Gastric precancerous lesions:occurrence, development factors, and treatment

Abstract

Patients with gastric precancerous lesions (GPL) have a higher risk of gastric cancer (GC). However, the transformation of GPL into GC is an ongoing process that takes several years. At present, several factors including H.Pylori (Hp), flora imbalance, inflammatory factors, genetic variations, Claudin-4, gastric stem cells, solute carrier family member 26 (SLC26A9), bile reflux, exosomes, and miR-30a plays a considerable role in the transformation of GPL into GC. Moreover, timely intervention in the event of GPL can reduce the risk of GC. In clinical practice, GPL is mainly treated with endoscopy, acid suppression therapy, Hp eradication, a cyclooxygenase-2 inhibitor, aspirin, and diet. Currently, the use of traditional Chinese medicine (TCM) or combination with western medication to remove Hp and the use of TCM to treat GPL are common in Asia, particularly China, and have also demonstrated excellent clinical efficacy. This review thoroughly discussed the combining of TCM and Western therapy for the treatment of precancerous lesions as conditions allow. Consequently, this review also focuses on the causes of the development and progression of GPL, as well as its current treatment. This may help us understand GPL and related treatment.

Keywords: H.pylori; gastric cancer; gastric precancerous lesions; traditional Chinese medicine; treatment.

Figure 1

Overview of the occurrence and development of GPL. The color change from left to right represents the process of GPL development. Inflammation runs through the occurrence and development of GPL. At the same time, it will lead to the loss of gastric stem cells SLC26A9, which will lead to the occurrence of GPL and GC. The multi-directional differentiation of gastric stem cells may also be the source of GPL and GC. Inflammatory factor IL-6, IL-1 in patients with GPL β, TNF- α, IL-10, IL-4, IFN- γ The formation of GC will be accelerated. Bile regeneration will cause the occurrence and development of GPL through the IL-6/JAK1/STAT3 signal pathway, and the active oxygen/nitrogen generated will cause DNA damage. The high expression of Claudin-4 will induce the formation of EMT and IM, and the induced IL-8 will accelerate the formation of GC. The ncRNA in Exosomes can also promote the development of GPL and the formation of GC. From the occurrence of GPL to the formation of GC, under the influence of various factors, chromatin modeling, driver gene abnormality, DNA metabolism change, etc. are phenomena that occur in this process, but they are also the driving force for GPL to develop towards GC.

Figure 2

GPL Treatment Overview. This figure illustrates some drugs or regimens that can help treat PLGC. Mainly including traditional Chinese medicine, Western medicine, and a combination of traditional Chinese and Western medicine treatment plan for inhibiting Hp;Therapeutic drugs that inhibit Inflammatory or and factors; Drugs that inhibit DNA damage caused by reactive oxygen species; Drugs that inhibit glycolysis in PLGC; Drugs that treat PGLC by upregulating PER3 and AQP4; By inhibiting TLRs/NF- κ B pathway and EGFR-PI3K-AKT pathway to treat PGLC drugs; A regimen that helps increase the sensitivity of tumor cells to chemotherapy.