BackgroundAdjuvant chemotherapy and targeted therapy have become standard postoperative therapeutic modalities for human epidermal growth factor receptor 2 (HER2)-positive breast cancer(HER2-positive,HR-negative), including triple-positive breast cancer(HER2-positive,HR-positive). However, these two types of breast cancer differ in terms of pathogenesis. This article analyzes these two types of breast cancer by comparing their prognoses.MethodsThe clinicopathological characteristics of 135 patients, including 60 patients with triple-positive breast cancer and 75 patients with HER2-positive breast cancer, were analyzed to compare the disease-free survival (DFS) and overall survival (OS) of the two groups over a 5-year period. A multifactorial Cox risk model was constructed by grouping age, menstrual status, maximum tumor diameter, number of lymph node metastases, pathological staging, and Ki-67 staining results. All statistical data were analyzed in detail using SPSS25.0 statistical software.ResultsThe 5-year OS rates of patients with breast cancer in the triple-positive and HER2-positive groups were 96.7% and 82.7%, respectively, and the 5-year DFS rates were 90% and 73.3%, respectively. The Cox results revealed that molecular staging was an independent factor affecting recurrent metastasis and survival of breast cancer patients (hazard ratio [HR] =2.199, 95% confidence interval [CI], 1.296-8.266; HR = 9.994, 95% CI, 2.019-49.465).ConclusionThe 5-year DFS and OS rates were significantly better in the triple-positive group than in the HER2-positive group. Subgroups received different prognosis for different chemotherapy regimens. Breast cancer patients should be treated according to the risk of recurrence with symptomatic treatment and precise regulation.

BackgroundN6-methyladenosine (m6A) modification is the most common RNA modification, but its potential role in the development of esophageal cancer and its specific mechanisms still need to be further investigated.MethodsBulk RNA-seq of 174 patients with esophageal squamous carcinoma from the TCGA-ESCC cohort, GSE53625, and single-cell sequencing data from patients with esophageal squamous carcinoma from GSE188900 were included in this study. Single-cell analysis of scRNA-seq data from GSE188900 of 4 esophageal squamous carcinoma samples and calculation of PROGENy scores. Demonstrate the scoring of tumor-associated pathways for different cell populations. Cell Chat was calculated for cell populations. thereafter, m6A-related differential genes were sought and risk models were constructed to analyze the relevant biological functions and impact pathways of potential m6A genes and their impact on immune infiltration and tumor treatment sensitivity in ESCC was investigated.ResultsBy umap downscaling analysis, ESCC single-cell data were labelled into clusters of seven immune cell classes. Cellchat analysis showed that the network interactions of four signaling pathways, MIF, AFF, FN1 and CD99, all showed different cell type interactions. The prognostic risk model constructed by screening for m6A-related differential genes was of significant value in the prognostic stratification of ESCC patients and had a significant impact on immune infiltration and chemotherapy sensitivity in ESCC patients.ConclusionIn our study, we explored a blueprint for the distribution of single cells in ESCC based on m6A methylation and constructed a risk model for immune infiltration analysis and tumor efficacy stratification in ESCC on this basis. This may provide important potential guidance for revealing the role of m6A in immune escape and treatment resistance in esophageal cancer.