N6-methyladenosine (m6A) is methylation that occurs in the N6-position of adenosine, which is the most prevalent internal modification on eukaryotic mRNA. Accumulating evidence suggests that m6A modulates gene expression, thereby regulating cellular processes ranging from cell self-renewal, differentiation, invasion and apoptosis. M6A is installed by m6A methyltransferases, removed by m6A demethylases and recognized by reader proteins, which regulate of RNA metabolism including translation, splicing, export, degradation and microRNA processing. Alteration of m6A levels participates in cancer pathogenesis and development via regulating expression of tumor-related genes like BRD4, MYC, SOCS2 and EGFR. In this review, we elaborate on recent advances in research of m6A enzymes. We also highlight the underlying mechanism of m6A in cancer pathogenesis and progression. Finally, we review corresponding potential targets in cancer therapy.

/pdf/functions-of-n6-methyladenosine-and-its-role-in-cancer-2mbjjwdcui.pdf

Functions of N6-methyladenosine and its role in cancer.

m6A Modification in Coding and Non-coding RNAs: Roles and Therapeutic Implications in Cancer

Cancers are not composed merely of cancer cells alone; instead, they are complex ‘ecosystems’ comprising many different cell types and noncellular factors. The tumour stroma is a critical component of the tumour microenvironment, where it has crucial roles in tumour initiation, progression, and metastasis. Most anticancer therapies target cancer cells specifically, but the tumour stroma can promote the resistance of cancer cells to such therapies, eventually resulting in fatal disease. Therefore, novel treatment strategies should combine anticancer and antistromal agents. Herein, we provide an overview of the advances in understanding the complex cancer cell–tumour stroma interactions and discuss how this knowledge can result in more effective therapeutic strategies, which might ultimately improve patient outcomes.

/pdf/targeting-the-tumour-stroma-to-improve-cancer-therapy-rewmxesg5f.pdf

Targeting the tumour stroma to improve cancer therapy

The role of m6A RNA methylation in cancer.

N6-methyladenosine (m6A) is considered the most common, abundant, and conserved internal transcript modification, especially in eukaryotic messenger RNA (mRNA). m6A is installed by m6A methyltransferases (METTL3/14, WTAP, RBM15/15B, VIRMA and ZC3H13, termed “writers”), removed by demethylases (FTO, ALKBH5, and ALKBH3, termed “erasers”), and recognized by m6A-binding proteins (YTHDC1/2, YTHDF1/2/3, IGF2BP1/2/3, HNRNP, and eIF3, termed “readers”). Accumulating evidence suggests that m6A RNA methylation greatly impacts RNA metabolism and is involved in the pathogenesis of many kinds of diseases, including cancers. In this review, we focus on the physiological functions of m6A modification and its related regulators, as well as on the potential biological roles of these elements in human tumors.

/pdf/the-potential-role-of-rna-n6-methyladenosine-in-cancer-1i1g16d2l1.pdf

The potential role of RNA N6-methyladenosine in Cancer progression

Objectives: To evaluate the positive rate of left posterior lymph nodes of the superior mesenteric artery (14cd-LN) in patients undergoing pancreaticoduodenectomy for pancreatic head carcinoma,to analyze the impact of 14cd-LN dissection on lymph node staging and tumor TNM staging. Methods: The clinical and pathological data of 103 consecutive patients with pancreatic cancer who underwent pancreaticoduodenectomy at Pancreatic Center,the First Affiliated Hospital of Nanjing Medical University from January to December 2022 were analyzed,retrospectively. There were 69 males and 34 females,with an age(M (IQR))of 63.0 (14.0) years (range:48.0 to 86.0 years). The χ2 test and Fisher's exact probability method was used for comparison of the count data between the groups,respectively. The rank sum test was used for comparison of the measurement data between groups. Univariate and multivariate Logistic regression analyzes were used for the analysis of risk factors. Results: All 103 patients underwent pancreaticoduodenectomy successfully using the left-sided uncinate process and the artery first approach. Pathological examination showed pancreatic ductal adenocarcinoma in all cases. The location of the tumors was the pancreatic head in 40 cases,pancreatic head-uncinate in 45 cases,and pancreatic head-neck in 18 cases. Of the 103 patients,38 cases had moderately differentiated tumor and 65 cases had poorly differentiated tumor. The diameter of the lesions was 3.2 (0.8) cm (range:1.7 to 6.5 cm),the number of lymph nodes harvested was 25 (10) (range:11 to 53),and the number of positive lymph nodes was 1 (3) (range:0 to 40). The lymph node stage was stage N0 in 35 cases (34.0%),stage N1 in 43 cases (41.7%),and stage N2 in 25 cases (24.3%). TNM staging was stage ⅠA in 5 cases (4.9%),stage ⅠB in 19 cases (18.4%),stage ⅡA in 2 cases (1.9%),stage ⅡB in 38 cases (36.9%),stage Ⅲ in 38 cases (36.9%),and stage Ⅳ in 1 case (1.0%). In 103 patients with pancreatic head cancer,the overall positivity rate for 14cd-LN was 31.1% (32/103),and the positive rates for 14c-LN and 14d-LN were 21.4% (22/103) and 18.4% (19/103),respectively. 14cd-LN dissection increased the number of lymph nodes (P<0.01) and positive lymph nodes (P<0.01). As a result of the 14cd-LN dissection,the lymph node stage was changed in 6 patients,including 5 patients changed from N0 to N1 and 1 patient changed from N1 to N2. Similarly,the TNM stage was changed in 5 patients,including 2 patients changed from stage ⅠB to ⅡB,2 patients changed from stage ⅡA to ⅡB,and 1 patient changed from stage ⅡB to Ⅲ. Tumors located in the pancreatic head-uncinate (OR=3.43,95%CI:1.08 to 10.93,P=0.037) and the positivity of 7,8,9,12 LN (OR=5.45,95%CI:1.45 to 20.44,P=0.012) were independent risk factors for 14c-LN metastasis; while tumors with diameter >3 cm (OR=3.93,95%CI:1.08 to 14.33,P=0.038) and the positivity of 7,8,9,12 LN (OR=11.09,95%CI:2.69 to 45.80,P=0.001) were independent risk factors for 14d-LN metastasis. Conclusion: Due to its high positive rate in pancreatic head cancer,dissection of 14cd-LN during pancreaticoduodenectomy should be recommended,which can increase the number of lymph nodes harvested,provide a more accurate lymph node staging and TNM staging.

[Clinical value of lymph node dissection of No. 14cd during pancreaticoduodenectomy in patients with pancreatic head carcinoma].

230 modified appleby procedure for locally advanced pancreatic cancer (lapc) after neoadjuvant therapy

Introduction: The tumor microenvironment is one of the significant factors contributing to the progression of pancreatic neuroendocrine tumors (panNETs). However, the underlying mechanism of how the tumor microenvironment impacts the prognosis of panNETs is not completely clear. 

Prognostic Implication of Tumor Immune Microenvironment for Pancreatic Neuroendocrine Tumors: A Bioinformatical Approach

Introduction: Pancreatic ductal adenocarcinoma (PDAC) is a highly invasive cancer with poor prognosis. As a member of the CAP superfamily, Peptidase inhibitor 16 (Pi16) is still unclear in most tumor studies. In our recent research, we were the first to find that Pi16 is highly expressed in PDAC tissues, and might regulate the proliferation and metastasis of PDAC by combining with Oligoadenylate synthetase L (OASL). Method: Immunohistochemistry and quantitative RT-PCR methods were used to detect the expression levels of Pi16 protein and mRNA in PDAC patients. The CRISPR-Cas9 technology was used to knocked out the expression of Pi16 in PDAC cell lines. Tests in vivo and in vitro were used to verify the effect of Pi16 on PDAC proliferation and metastasis. By RNA sequencing, we found that OASL can serve as a potential downstream of Pi16. Results: The expression of Pi16 was higher in cancer tissues compared with matched adjacent tissues. High expression of Pi16 was associated with PDAC progression and poor prognosis. Overexpression of ROBO1 could promote the proliferation and metastasis of PDAC cells in vitro. It was found that Pi16 could bind to OASL by bioinformatics analysis and Co-immunoprecipitation (Co-IP) assay. Moreover, the function recovery test confirmed that Pi16 could promote the proliferation and metastasis of PDAC via OASL. Conclusions: Our present study demonstrates that Pi16 might participate in the occurrence and development of PDAC by regulating cell proliferation and metastasis by combining with OASL, and indicates that Pi16 might be a new promising therapeutic target for PDAC.Tabled 1VariablePi16 expressionHighLowP valueAge (year) ≤ 607140.267> 602224Histological grade I/I-II19260.802II/II-III/III1012T stage T1,T222310.568T3,T477Clinical stage I-IIa11240.041IIb-IV1814 Open table in a new tab 

Peptidase Inhibitor 16 Promote Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma via Oligoadenylate Synthetase L

Su1434 DISEASE BURDEN AND MANAGEMENT OF PANCREATIC EXOCRINE INSUFFICIENCY IN PATIENTS AFTER PANCREATIC RESECTION IN CHINA: A CROSS-SECTIONAL STUDY

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