Table 2. GC classification algorithm based on immunohistochemistry and in-situ hybridization.
Sample size | Markers | Findings | References |
---|---|---|---|
438 GC patients | EBER, MLH1, PMS2, MSH2, MSH6, HER2, EGFR, MET, PTEN, TP53 | Relationship between protein/RNA expression levels and unique clinical characteristics | Kim et al. [24] |
244 GC patients | EBER, MLH1, MSH2, MSH6, PMS2, TP53, E-cadherin, EGFR, HER2, Lauren classification | Association of molecular markers and clinicopathological characteristics including sex, tumor location, and overall survival | Birkman et al. [25] |
146 GC patients | EBER, MLH1, PMS2, MSH2, MSH6, TP53, E-cadherin | Clinicopathologic features including significant differences in prognosis corresponding to earlier molecular classification | Setia et al. [26] |
349 GC patients | EBER, MLH1, E-cadherin, TP53, HER2 | Clinicopathologic features including significant differences in prognosis corresponding to earlier molecular classification | Ahn et al. [27] |
206 GC patients | MLH1, PMS2, MSH2, MSH6, TP53, E-cadherin, | Subtypes associated with survival, recurrence rate, and other clinical characteristics corresponding to TCGA classification | Díaz Del Arco et al. [28] |
104 GC patients | ERER, MLH1, TP53 | Subtypes associated with survival and HER2 overexpression comparable to TCGA classification | Gonzalez et al. [29] |
993 GC patients | EBER, TP53, EGFR, HER2, MET, Lauren classification | Survival predicting histo-molecular classification and screening protocol for RTK amplified GCs | Park et al. [30] |
GC = gastric cancer; EBER = Epstein–Barr encoding region; MLH1 = mutL homolog 1; TP53 = tumor suppressor p53; PMS2 = PMS1 homolog 2; MET =mesenchymal epithelial transtion; PTEN = phosphatase and tensin homologue deleted on chromosome 10; HER2 = human epidermal growth factor receptor 2; EGFR = epidermal growth factor receptor; TCGA = The Cancer Genomic Atlas; RTK = receptor tyrosine kinase; MSH = mutS homologue.