up and identify clinical and morphological predictors of malignancy.\u0000 \u0000 \u0000 \u0000 We performed a retrospective analysis of data from all patients with a presumed BD-IPMN diagnosis at the CIUSSS de l’Estrie CHUS, from 2004-2018.\u0000 \u0000 \u0000 \u0000 The final database included 380 patients with presumed BD-IPMN with a median follow up of 43,9 months (IQR 28,6-73,3 months). Mean age at diagnosis was 65,5 years [27-90], 159 patients (42,8%) were male and 17 patients (4,5%) underwent resection of their lesion during their surveillance period. In our cohort, 132 patients (34,7%) had a follow-up > 5 years.\u0000 Overall risk of malignancy was 2.1% [0.9%-4.1%]. During follow-up, neoplastic transformation was observed in 2/132 patients (1,5%) surveilled > 5 years. Malignancy was significantly associated with cyst growth > 2,5 mm/year (57,1% vs 5,8% p < 0,001) dilated MPD (71,4% vs 4,9% p<0,001), solid component (71,4% vs 1,3% p<0,001), positive cytology (37,5% vs 0,5% p<0,001), development of high-risk stigmatas (87,5% vs 1,9% p <0,001) or worrisome features (87,5% vs 23,9% p<0,001) during follow up and symptoms of jaundice (25% vs 0,5% p=0,002) and abdominal pain (50% vs 9,4% p=0,005).\u0000 \u0000 \u0000 \u0000 While overall malignancy risk remains low in presumed BD-IPMN, continuous surveillance should be pursued after 5 years in surgically fit individuals, particularly in patients who develop our identified risk factors.\u0000","PeriodicalId":92925,"journal":{"name":"Journal of pancreatology","volume":"6 5‐6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138972469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chronic pancreatitis (CP) is a multifaceted disorder influenced by environmental and genetic factors, with smoking and alcohol consumption being major contributors. Recent developments encompass the advent of innovative transgenic models and the identification of susceptibility genes, shedding light on the genetic aspect of CP. The pathogenesis of this disease involves a complex interplay of pancreatic acinar cell dysfunction, inflammatory reactions, and fibrosis. Current research delves into understanding these molecular mechanisms. Pain, a pivotal symptom of CP, has been increasingly studied to develop effective therapeutic interventions. Diagnostic advancements, including endoscopic ultrasound, radiomics, and blood-based markers, have shown potential in enhancing early CP detection. Moreover, recent clinical trials have optimized treatment approaches, such as pancreatic stone fragmentation, stent placement, and decision-making between endoscopic and surgical procedures. Emerging therapies, including chemical pancreatectomy and gene therapy, present promising opportunities for improved CP management.
{"title":"A Comprehensive Review of Recent Advances in Chronic Pancreatitis","authors":"Shenghan Mao, Wen‐Bin Zou, Xiaotong Mao, Zhao-Shen Li, Zhuan Liao","doi":"10.1097/jp9.0000000000000161","DOIUrl":"https://doi.org/10.1097/jp9.0000000000000161","url":null,"abstract":"Chronic pancreatitis (CP) is a multifaceted disorder influenced by environmental and genetic factors, with smoking and alcohol consumption being major contributors. Recent developments encompass the advent of innovative transgenic models and the identification of susceptibility genes, shedding light on the genetic aspect of CP. The pathogenesis of this disease involves a complex interplay of pancreatic acinar cell dysfunction, inflammatory reactions, and fibrosis. Current research delves into understanding these molecular mechanisms. Pain, a pivotal symptom of CP, has been increasingly studied to develop effective therapeutic interventions. Diagnostic advancements, including endoscopic ultrasound, radiomics, and blood-based markers, have shown potential in enhancing early CP detection. Moreover, recent clinical trials have optimized treatment approaches, such as pancreatic stone fragmentation, stent placement, and decision-making between endoscopic and surgical procedures. Emerging therapies, including chemical pancreatectomy and gene therapy, present promising opportunities for improved CP management.","PeriodicalId":92925,"journal":{"name":"Journal of pancreatology","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139002751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human chemokines are linked to tumour survival and perform a critical role in the pancreatic adenocarcinoma (PAAD) microenvironment. It is not known if abnormal expression of chemokines contributes to the prognostic features of PAAD. Therefore, this study explored gene alteration profiles of chemokines in PAAD and constructed a chemokine family-based prognosis signature (CPS). RNA-Seq and clinical data from 176 PAAD patients were obtained from The Cancer Genome Atlas (TCGA) database. Bioinformatics analysis tools were used to assess the expression and prognostic value of chemokines. A profile affecting patient survival was obtained using unsupervised hierarchical clustering and a prognostic model of chemokine-related genes was constructed to explore the immune landscape. 29 chemokines were highly expressed in PAAD tissues, and 10 were significantly associated with poor prognosis. Hierarchical clustering resulted in the classification of the PAAD cohort into 2 clusters. High levels of chemokines indicated a worse prognosis (for HR=5.4, CI=1.7-17, P=0.004). A CPS containing 7 hub genes was constructed using the least absolute shrinkage and selection operator (LASSO) and stepwise multivariable Cox analysis. This signature separated PAAD patients into high and low risk groups and was confirmed as an independent prognostic factor. An ESTIMATE score and TIMER2.0 analysis further reflected the immune profile of PAAD, which had a higher percentage of localized immune cell infiltration with predominantly suppressive cells. This is the first chemokine family-based model for predicting outcomes in PAAD patients. Our work highlights the need to understand the mechanism of chemokine contributions to PAAD occurrence.
{"title":"Chemokine expression profiles predict overall survival and immune infiltration in patients with pancreatic adenocarcinoma","authors":"Xinyu Peng, Shengnan Lv, Yuxiang Fan, Jian Zhang, Huan Liu, Yan Liu, Feng Wei","doi":"10.1097/jp9.0000000000000164","DOIUrl":"https://doi.org/10.1097/jp9.0000000000000164","url":null,"abstract":"\u0000 \u0000 Human chemokines are linked to tumour survival and perform a critical role in the pancreatic adenocarcinoma (PAAD) microenvironment. It is not known if abnormal expression of chemokines contributes to the prognostic features of PAAD. Therefore, this study explored gene alteration profiles of chemokines in PAAD and constructed a chemokine family-based prognosis signature (CPS).\u0000 \u0000 \u0000 \u0000 RNA-Seq and clinical data from 176 PAAD patients were obtained from The Cancer Genome Atlas (TCGA) database. Bioinformatics analysis tools were used to assess the expression and prognostic value of chemokines. A profile affecting patient survival was obtained using unsupervised hierarchical clustering and a prognostic model of chemokine-related genes was constructed to explore the immune landscape.\u0000 \u0000 \u0000 \u0000 29 chemokines were highly expressed in PAAD tissues, and 10 were significantly associated with poor prognosis. Hierarchical clustering resulted in the classification of the PAAD cohort into 2 clusters. High levels of chemokines indicated a worse prognosis (for HR=5.4, CI=1.7-17, P=0.004). A CPS containing 7 hub genes was constructed using the least absolute shrinkage and selection operator (LASSO) and stepwise multivariable Cox analysis. This signature separated PAAD patients into high and low risk groups and was confirmed as an independent prognostic factor. An ESTIMATE score and TIMER2.0 analysis further reflected the immune profile of PAAD, which had a higher percentage of localized immune cell infiltration with predominantly suppressive cells.\u0000 \u0000 \u0000 \u0000 This is the first chemokine family-based model for predicting outcomes in PAAD patients. Our work highlights the need to understand the mechanism of chemokine contributions to PAAD occurrence.\u0000","PeriodicalId":92925,"journal":{"name":"Journal of pancreatology","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138974674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ectopic accumulation of fat can cause a variety of metabolic diseases, and the emerging non-alcoholic fatty pancreas disease (NAFPD) is increasingly being recognized by clinicians as a cause for concern. NAFPD is a disease caused by abnormal accumulation of adipose tissue in the pancreas, which is related to obesity. The main feature of NAFPD is death of acinar cells, which are then replaced by adipose cells. However, the underlying molecular mechanisms have not been fully explored. Obesity, aging, and metabolic syndrome are independent risk factors for the occurrence and development of NAFPD. Studies have shown that NAFPD leads to insulin resistance and pancreatic dysfunction, increases the risk of diabetes, worsens the severity of pancreatitis, and is significantly correlated with pancreatic cancer and postoperative pancreatic fistula. There is no standard treatment for NAFPD; exercise, a balanced diet, and lifestyle can help reduce pancreatic fat; however, other treatment modalities such as drugs and bariatric surgery are still being explored. The specific pathological mechanism of NAFPD remains unclear, and its potential association with various clinical diseases requires further study. This review summarizes the etiology, diagnosis, clinical consequences, and potential therapeutic strategies of NAFPD.
{"title":"Non-alcoholic Fatty Pancreas Disease (NAFPD): An updated review","authors":"C. Pang, Peng Dong, Jian Yang, Zhiyao Fan, Zhiqiang Cheng, Hanxiang Zhan","doi":"10.1097/jp9.0000000000000157","DOIUrl":"https://doi.org/10.1097/jp9.0000000000000157","url":null,"abstract":"Ectopic accumulation of fat can cause a variety of metabolic diseases, and the emerging non-alcoholic fatty pancreas disease (NAFPD) is increasingly being recognized by clinicians as a cause for concern. NAFPD is a disease caused by abnormal accumulation of adipose tissue in the pancreas, which is related to obesity. The main feature of NAFPD is death of acinar cells, which are then replaced by adipose cells. However, the underlying molecular mechanisms have not been fully explored. Obesity, aging, and metabolic syndrome are independent risk factors for the occurrence and development of NAFPD. Studies have shown that NAFPD leads to insulin resistance and pancreatic dysfunction, increases the risk of diabetes, worsens the severity of pancreatitis, and is significantly correlated with pancreatic cancer and postoperative pancreatic fistula. There is no standard treatment for NAFPD; exercise, a balanced diet, and lifestyle can help reduce pancreatic fat; however, other treatment modalities such as drugs and bariatric surgery are still being explored. The specific pathological mechanism of NAFPD remains unclear, and its potential association with various clinical diseases requires further study. This review summarizes the etiology, diagnosis, clinical consequences, and potential therapeutic strategies of NAFPD.","PeriodicalId":92925,"journal":{"name":"Journal of pancreatology","volume":"18 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139007890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-12DOI: 10.1097/jp9.0000000000000160
Shuai Wu, Jiaqiang Ren, Weikun Qian, M. Gong, Jie Li, Tao Qin, Simei Zhang, Wunai Zhang, Hao Sun, Zheng Wu, Zheng Wang, Qingyong Ma, Wanxing Duan
Pancreatic cancer is a highly malignant tumor of the digestive tract with a dismal prognosis. A key challenge of pancreatic cancer is its resistance to chemotherapy. The c-Met/PARP1 axis plays an important role in the therapeutic resistance of breast cancer and hepatocellular carcinoma. Therefore, this study aims to explore potential therapeutic targets for improving chemotherapy for pancreatic cancer and the underlying mechanisms. Gemcitabine-resistant pancreatic cancer cell lines were constructed by our laboratory using a continuous low-concentration gemcitabine induction method. The proliferation and apoptosis of combination therapy were examined using flow cytometry and comet assay. Synergistic effects of two drugs were determined by Chou-Talalay's combination index (CI). The interactions between proteins were predicted using the AutoDock model and detected through Coimmunoprecipitation assays. The combination of resveratrol and gemcitabine inhibited proliferation and promoted apoptosis of pancreatic cancer cells. We found that c-Met and PARP1 were highly expressed in gemcitabine-resistant pancreatic cancer cells. However, resveratrol inhibited their expression and improved the effectiveness of gemcitabine-induced DNA damage. In addition, our data demonstrated that resveratrol and gemcitabine had synergistic effects (CI < 1). Furthermore, the protein interactions between c-Met and PARP1 were attenuated after the early stage of resveratrol intervention. Using AutoDock models, we predicted the potential binding sites where resveratrol could impact the protein interaction between c-Met (tyrosine kinase domain) and PARP1 (CAT domain). Our results suggested that the synergistic effects of resveratrol with gemcitabine depend on the c-Met/PAPR1 axis. Using resveratrol as a combined chemotherapy agent may have clinical benefits for patients with refractory pancreatic cancer.
{"title":"Synergistic effects of resveratrol with gemcitabine in pancreatic cancer chemotherapy by inhibiting the c-Met/PARP1 axis","authors":"Shuai Wu, Jiaqiang Ren, Weikun Qian, M. Gong, Jie Li, Tao Qin, Simei Zhang, Wunai Zhang, Hao Sun, Zheng Wu, Zheng Wang, Qingyong Ma, Wanxing Duan","doi":"10.1097/jp9.0000000000000160","DOIUrl":"https://doi.org/10.1097/jp9.0000000000000160","url":null,"abstract":"\u0000 \u0000 Pancreatic cancer is a highly malignant tumor of the digestive tract with a dismal prognosis. A key challenge of pancreatic cancer is its resistance to chemotherapy. The c-Met/PARP1 axis plays an important role in the therapeutic resistance of breast cancer and hepatocellular carcinoma. Therefore, this study aims to explore potential therapeutic targets for improving chemotherapy for pancreatic cancer and the underlying mechanisms.\u0000 \u0000 \u0000 \u0000 Gemcitabine-resistant pancreatic cancer cell lines were constructed by our laboratory using a continuous low-concentration gemcitabine induction method. The proliferation and apoptosis of combination therapy were examined using flow cytometry and comet assay. Synergistic effects of two drugs were determined by Chou-Talalay's combination index (CI). The interactions between proteins were predicted using the AutoDock model and detected through Coimmunoprecipitation assays.\u0000 \u0000 \u0000 \u0000 The combination of resveratrol and gemcitabine inhibited proliferation and promoted apoptosis of pancreatic cancer cells. We found that c-Met and PARP1 were highly expressed in gemcitabine-resistant pancreatic cancer cells. However, resveratrol inhibited their expression and improved the effectiveness of gemcitabine-induced DNA damage. In addition, our data demonstrated that resveratrol and gemcitabine had synergistic effects (CI < 1). Furthermore, the protein interactions between c-Met and PARP1 were attenuated after the early stage of resveratrol intervention. Using AutoDock models, we predicted the potential binding sites where resveratrol could impact the protein interaction between c-Met (tyrosine kinase domain) and PARP1 (CAT domain).\u0000 \u0000 \u0000 \u0000 Our results suggested that the synergistic effects of resveratrol with gemcitabine depend on the c-Met/PAPR1 axis. Using resveratrol as a combined chemotherapy agent may have clinical benefits for patients with refractory pancreatic cancer.\u0000","PeriodicalId":92925,"journal":{"name":"Journal of pancreatology","volume":"6 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139009433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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