Objective To explore the predictive value of radiomics for postoperative pancreatic fistula, infection, and long-term survival in patients with pancreatic ductal adenocarcinoma (PDAC). Methods 206 patients who received radical resection of pancreatic cancer in Zhongshan Hospital, Fudan University from January 2014 to December 2020 and were pathologically confirmed as PDAC after surgery were retrospectively selected, all of whom had complete surgical data and long-term follow-up data. Pyradiomics was used to analyze the enhanced CT images of all patients and extract radiomics features. LASSO dimensionality reduction combined with logistic regression analysis was used to construct a predictive model for pancreatic fistula and abdominal infection after PDAC surgery, and evaluating the model’s effectiveness using ROC curves. A long-term survival prediction model for PDAC patients was constructed using LASSO dimensionality reduction combined with Cox regression analysis, and patient risk scores were calculated. The patients were divided into high-risk and low-risk groups based on the median, and the survival curves were compared to evaluate the effectiveness of the model. The imaging omics features with the highest weight were divided into high expression group and low expression group according to the median, and the prognostic differences and clinical features were compared. Radiomics and clinical features were combined to analyze the influencing factors of long-term prognosis and construct a clinical imaging comprehensive model. Results A total of 1 595 radiomics features were extracted. A predictive model for pancreatic fistula and infection after PDAC surgery was constructed, with AUC values of 0.81 and 0.79, respectively. The PDAC long-term survival prediction model was successfully constructed, and the prognosis of the high-risk group was worse than that of the low-risk group (P<0.001). The weight of the radiomics feature “log-sigma-5-mm-3D_glszm_ZonePercentage” was 59.557. The CA19-9 level in the high expression group is higher than that in the low expression group (P=0.017), and there is a statistically significant difference in survival curves between the two groups (P=0.021). The comprehensive clinical imaging model suggested that age, AJCC stage, lymph infiltration, CA19-9 level and imaging characteristics were risk factors for long-term prognosis of PDAC patients (HR=1.028, 4.084, 2.566, 1.232 and 2.536). Conclusions The predictive model based on radiomics has good predictive performance for pancreatic fistula, infection, and long-term prognosis after PDAC surgery. Patients with high expression of the radiomics feature “log-sigma-5-mm-3D_glszm_ZonePercentage” face poorer prognosis.

Pancreatic cancer is a extremely high malignant digestive cancer, which usually occurred in the elderly. The cases and the portion of the elder patients in all pancreatic cancer patients are gradually increasing, resulted from the aging population in China. However, the management of the elder pancreatic cancer patients is challenging due to the multiple comorbidity, the poor tolerance to treatment and lack of social support. Meanwhile, these patients could be neglected by physician and relatives easily. More detailed physical, psychological and social support evaluations ought to be done before treatment in the elderly. The clinical care should be individualized based on the evaluations and tumor stage, in order to improve the prognosis and quality of life.

Cancer-related sarcopenia is mainly characterized by protein degradation and muscle depletion caused by catabolism, leading to a decrease in the quality, strength, and function of skeletal muscles. Pancreatic cancer has the highest incidence of cancer-associated sarcopenia. More than 80% of pancreatic cancer patients have the Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations, which promote the progress of sarcopenia. The authors systematically elaborate the interaction mechanism between KRAS-mutant pancreatic cancer and sarcopenia, mainly in four aspects: (1) KRAS driven metabolic reprogramming leads to depletion of muscle energy reserves, affecting the redistribution of muscle fiber energy and resulting in unidirectional energy flow for cancer cell proliferation. (2) By altering the cytokine profile, activating the ubiquitin protease system and the autophagy lysosome pathway, the cancer cells promote myotube degradation, inhibit muscle regeneration, disrupt muscle homeostasis, and lead to unidirectional flow of nutrients to support tumor growth. (3) Oxidative stress caused by cancer cells damages skeletal muscles. (4) Cancer cells induce immune cell remodeling in skeletal muscle. Meanwhile, the authors review the treatment progress of KRAS-mutant pancreatic cancer-related sarcopenia. With the deepening research of KRAS-mutant pancreatic cancer-related sarcopenia, targeted therapy and personalized intervention are expected to become important means to improve the prognosis and quality of life of patients.

Pancreatic cancer is a extremely high malignant digestive cancer, which usually occurred in the elderly. The cases and the portion of the elder patients in all pancreatic cancer patients are gradually increasing, resulted from the aging population in China. However, the management of the elder pancreatic cancer patients is challenging due to the multiple comorbidity, the poor tolerance to treatment and lack of social support. Meanwhile, these patients could be neglected by physician and relatives easily. More detailed physical, psychological and social support evaluations ought to be done before treatment in the elderly. The clinical care should be individualized based on the evaluations and tumor stage, in order to improve the prognosis and quality of life.

Cancer-related sarcopenia is mainly characterized by protein degradation and muscle depletion caused by catabolism, leading to a decrease in the quality, strength, and function of skeletal muscles. Pancreatic cancer has the highest incidence of cancer-associated sarcopenia. More than 80% of pancreatic cancer patients have the Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations, which promote the progress of sarcopenia. The authors systematically elaborate the interaction mechanism between KRAS-mutant pancreatic cancer and sarcopenia, mainly in four aspects: (1) KRAS driven metabolic reprogramming leads to depletion of muscle energy reserves, affecting the redistribution of muscle fiber energy and resulting in unidirectional energy flow for cancer cell proliferation. (2) By altering the cytokine profile, activating the ubiquitin protease system and the autophagy lysosome pathway, the cancer cells promote myotube degradation, inhibit muscle regeneration, disrupt muscle homeostasis, and lead to unidirectional flow of nutrients to support tumor growth. (3) Oxidative stress caused by cancer cells damages skeletal muscles. (4) Cancer cells induce immune cell remodeling in skeletal muscle. Meanwhile, the authors review the treatment progress of KRAS-mutant pancreatic cancer-related sarcopenia. With the deepening research of KRAS-mutant pancreatic cancer-related sarcopenia, targeted therapy and personalized intervention are expected to become important means to improve the prognosis and quality of life of patients.

In the past two decades, significant advances have been made in the treatment of pancreatic cancer.Numerous first-line treatments, such as gemcitabine combined with erlotinib, gemcitabine combined with albumin-bound paclitaxel, FOLFIRINOX, and NALIRIFOX, have emerged;surgery-centered treatment has gradually become the mains clinical strategy.However, behind these achievements, the new drugs developed with substantial funding have not extended the median survival time of patients with advanced pancreatic cancer to more than one year; the 5-year survival rate for postoperative patients remains below 30%. While harboring hope and being proactive, researchers must also soberly reflect and continually reassess our direction, in anticipation of bringing tangible clinical benefits to pancreatic cancer patients at an early date.

The incidence of pancreatic cystic neoplasms increased dramatically. The clinically optimal management guideline for pancreatic cysts has continued to improve in previous decades. Some issues in diagnosis and treatment require careful consideration and decision-making to achieve the best therapeutic effect and avoid overtreatment. This article analyzes the new progress in the differential diagnosis of pancreatic cystic tumors, surgical decision-making and scope of surgery, and long-term follow-up of patients who have not undergone surgery. In general, the current diagnosis and treatment decisions for pancreatic cystic tumors are more comprehensive and scientific as evidence becomes increasingly abundant, emphasizing the risks and benefits of precise diagnosis and treatment and balanced treatment.

In the past two decades, significant advances have been made in the treatment of pancreatic cancer.Numerous first-line treatments, such as gemcitabine combined with erlotinib, gemcitabine combined with albumin-bound paclitaxel, FOLFIRINOX, and NALIRIFOX, have emerged;surgery-centered treatment has gradually become the mains clinical strategy.However, behind these achievements, the new drugs developed with substantial funding have not extended the median survival time of patients with advanced pancreatic cancer to more than one year; the 5-year survival rate for postoperative patients remains below 30%. While harboring hope and being proactive, researchers must also soberly reflect and continually reassess our direction, in anticipation of bringing tangible clinical benefits to pancreatic cancer patients at an early date.

The incidence of pancreatic cystic neoplasms increased dramatically. The clinically optimal management guideline for pancreatic cysts has continued to improve in previous decades. Some issues in diagnosis and treatment require careful consideration and decision-making to achieve the best therapeutic effect and avoid overtreatment. This article analyzes the new progress in the differential diagnosis of pancreatic cystic tumors, surgical decision-making and scope of surgery, and long-term follow-up of patients who have not undergone surgery. In general, the current diagnosis and treatment decisions for pancreatic cystic tumors are more comprehensive and scientific as evidence becomes increasingly abundant, emphasizing the risks and benefits of precise diagnosis and treatment and balanced treatment.

Intraductal papillary mucinous neoplasm (IPMN) is the most common pancreatic cystic neoplasm with a tendency to malignancy,and the 5-year survival rate of patients with invasive IPMN is less than 40%. Therefore,early detection of malignant cases and surgical intervention will significantly improve patient outcomes. The clinical guidelines recommended risk factors for IPMN malignancy according to imaging characteristics,clinical manifestations and serum tumor markers,among which dilation of the main pancreatic duct≥10 mm,the presence of solid components or enhanced mural nodules,and obstructive jaundice were recognized as high-risk factors. However,clinical practice has shown that the risk factors recommended by the current guidelines are not highly accurate in predicting IPMN malignancy,and the main problem is that the guidelines are less specific and allow follow-up cases to undergo unnecessary surgical resection. In recent years,the development of new technologies and methods such as genomics,radiomics,and artificial intelligence has greatly promoted the research progress of IPMN. Endoscopic ultrasound-guided fine needle aspiration of cystic fluid combined with molecular detection such as DNA and RNA,as well as radiomics combined with machine learning modeling,have shown superiority in improving the prediction accuracy of malignant IPMN,and will become an important tool to assist the diagnosis and treatment of IPMN in the future.