Diabetes mellitus promoted lymph node metastasis in gastric cancer: a 15–year single-institution experience

Abstract

Background:Previous studies have revealed that diabetes mellitus (DM) promotes disease progress of gastric cancer (GC). This study aimed to further investigating whether DM advanced lymph nodes (LNs) metastasis in GC.Methods:The clinicopathologic data of GC patients with >15 examined LN (ELN) between October 2004 and December 2019 from a prospectively maintained database were included. The observational outcomes included the number (N3b status) and anatomical distribution (N3 stations) of metastatic LN (MLN).Results:A total of 2142 eligible patients were included in the study between October 2004 and December 2019. N3 stations metastasis (26.8% in DM vs. 19.3% in non-DM, P = 0.026) and N3b status (18.8% in DM vs. 12.8% in non-DM, P = 0.039) were more advanced in the DM group, and multivariate logistic regression analyses confirmed that DM was an independent factor of developing N3 stations metastasis (odds ratio [OR] = 1.771, P = 0.011) and N3b status (OR = 1.752, P = 0.028). Also, multivariate analyses determined DM was independently associated with more MLN (β = 1.424, P = 0.047). The preponderance of N3 stations metastasis (DM vs. non-DM, T1–2: 2.2% vs. 4.9%, T3: 29.0% vs. 20.3%, T4a: 38.9% vs. 25.8%, T4b: 50.0% vs. 36.6%; ELN16–29: 8.6% vs. 10.4%, ELN30–44: 27.9% vs. 20.5%, ELN ≥ 45: 37.7% vs. 25.3%), N3b status (DM vs. non-DM, T1–2: 0% vs. 1.7%, T3: 16.1% vs. 5.1%, T4a: 27.8% vs. 19.1%, T4b: 44.0% vs. 28.0%; ELN16–29: 8.6% vs. 7.9%, ELN30–44: 18.0% vs. 11.8%, ELN ≥ 45: 26.4% vs. 17.3%), and the number of MLN (DM vs. non-DM, T1–2: 0.4 vs. 1.1, T3: 8.6 vs. 5.2, T4a: 9.7 vs. 8.6, T4b: 17.0 vs. 12.8; ELN16–29: 3.6 vs. 4.6, ELN30–44: 5.8 vs. 5.5, ELN ≥ 45: 12.0 vs. 7.7) of DM group increased with the advancement of primary tumor depth stage and raising of ELN.Conclusions:DM was an independent risk factor for promoting LN metastasis. The preponderance of LN involvement in the DM group was aggravated with the advancement of tumor depth.

Relationship Between Programmed Death Ligand 1 Expression and Other Clinicopathological Features in a Large Cohort of Gastric Cancer Patients

“…All cases were reviewed by two pathologists, and histological diagnoses were confirmed without discrepancy. Clinical characteristics including age, body mass index (BMI), sex, diabetes (12), tumor location (13), histology, Lauren classification, grade, Tumor size, T stage (14), N stage (15,16), M stage (14), Ki-67 index, S-100, CD-31, D240, EBV, MMR, and, HER2 statuses, and routine blood indicators [white blood cell (WBC), mononuclear cell (MONO), eosinophilic granulocyte (EOS), neutrophil (NEU), lymphocyte (LYM), and platelet (PLT) counts, the neutrophil/lymphocyte ratio (NLR), and ABO blood group] were obtained from medical records, pathology reports, discharge summaries, and extracted from the prospective database. All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1964 and later versions.…”

Advances in Treatment Models of Advanced Gastric Cancer

“…[67][68][69] Luckily, with persistent effort, new treatment models of AGC, especially conversion therapy and immunotherapy, have brought a new sense of hope and vision. Taking into consideration the high heterogeneity of GC [70][71][72][73] , it is particularly important to further screen subgroups sensitive to each treatment model to develop individual and tailored treatments for AGC. Meanwhile, how to improving the response to immunotherapy and overcome drug resistance via tumor microenvironment changes caused by immunotherapy and chemotherapy are also future research directions.…”

Diabetes Mellitus and Gastric Cancer: Correlation and Potential Mechanisms

“…Additionally, insulin resistance in DM promotes inflammation and activates nuclear factor-κB (NF-κB), which is a light-chain enhancer of activated B cell signaling that plays a major role in GC development and progression [61]. Hyperglycemia can also provide more glucose to tumor cells, promote tumor proliferation and migration, and activate GC cells to migrate to lymph nodes [62]. In addition, abnormal fluctuations in glucose levels in DM patients also increase oxidative stress, endothelial dysfunction, and subclinical inflammation.…”