Breast cancer is one of the common malignant tumors in women, which seriously affects women’s life and health, and its incidence is increasing year by year. Chemotherapy is an important part of the comprehensive treatment of breast cancer. Currently, chemotherapy for breast cancer is mostly based on the clinical stage and pathological type of breast cancer, which makes the treatment blind due to the heterogeneity of tumors and their insensitivity to chemotherapy drugs. Chemotherapeutic drugs are cytotoxic in themselves, and during the process of chemotherapy, the cancer may not be controlled, but there may be adverse reactions, which bring unnecessary pain to the patient and affect the quality of life and even the prognosis of the tumor. Therefore, it is necessary to find some indicators that can predict the efficacy of chemotherapy for breast cancer, in order to guide the selection of chemotherapy drugs and the application of chemotherapy regimens, thus improving the efficacy of chemotherapy. With the rapid development of molecular biology, it has been recognized that gene expression in breast cancer is closely related to the occurrence, development, metastasis and prognosis of tumors, and also has some connection with the chemotherapeutic efficacy of tumors. I. Oncogene c-erbB-2 Oncogenes are nucleic acid sequences in living organisms that can cause malignant transformation of cells. The oncogenes associated with breast cancer are c-erbB-2, ras, c-myc and so on. The c-erbB-2 oncogene, also known as HER-2 or neu, was originally identified in a rat neuroblastoma cell line caused by ethylnitrosourea. c-erbB-2 oncogene is located in the q21 region of chromosome 17 and has homology with EGFR gene. Herceptin (trade name Herceptin), whose main component is Trastuzumab, Pegram et al [1] used fluorescence in situ hybridization to detect HER-2 gene amplification in breast cancer and found that the HER-2 gene amplification group had a high overall response rate and a long mean time to progression to chemotherapy with doxorubicin, allyloxacin, cisplatin, or carboplatin, and concluded that the combination of doxorubicin, allyloxacin, and platinum salts Campiglio et al [2] studied 220 breast cancers with tumors larger than 2.5 cm, all receiving three courses of adriamycin chemotherapy, and found that HER-2(+) patients were more responsive to adriamycin than HER-2(-) patients, and concluded that HER-2 expression could be used as a predictor of responsiveness to adriamycin in an in vivo trial. Dileo et al [3] studied 430 cases of early-stage breast cancer treated with EPI, CTX or CMF regimen chemotherapy and found that anthracycline-based chemotherapy was more effective than CMF in cases with HER-2 amplification, suggesting that HER-2 is predictive of breast cancer treated with anthracycline-based adjuvant chemotherapy by a mechanism possibly related to amplification of the Topo IIα gene. In a study by Gregory et al [4], c-erbB-2-positive patients were found to show unresponsiveness to methotrexate, mitoxantrone chemotherapy, and triamcinolone endocrine therapy; the results of a study by Nieto et al [5] also pointed out that overexpression of c-erbB-2 was a predictor of recurrence-free survival and overall survival in high-risk early-stage breast cancer treated with high-dose cyclophosphamide, cisplatin, and capsaicin regimens of chemotherapy Lee et al [6] found that Herceptin enhanced paclitaxel-induced apoptosis and cytotoxicity and inhibited tumor growth in xenografts in an in vitro assay; Herceptin inhibited ErbB-2-mediated Cdc-Tyr-15 phosphorylation and p21CIP1 upregulation for ErbB-2 overexpressing cell lines, suggesting that Herceptin makes ErbB-2 overexpressing breast cancer more sensitive to paclitaxel-induced cell death. Luo Rongcheng et al [7] studied 60 cases of Her-2/neu overexpressed metastatic breast cancer, 22 cases with Herceptin+Tysol and 38 cases with Tysol+Adriamycin, the efficiency of Herceptin+Tysol group was 68.2%, which was significantly higher than 44.7% of Tysol+Adriamycin group; there were 6 cases of Her-2/neu(++) and 50% of CR+PR. Her-2/neu(++++) had 16 cases with CR+PR of 75%; it was concluded that Herceptin combined with tamsulosin could improve the efficacy of metastatic breast cancer, and the recent remission rate was correlated with Her-2/neu expression status. The above data show that the expression status of c-erbB-2 gene is still a promising predictor of breast cancer chemotherapy efficacy. P53 is an important negative regulator of cell growth and is involved in cell cycle control, DNA repair and synthesis, cell differentiation, genomic plasticity, and programmed cell death. Chemotherapeutic drugs act mostly by interfering with DNA synthesis, directly damaging DNA or otherwise interfering to inhibit cell division. Wild-type P53 induces cell growth arrest in G1 phase or programmed cell death in the presence of chemotherapeutic drug damage to cellular DNA. the P21 gene encodes an arginine-rich protein of 164 amino acids. the P21 protein is the target protein of P53 action, which arrests cells in G1 phase by binding to CDK2 and inhibiting activity. mutations in both P53/P21 genes Kandioler-Eckersberger et al [8] showed that TP53 mutations and overexpression of P53 protein are associated with breast cancer response to FEC regimens, paclitaxel chemotherapy, and that response to FEC regimens is dependent on normal p53 function, while cases with loss of p53 function can derive greater benefit.A study by Domagala et al [9] suggested a 5-year survival rate of 58% for P21-/P53+ presentation and 83% for P21+/P53-, suggesting that P21/P53 presentation is associated with response to adjuvant chemotherapy with CMF regimen.Rahko et al [10] studied 254 cases of early-stage breast cancer and found that p53 expression was associated with shorter overall survival, disease-free survival, and poor responsiveness to anthracycline-based chemotherapy in p53-positive cases, suggesting that p53 expression is predictive of resistance to anthracyclines. In contrast to the above findings, Nieto et al [5] concluded that P53 mutations lacked predictive value for recurrence-free survival and overall survival in high-risk early breast cancer treated with high-dose cyclophosphamide, cisplatin, and capsaicin regimens of chemotherapy. sjostrom et al [11] showed no association between P53 status and response to chemotherapy with methotrexate, 5-fluorouracil, and doxorubicin. For P21 gene expression, Thor et al [12] showed that P21-negative lymph node-negative breast cancer patients had longer tumor-free survival, possibly because the absence of P21 expression enhanced the sensitivity of tumor cells to chemotherapy. Although there is still a debate on oncogene expression and the prediction of chemotherapeutic efficacy in breast cancer, it would be interesting to do further studies. One of the main mechanisms of antitumor therapy with chemotherapeutic agents is the induction of apoptosis, therefore, the expression status of genes regulating apoptosis can be used as a predictor of chemotherapeutic efficacy in breast cancer. The genes regulating apoptosis include P53, bcl-2, P16, c-myc, Rb and so on. P53 is an oncogene that promotes apoptosis and has been described above as an indicator of chemotherapy efficacy. bcl-2 gene family is divided into two categories, one is apoptosis suppressor genes, including bcl-2, bcl-xl; the other is apoptosis promoter genes, such as bax, bak, bcl-xs, bad, etc. xs,bad, etc. Overexpression of bcl-2 gene and mutation of P53 can inhibit apoptosis, thus giving tumor cells a multidrug resistance phenotype. determination of apoptotic potential of tumor cells and expression of various genes controlling apoptosis can predict the sensitivity or resistance of patients to different treatments. buchholz et al [13] examined 24 cases of breast cancer treated with doxorubicin and cisplatin chemotherapy in Bonetti et al [14] found that 17 of 55 breast cancers treated with chemotherapy with CMF and FEC regimens were effective (5 complete remissions and 12 partial remissions), of which 14 were bcl-2(-) and only 3 were bcl-2(+); it was concluded that bcl-2 expression was associated with resistance to chemotherapy in breast cancer patients; in another study it was also shown that bcl-2 expression in breast cancer was associated with resistance to cytotoxic drugs and that its expression level correlated with the level of clinical resistance to chemotherapy [15]. In a study done by Sjostrom et al [16] in which multifactorial analysis of tumor biological indicators predicted the efficacy of chemotherapy to FEC regimen in 173 breast cancers, bax expression correlated with overall survival (os) and time to treatment progression (TTP), independently predicting chemotherapy efficacy. bax expression was also proposed in a study by Kymionis et al [17] to be associated with tumor size, low histological grade ER(+), PR(+), disease-free survival, and overall survival, with predictive value for chemotherapy responsiveness in breast cancer patients without lymph node metastases on CMF regimens. While Sjöström et al [18] studied 283 breast cancers that failed anthracycline chemotherapy and received doxorubicin and aminoglutethimide and 5-fluorouracil chemotherapy, respectively, and found that low bcl-2 expression was significantly associated with progression and short overall survival, yet no association was found between the bcl-2 family and responsiveness to chemotherapy with doxorubicin or aminoglutethimide and 5-fluorouracil. Multidrug resistance-related genes Multidrug resistance (MDR) is one of the major causes of chemotherapy failure in advanced breast cancer. The expression of multidrug resistance-related genes is significantly related to the efficacy of chemotherapy in breast cancer, but current research data suggest that their predictive validity of chemotherapy is still controversial. Multidrug resistance-related genes include MDR1, multidrug resistance-associated protein (MRP), lung resistance protein (LRP), glutathione S-transferase (GST), topoisomerase II (Topo IIα), and breast cancer resistance protein (BCRP). It has been shown that breast cancer tissues have overexpression of multiple drug resistance proteins, and mdr-1 gene overexpression and the encoded product p-gp-mediated MDR are the main mechanisms of multidrug resistance in breast cancer; clinical studies have shown that p-gp expression is associated with chemotherapy efficacy, remission rate, survival and estimated prognosis [19].Takamura et al [20] studied 45 cases of early breast cancer and 25 cases of locally Mechetner et al[21] also showed that the degree of p-gp expression correlated with resistance to paclitaxel and adriamycin, but not 5-Fu. MacGrogan et al [22] selected 125 breast cancer patients who received three courses of epi-adriamycin, cyclophosphamide, and vincristine chemotherapy followed by three courses of mitomycin, vincristine, and tiotipine chemotherapy and found that patients with high Topo IIα expression were associated with tumor regression during chemotherapy and could be used as an independent predictor of tumor regression, and concluded that Topo IIα expression and tumor chemotherapy The relationship between Topo IIα expression and tumor chemotherapy sensitivity has important practical implications.A study by Harris et al [23] found that MCF-7 cell lines were sensitive to adriamycin after trans-heregulin β-2 and found an increase in Topo IIα expression, which was speculated to be a possible mechanism for the increased sensitivity of tumor cells to adriamycin.Burger et al [24] studied 59 cases treated with first-line chemotherapeutic agents for systemic chemotherapy of early-stage breast cancer treated with systemic chemotherapy with first-line chemotherapeutic agents, and examined the mRNA levels of BCRP, LRP, MRP1, MRP2, and MDR1, respectively, and found that the overall response rate to chemotherapy was significantly lower in the group with high MDR1 expression than in the group with low MDR1 expression; the expression of BCRP, MRP1, and LRP was associated with poorer progression-free survival in the group receiving chemotherapy with the FEC regimen; the authors concluded that MDR1 expression was associated with first-line drug chemotherapy and that its high expression level is a predictor of poorer prognosis in advanced breast cancer, while BCRP, LRP, and MRP1 have some predictive value for clinical prognosis.Arnal et al [25], on the other hand, concluded that mdr1 gene overexpression is not a characteristic of breast cancer, but a general phenomenon occurring in both normal and tumor cells, which could also explain the This could also explain the lack of association between mdr1 expression and clinical prognosis of breast cancer. The discrepancy between the above findings of MDR-related genes in the prediction of breast cancer chemotherapy efficacy may be related to the more complex mechanism of tumor drug resistance, as well as the interaction of MDR-related genes with other genes and tumor types. Therefore, the value of MDR-related gene expression in predicting chemotherapeutic efficacy remains to be further investigated by the development of tumor molecular biology. The relationship between gene expression and chemotherapy efficacy in breast cancer is still controversial in the above mentioned studies. So far, there is no gene expression with satisfactory specificity and sensitivity for the prediction of chemotherapy efficacy. Therefore, the combined detection of multiple gene expressions and related tumor biological indicators is very meaningful in the prediction of chemotherapy efficacy in breast cancer. As the research on tumor molecular biology continues, some genes with good sensitivity and specificity will be identified for predicting the efficacy of chemotherapy in breast cancer, thus guiding the selection of clinical chemotherapy regimens and drugs, enhancing the purpose of chemotherapy, and implementing targeted individualized chemotherapy.