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International Journal of Surgery... Sep 2022Validity of the laparoscopic approach in pancreatic head lesion remains debatable. This study aims to compare the safety and effectiveness of laparoscopic... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Validity of the laparoscopic approach in pancreatic head lesion remains debatable. This study aims to compare the safety and effectiveness of laparoscopic pancreatoduodenectomy (LPD) and open pancreatoduodenectomy (OPD) and investigate the source of heterogeneity from surgeons' and patients' perspectives.
METHOD
We searched PubMed, Cochrane, Embase, and Web of Science for studies published before February 1, 2021. Of 6578 articles, 81 were full-text reviewed. The primary outcome was mortality. Three independent reviewers screened and extracted the data and resolved disagreements by consensus. Studies were evaluated for quality using ROB2.0 and ROBINS-I. According to different study designs, sensitivity and meta-regression analyses were conducted to explore the heterogeneity source. This meta-analyses was also conducted to explore the learning curve's heterogeneity. This study was registered with PROSPERO, CRD42021234579.
RESULTS
We analyzed 34 studies involving 46,729 patients (4705 LPD and 42,024 OPD). LPD was associated with lower (P = 0.025) in unmatched studies (P = 0.017). No differences in mortality existed in randomized controlled trials (P = 0.854) and matched studies (P = 0.726). Sensitivity analysis found no significant difference in mortality in elderly patients, patients with pancreatic cancer, and in high- and low-volume hospitals (all P > 0.05). In studies at the early period of LPD (<40 cases), higher mortality (P < 0.001) was found (all P < 0.05).LPD showed non-inferiority in length of stay, complications, and survival outcomes in all analyses.
CONCLUSION
In high-volume centers with adequate surgical experience, LPD in selected patients appears to be a valid alternative to LPD with comparable mortality, LOS, complications, and survival outcomes.
Topics: Aged; Hospitals, Low-Volume; Humans; Laparoscopy; Length of Stay; Pancreatic Neoplasms; Pancreaticoduodenectomy; Postoperative Complications; Retrospective Studies
PubMed: 35988720
DOI: 10.1016/j.ijsu.2022.106799 -
Signal Transduction and Targeted Therapy Mar 2023Research on obesity- and diabetes mellitus (DM)-related carcinogenesis has expanded exponentially since these two diseases were recognized as important risk factors for...
Research on obesity- and diabetes mellitus (DM)-related carcinogenesis has expanded exponentially since these two diseases were recognized as important risk factors for cancers. The growing interest in this area is prominently actuated by the increasing obesity and DM prevalence, which is partially responsible for the slight but constant increase in pancreatic cancer (PC) occurrence. PC is a highly lethal malignancy characterized by its insidious symptoms, delayed diagnosis, and devastating prognosis. The intricate process of obesity and DM promoting pancreatic carcinogenesis involves their local impact on the pancreas and concurrent whole-body systemic changes that are suitable for cancer initiation. The main mechanisms involved in this process include the excessive accumulation of various nutrients and metabolites promoting carcinogenesis directly while also aggravating mutagenic and carcinogenic metabolic disorders by affecting multiple pathways. Detrimental alterations in gastrointestinal and sex hormone levels and microbiome dysfunction further compromise immunometabolic regulation and contribute to the establishment of an immunosuppressive tumor microenvironment (TME) for carcinogenesis, which can be exacerbated by several crucial pathophysiological processes and TME components, such as autophagy, endoplasmic reticulum stress, oxidative stress, epithelial-mesenchymal transition, and exosome secretion. This review provides a comprehensive and critical analysis of the immunometabolic mechanisms of obesity- and DM-related pancreatic carcinogenesis and dissects how metabolic disorders impair anticancer immunity and influence pathophysiological processes to favor cancer initiation.
Topics: Humans; Carcinogenesis; Diabetes Mellitus; Obesity; Pancreas; Pancreatic Neoplasms; Tumor Microenvironment
PubMed: 36964133
DOI: 10.1038/s41392-023-01376-w -
Annals of Surgical Oncology Jul 2023Pancreatic cancer often presents as locally advanced (LAPC) or borderline resectable (BRPC). Neoadjuvant systemic therapy is recommended as initial treatment. It is... (Meta-Analysis)
Meta-Analysis Review
FOLFIRINOX or Gemcitabine-based Chemotherapy for Borderline Resectable and Locally Advanced Pancreatic Cancer: A Multi-institutional, Patient-Level, Meta-analysis and Systematic Review.
BACKGROUND
Pancreatic cancer often presents as locally advanced (LAPC) or borderline resectable (BRPC). Neoadjuvant systemic therapy is recommended as initial treatment. It is currently unclear what chemotherapy should be preferred for patients with BRPC or LAPC.
METHODS
We performed a systematic review and multi-institutional meta-analysis of patient-level data regarding the use of initial systemic therapy for BRPC and LAPC. Outcomes were reported separately for tumor entity and by chemotherapy regimen including FOLFIRINOX (FIO) or gemcitabine-based.
RESULTS
A total of 23 studies comprising 2930 patients were analyzed for overall survival (OS) calculated from the beginning of systemic treatment. OS for patients with BRPC was 22.0 months with FIO, 16.9 months with gemcitabine/nab-paclitaxel (Gem/nab), 21.6 months with gemcitabine/cisplatin or oxaliplatin or docetaxel or capecitabine (GemX), and 10 months with gemcitabine monotherapy (Gem-mono) (p < 0.0001). In patients with LAPC, OS also was higher with FIO (17.1 months) compared with Gem/nab (12.5 months), GemX (12.3 months), and Gem-mono (9.4 months; p < 0.0001). This difference was driven by the patients who did not undergo surgery, where FIO was superior to other regimens. The resection rates for patients with BRPC were 0.55 for gemcitabine-based chemotherapy and 0.53 with FIO. In patients with LAPC, resection rates were 0.19 with Gemcitabine and 0.28 with FIO. In resected patients, OS for patients with BRPC was 32.9 months with FIO and not different compared to Gem/nab, (28.6 months, p = 0.285), GemX (38.8 months, p = 0.1), or Gem-mono (23.1 months, p = 0.083). A similar trend was observed in resected patients converted from LAPC.
CONCLUSIONS
In patients with BRPC or LAPC, primary treatment with FOLFIRINOX compared with Gemcitabine-based chemotherapy appears to provide a survival benefit for patients that are ultimately unresectable. For patients that undergo surgical resection, outcomes are similar between GEM+ and FOLFIRINOX when delivered in the neoadjuvant setting.
Topics: Humans; Gemcitabine; Antineoplastic Combined Chemotherapy Protocols; Oxaliplatin; Pancreatic Neoplasms; Fluorouracil; Leucovorin; Neoadjuvant Therapy; Paclitaxel; Multicenter Studies as Topic
PubMed: 37020094
DOI: 10.1245/s10434-023-13353-2 -
The Lancet. Oncology Jun 201635% of patients with pancreatic cancer have unresectable locally advanced disease at diagnosis. Several studies have examined systemic chemotherapy with FOLFIRINOX... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
35% of patients with pancreatic cancer have unresectable locally advanced disease at diagnosis. Several studies have examined systemic chemotherapy with FOLFIRINOX (leucovorin and fluorouracil plus irinotecan and oxaliplatin) in patients with locally advanced pancreatic cancer. We aimed to assess the effectiveness of FOLFIRINOX as first-line treatment in this patient population.
METHODS
We systematically searched Embase, MEDLINE (OvidSP), Web of Science, Scopus, PubMed Publisher, Cochrane, and Google Scholar from July 1, 1994, to July 2, 2015, for studies of treatment-naive patients of any age who received FOLFIRINOX as first-line treatment of locally advanced pancreatic cancer. Our primary outcome was overall survival. Secondary outcomes were progression-free survival; rates of grade 3 or 4 adverse events; and the proportion of patients who underwent radiotherapy or chemoradiotherapy, surgical resection after FOLFIRINOX, and R0 resection. We evaluated survival outcomes with the Kaplan-Meier method with patient-level data. Grade 3 or 4 adverse events, and the proportion of patients who underwent subsequent radiotherapy or chemoradiotherapy or resection, were pooled in a random-effects model.
FINDINGS
We included 13 studies comprising 689 patients, of whom 355 (52%) patients had locally advanced pancreatic cancer. 11 studies, comprising 315 patients with locally advanced disease, reported survival outcomes and were eligible for patient-level meta-analysis. Median overall survival from the start of FOLFIRINOX ranged from 10·0 months (95% CI 4·0-16·0) to 32·7 months (23·1-42·3) across studies with a pooled patient-level median overall survival of 24·2 months (95% CI 21·7-26·8). Median progression-free survival ranged from 3·0 months (95% CI not calculable) to 20·4 months (6·5-34·3) across studies with a patient-level median progression-free survival of 15·0 months (95% 13·8-16·2). In ten studies comprising 490 patients, 296 grade 3 or 4 adverse events were reported (60·4 events per 100 patients). No deaths were attributed to FOLFIRINOX toxicity. The proportion of patients who underwent radiotherapy or chemoradiotherapy ranged from 31% to 100% across studies. In eight studies, 154 (57%) of 271 patients received radiotherapy or chemoradiotherapy after FOLFIRINOX. The pooled proportion of patients who received any radiotherapy treatment was 63·5% (95% CI 43·3-81·6, I(2) 90%). The proportion of patients who underwent surgical resection for locally advanced pancreatic cancer ranged from 0% to 43%. The proportion of patients who had R0 resection of those who underwent resection ranged from 50% to 100% across studies. In 12 studies, 91 (28%) of 325 patients underwent resection after FOLFIRINOX. The pooled proportion of patients who had resection was 25·9% (95% CI 20·2-31·9, I(2) 24%). R0 resection was reported in 60 (74%) of 81 patients. The pooled proportion of patients who had R0 resection was 78·4% (95% CI 60·2-92·2, I(2) 64%).
INTERPRETATION
Patients with locally advanced pancreatic cancer treated with FOLFIRINOX had a median overall survival of 24·2 months-longer than that reported with gemcitabine (6-13 months). Future research should assess these promising results in a randomised controlled trial, and should establish which patients might benefit from radiotherapy or chemoradiotherapy or resection after FOLFIRINOX.
FUNDING
None.
Topics: Antineoplastic Combined Chemotherapy Protocols; Camptothecin; Chemotherapy, Adjuvant; Deoxycytidine; Fluorouracil; Humans; Irinotecan; Leucovorin; Neoplasm Staging; Organoplatinum Compounds; Oxaliplatin; Pancreatic Neoplasms; Prognosis; Survival Rate; Gemcitabine
PubMed: 27160474
DOI: 10.1016/S1470-2045(16)00172-8 -
The Cochrane Database of Systematic... Mar 2021Cancer cachexia is a multifactorial syndrome characterised by an ongoing loss of skeletal muscle mass, with or without a loss of fat mass, leading to progressive... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Cancer cachexia is a multifactorial syndrome characterised by an ongoing loss of skeletal muscle mass, with or without a loss of fat mass, leading to progressive functional impairment. Physical exercise may attenuate cancer cachexia and its impact on patient function. This is the first update of an original Cochrane Review published in Issue 11, 2014, which found no studies to include.
OBJECTIVES
To determine the effectiveness, acceptability and safety of exercise, compared with usual care, no treatment or active control, for cancer cachexia in adults.
SEARCH METHODS
We searched CENTRAL, MEDLINE, Embase, and eight other databases to March 2020. We searched for ongoing studies in trial registries, checked reference lists and contacted experts to seek relevant studies.
SELECTION CRITERIA
We sought randomised controlled trials in adults with cancer cachexia, that compared a programme of exercise alone or in combination with another intervention, with usual care, no treatment or an active control group.
DATA COLLECTION AND ANALYSIS
Two review authors independently assessed titles and abstracts for relevance and extracted data on study design, participants, interventions and outcomes from potentially relevant articles. We used standard methodological procedures expected by Cochrane. Our primary outcome was lean body mass and secondary outcomes were adherence to exercise programme, adverse events, muscle strength and endurance, exercise capacity, fatigue and health-related quality of life. We assessed the certainty of evidence using GRADE and included two Summary of findings tables.
MAIN RESULTS
We included four new studies in this update which overall randomised 178 adults with a mean age of 58 (standard deviation (SD) 8.2) years. Study sample size ranged from 20 to 60 participants and in three studies the proportion of men ranged from 52% to 82% (the fourth study was only available in abstract form). Three studies were from Europe: one in the UK and Norway; one in Belgium and one in Germany. The remaining study was in Canada. The types of primary cancer were head and neck (two studies), lung and pancreas (one study), and mixed (one study). We found two comparisons: exercise alone (strength-based exercise) compared to usual care (one study; 20 participants); and exercise (strength-based exercise/endurance exercise) as a component of a multimodal intervention (pharmacological, nutritional or educational (or a combination) interventions) compared with usual care (three studies, 158 participants). Studies had unclear and high risk of bias for most domains. Exercise plus usual care compared with usual care We found one study (20 participants). There was no clear evidence of a difference for lean body mass (8 weeks: MD 6.40 kg, 95% CI -2.30 to 15.10; very low-certainty evidence). For our secondary outcomes, all participants adhered to the exercise programme and no participant reported any adverse event during the study. There were no data for muscle strength and endurance, or maximal and submaximal exercise capacity. There was no clear evidence of a difference for either fatigue (4 to 20 scale, lower score was better) (8 weeks: MD -0.10, 95% CI -4.00 to 3.80; very low-certainty evidence) or health-related quality of life (0 to 104 scale, higher score was better) (8 weeks: MD 4.90, 95% CI -15.10 to 24.90; very low-certainty evidence). Multimodal intervention (exercise plus other interventions) plus usual care compared with usual care We found three studies but outcome data were only available for two studies. There was no clear evidence of a difference for lean body mass (6 weeks: MD 7.89 kg, 95% CI -9.57 to 25.35; 1 study, 44 participants; very low-certainty evidence; 12 weeks: MD -2.00, 95% CI -8.00 to 4.00; one study, 60 participants; very low-certainty evidence). For our secondary outcomes, there were no data reported on adherence to the exercise programme, endurance, or maximal exercise capacity. In one study (44 participants) there was no clear evidence of a difference for adverse events (patient episode report) (6 weeks: risk ratio (RR) 1.18, 95% CI 0.67 to 2.07; very low-certainty evidence). Another study assessed adverse events but reported no data and the third study did not assess this outcome. There was no clear evidence of a difference in muscle strength (6 weeks: MD 3.80 kg, 95% CI -2.87 to 10.47; 1 study, 44 participants; very low-certainty evidence; 12 weeks MD -5.00 kg, 95% CI -14.00 to 4.00; 1 study, 60 participants; very low-certainty evidence), submaximal exercise capacity (6 weeks: MD -16.10 m walked, 95% CI -76.53 to 44.33; 1 study, 44 participants; very low-certainty evidence; 12 weeks: MD -62.60 m walked, 95% CI -145.87 to 20.67; 1 study, 60 participants; very low-certainty evidence), fatigue (0 to 10 scale, lower score better) (6 weeks: MD 0.12, 95% CI -1.00 to 1.24; 1 study, 44 participants; very low-certainty evidence) or health-related quality of life (0 to 104 scale, higher score better) (12 weeks: MD -2.20, 95% CI -13.99 to 9.59; 1 study, 60 participants; very low-certainty evidence).
AUTHORS' CONCLUSIONS
The previous review identified no studies. For this update, our conclusions have changed with the inclusion of four studies. However, we are uncertain of the effectiveness, acceptability and safety of exercise for adults with cancer cachexia. Further high-quality randomised controlled trials are still required to test exercise alone or as part of a multimodal intervention to improve people's well-being throughout all phases of cancer care. We assessed the certainty of the body of evidence as very low, downgraded due to serious study limitations, imprecision and indirectness. We have very little confidence in the results and the true effect is likely to be substantially different from these. The findings of at least three more studies (one awaiting classification and two ongoing) are expected in the next review update.
Topics: Bias; Cachexia; Combined Modality Therapy; Exercise; Exercise Tolerance; Fatigue; Female; Head and Neck Neoplasms; Humans; Lung Neoplasms; Male; Middle Aged; Muscle Strength; Neoplasms; Pancreatic Neoplasms; Patient Compliance; Physical Endurance; Quality of Life; Randomized Controlled Trials as Topic; Thinness
PubMed: 33735441
DOI: 10.1002/14651858.CD010804.pub3 -
JAMA Network Open Jan 2024The NAPOLI 3 trial showed the superiority of fluorouracil, leucovorin, liposomal irinotecan, and oxaliplatin (NALIRIFOX) over the combination of gemcitabine and... (Meta-Analysis)
Meta-Analysis
IMPORTANCE
The NAPOLI 3 trial showed the superiority of fluorouracil, leucovorin, liposomal irinotecan, and oxaliplatin (NALIRIFOX) over the combination of gemcitabine and nab-paclitaxel (GEM-NABP) as first-line treatment of metastatic pancreatic ductal adenocarcinoma (PDAC). Analyses comparing NALIRIFOX and GEM-NABP with fluorouracil, leucovorin, irinotecan, and oxaliplatin (FOLFIRINOX) have not yet been reported.
OBJECTIVE
To derive survival, response, and toxic effects data from phase 3 clinical trials and compare NALIRIFOX, FOLFIRINOX, and GEM-NABP.
DATA SOURCES
After a systematic search of PubMed, Scopus, Embase, and American Society of Clinical Oncology and European Society for Medical Oncology meetings' libraries, Kaplan-Meier curves were extracted from phase 3 clinical trials conducted from January 1, 2011, until September 12, 2023.
STUDY SELECTION
Phase 3 clinical trials that tested NALIRIFOX, FOLFIRINOX, or GEM-NABP as first-line treatment of metastatic PDAC and reported overall survival (OS) and progression-free survival (PFS) curves were selected. This study followed the Preferred Reporting Items for Systematic Reviews and Meta-analyses of Individual Participant Data reporting guidelines.
DATA EXTRACTION AND SYNTHESIS
Individual patient OS and PFS data were extracted from Kaplan-Meier plots of original trials via a graphic reconstructive algorithm. Overall response rates (ORRs) and grade 3 or higher toxic effects rates were also collected. A pooled analysis was conducted, and results were validated via a network meta-analysis.
MAIN OUTCOMES AND MEASURES
The primary end point was OS. Secondary outcomes included PFS, ORR, and toxic effects rates.
RESULTS
A total of 7 trials with data on 2581 patients were analyzed, including 383 patients treated with NALIRIFOX, 433 patients treated with FOLFIRINOX, and 1756 patients treated with GEM-NABP. Median PFS was longer in patients treated with NALIRIFOX (7.4 [95% CI, 6.1-7.7] months) or FOLFIRINOX (7.3 [95% CI, 6.5-7.9] months; [HR], 1.21 [95% CI, 0.86-1.70]; P = .28) compared with patients treated with GEM-NABP (5.7 [95% CI, 5.6-6.1] months; HR vs NALIRIFOX, 1.45 [95% CI, 1.22-1.73]; P < .001). Similarly, GEM-NABP was associated with poorer OS (10.4 [95% CI, 9.8-10.8]; months) compared with NALIRIFOX (HR, 1.18 [95% CI, 1.00-1.39]; P = .05], while no difference was observed between FOLFIRINOX (11.7 [95% CI, 10.4-13.0] months) and NALIRIFOX (11.1 [95% CI, 10.1-12.3] months; HR, 1.06 [95% CI, 0.81-1.39]; P = .65). There were no statistically significant differences in ORR among NALIRIFOX (41.8%), FOLFIRINOX (31.6%), and GEM-NABP (35.0%). NALIRIFOX was associated with lower incidence of grade 3 or higher hematological toxic effects (eg, platelet count decreased 1.6% vs 11.8% with FOLFIRINOX and 10.8% with GEM-NABP), but higher rates of severe diarrhea compared with GEM-NABP (20.3% vs 15.7%).
CONCLUSIONS AND RELEVANCE
In this systematic review and meta-analysis, NALIRIFOX and FOLFIRINOX were associated with similar PFS and OS as first-line treatment of advanced PDAC, although NALIRIFOX was associated with a different toxicity profile. Careful patient selection, financial toxic effects consideration, and direct comparison between FOLFIRINOX and NALIRIFOX are warranted.
Topics: Humans; Pancreatic Neoplasms; Irinotecan; Antineoplastic Combined Chemotherapy Protocols; Leucovorin; Oxaliplatin; Gemcitabine; Fluorouracil; Adenocarcinoma
PubMed: 38190183
DOI: 10.1001/jamanetworkopen.2023.50756 -
BMJ Clinical Evidence May 2010Pancreatic cancer is the fourth most common cause of cancer death in higher-income countries, with 5-year survival only 10% even in people presenting with early-stage... (Review)
Review
INTRODUCTION
Pancreatic cancer is the fourth most common cause of cancer death in higher-income countries, with 5-year survival only 10% even in people presenting with early-stage cancer. Risk factors include smoking, high alcohol intake, and dietary factors, while diabetes mellitus and previous pancreatitis may also increase the risk.
METHODS AND OUTCOMES
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of surgical treatments in people with pancreatic cancer considered suitable for complete tumour resection? What are the effects of interventions to prevent pancreatic leak after pancreaticoduodenectomy in people with pancreatic cancer considered suitable for complete tumour resection? What are the effects of adjuvant treatments in people with completely resected pancreatic cancer? What are the effects of interventions in people with non-resectable (locally advanced or advanced) pancreatic cancer? We searched: Medline, Embase, The Cochrane Library, and other important databases up to August 2009 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
RESULTS
We found 46 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
CONCLUSIONS
In this systematic review we present information relating to the effectiveness and safety of the following interventions: chemoradiotherapy; chemoradiotherapy for non-resectable pancreatic cancer; chemoradiotherapy for resected pancreatic cancer; fibrin glue; fluorouracil-based chemotherapy (adjuvant) for resected pancreatic cancer (with or without surgery); fluorouracil-based chemotherapy for non-resectable pancreatic cancer; fluorouracil-based chemotherapy (systemic); fluorouracil-based combination chemotherapy; fluorouracil-based monotherapy for non-resectable pancreatic cancer; gemcitabine-based chemotherapy (adjuvant) for resected pancreatic cancer; gemcitabine-based chemotherapy (systemic); gemcitabine-based combination chemotherapy; gemcitabine-based monotherapy for non-resectable pancreatic cancer; lymphadenectomy (extended [radical], or standard) in people having pancreaticoduodenectomy; pancreatic duct occlusion; pancreaticoduodenectomy (pylorus-preserving); pancreaticoduodenectomy (Whipple's procedure); pancreaticogastrostomy reconstruction; pancreaticojejunostomy; and somatostatin and somatostatin analogues.
Topics: Fluorouracil; Humans; Pancreatectomy; Pancreatic Neoplasms; Pancreaticoduodenectomy; Pylorus
PubMed: 21729338
DOI: No ID Found -
Correlation between pancreatic cancer and metabolic syndrome: A systematic review and meta-analysis.Frontiers in Endocrinology 2023Pancreatic cancer is a globally frequent cause of death, which can be caused by many factors. This meta-analysis was performed to assess the correlation between... (Meta-Analysis)
Meta-Analysis
OBJECTIVE
Pancreatic cancer is a globally frequent cause of death, which can be caused by many factors. This meta-analysis was performed to assess the correlation between pancreatic cancer and metabolic syndrome (MetS).
METHODS
Publications were identified by searching PubMed, EMBASE, and the Cochrane Library for studies published until November 2022. Case-control and cohort studies published in English that provided information on the odds ratio (OR), relative risk (RR), or hazard ratio (HR) of metabolic syndrome and pancreatic cancer were included in the meta-analysis. Two researchers separately retrieved the core data from the included Random effects meta-analysis was conducted to summarize the findings. Results were presented as relative risk (RR) and 95% confidence interval (CI).
RESULTS
MetS showed a strong association with an increased risk of developing pancreatic cancer (RR1.34, 95% CI1.23-1.46, <0.001), and gender differences were also observed (men: RR 1.26, 95% CI 1.03-1.54, =0.022; women: RR 1.64, 95% CI 1.41-1.90, < 0.001). Moreover, an increased risk of developing pancreatic cancer was strongly linked to hypertension, poor high-density lipoprotein cholesterol, and hyperglycemia (hypertension: RR 1.10 CI 1.01-1.19, =0.027; low high-density lipoprotein cholesterol: RR 1.24 CI 1.11-1.38, <0.001; hyperglycemia: RR 1.55, CI 1.42-1.70, < 0.001). However, pancreatic cancer was independent of obesity and hypertriglyceridemia (obesity: RR 1.13 CI 0.96-1.32, =0.151, hypertriglyceridemia: RR 0.96, CI 0.87-1.07, =0.486).
CONCLUSIONS
Although further prospective studies are required for confirmation, this meta-analysis indicated a strong relationship between MetS and pancreatic cancer. Regardless of gender, a greater risk of pancreatic cancer existed in people with MetS. Patients with MetS were more likely to develop pancreatic cancer, regardless of gender. Hypertension, hyperglycemia, and low HDL-c levels may largely account for this association. Further, the prevalence of pancreatic cancer was independent of obesity and hypertriglyceridemia.
SYSTEMATIC REVIEW REGISTRATION
https://www.crd.york.ac.uk/prospero/, identifier CRD42022368980.
Topics: Male; Humans; Female; Metabolic Syndrome; Obesity; Hyperglycemia; Hypertension; Hyperlipidemias; Hypertriglyceridemia; Pancreatic Neoplasms; Lipoproteins, HDL; Cholesterol
PubMed: 37113491
DOI: 10.3389/fendo.2023.1116582 -
Histopathology Sep 2022Intraductal tubulopapillary neoplasm (ITPN) of the pancreas is a recently recognized pancreatic tumor entity. Here we aimed to determine the most important features with... (Review)
Review
AIMS
Intraductal tubulopapillary neoplasm (ITPN) of the pancreas is a recently recognized pancreatic tumor entity. Here we aimed to determine the most important features with a systematic review coupled with an integrated statistical approach.
METHODS AND RESULTS
PubMed, SCOPUS, and Embase were searched for studies reporting data on pancreatic ITPN. The clinicopathological, immunohistochemical, and molecular data were summarized. Then a comprehensive survival analysis and a comparative analysis of the molecular alterations of ITPN with those of pancreatic ductal adenocarcinoma (PDAC) and intraductal papillary mucinous neoplasm (IPMN) from reference cohorts (including the International Cancer Genome Consortium- ICGC dataset and The Cancer Genome Atlas, TCGA program) were conducted. The core findings of 128 patients were as follows: (i) Clinicopathological parameters: pancreatic head is the most common site; presence of an associated adenocarcinoma was reported in 60% of cases, but with rare nodal metastasis. (ii) Immunohistochemistry: MUC1 (>90%) and MUC6 (70%) were the most frequently expressed mucins. ITPN lacked the intestinal marker MUC2; unlike IPMN, it did not express MUC5AC. (iii) Molecular landscape: Compared with PDAC/IPMN, the classic pancreatic drivers KRAS, TP53, CDKN2A, SMAD4, GNAS, and RNF43 were less altered in ITPN (P < 0.001), whereas MCL amplifications, FGFR2 fusions, and PI3KCA mutations were commonly altered (P < 0.001). (iv) Survival analysis: ITPN with a "pure" branch duct involvement showed the lowest risk of recurrence.
CONCLUSION
ITPN is a distinct pancreatic neoplasm with specific clinicopathological and molecular characteristics. Its recognition is fundamental for its clinical/prognostic implications and for the enrichment of potential targets for precision oncology.
Topics: Carcinoma, Pancreatic Ductal; Carcinoma, Papillary; Humans; Pancreas; Pancreatic Intraductal Neoplasms; Pancreatic Neoplasms; Precision Medicine
PubMed: 35583805
DOI: 10.1111/his.14698 -
Cell Proliferation Oct 2023The liver is a common secondary metastasis site of many malignant tumours, such as the colorectum, pancreas, stomach, breast, prostate, and lung cancer. The clinical... (Review)
Review
The liver is a common secondary metastasis site of many malignant tumours, such as the colorectum, pancreas, stomach, breast, prostate, and lung cancer. The clinical management of liver metastases is challenging because of their strong heterogeneity, rapid progression, and poor prognosis. Now, exosomes, small membrane vesicles that are 40-160 nm in size, are released by tumour cells, namely, tumour-derived exosomes (TDEs), and are being increasingly studied because they can retain the original characteristics of tumour cells. Cell-cell communication via TDEs is pivotal for liver pre-metastatic niche (PMN) formation and liver metastasis; thus, TDEs can provide a theoretical basis to intensively study the potential mechanisms of liver metastasis and new insights into the diagnosis and treatment of liver metastasis. Here, we systematically review current research progress about the roles and possible regulatory mechanisms of TDE cargos in liver metastasis, focusing on the functions of TDEs in liver PMN formation. In addition, we discuss the clinical utility of TDEs in liver metastasis, including TDEs as potential biomarkers, and therapeutic approaches for future research reference in this field.
Topics: Humans; Exosomes; Liver Neoplasms; Cell Communication; Pancreas; Biomarkers, Tumor; Tumor Microenvironment; Neoplasm Metastasis
PubMed: 36941028
DOI: 10.1111/cpr.13452