Mastocytosis is a non-inflammatory, non-tumorigenic group of lesions with varying degrees of parenchymal and mesenchymal hyperplasia and incomplete replenishment in women caused by endocrine dysfunction. There has been widespread concern about whether mammary gland hyperplasia can develop into cancer. Many scholars have done a lot of research in this area, and there are always controversies. Various names have been given to mastocytosis for a long time, such as cystic hyperplasia, cystic mastopathy, benign mastopathy, mammary gland structural dysplasia, and so on. Foreign countries call them fibrocystic mastopathy, while in China, this group of breast hyperplasia diseases with not completely uniform histology is collectively called mastoproliferative disorders. We will try to review the relationship between simple hyperplasia and atypical hyperplasia of ducts and lobules and breast cancer in mastoproliferative disorders from the epidemiological and genetic aspects as follows. The basic pathological changes of mastocytosis in the Diagnostic Pathology published in 1994 include lobular hyperplasia, ductal hyperplasia, cyst formation, fibrous tissue hyperplasia, sweat gland hyperplasia, inflammatory cell infiltration, fibromatous changes, atypical hyperplasia and carcinoma, etc. In 1997, the Pathology Branch of Chinese Medical Association made a detailed classification of mastocytosis. Histological classification. It was classified into five tissue types: cystic predominant, adenopathy predominant, fibroadenoma-like structure predominant, intraductal papilloma predominant, and atypical hyperplasia. The most recent classification of breast diseases is the “Pathological and Genetic Classification of Neoplasms of the Female Breast and Genital Organs” published by the WHO in 2003. Benign epithelial lesions of the breast are classified into lobular neoplasia, intraductal proliferative lesions, papillary tumors, benign epithelial hyperplasia and myoepithelial hyperplasia, which are not consistent with the domestic nomenclature for mastocytosis. This shows that mastocytosis is a group of breast diseases with complex histological origin and diverse clinicopathological manifestations, and is not a single disease. Epidemiological basis The hyperplasia and atypical hyperplasia of breast ducts and lobules are benign lesions, and many scholars have made many clinical observations and follow-up studies on whether breast cancer can occur in mammary hyperplasia over the years. As early as 1985, Dupont and Page showed that the incidence of breast cancer in patients with benign breast hyperplasia was nearly two times higher than that in patients without hyperplasia in a study of more than 2,000 patients with breast hyperplasia. Subsequently, a study by Carter on more than 16,000 cases of benign breast disease showed that the risk of breast cancer in patients with breast hyperplasia was 1.5 times higher, and in 2004 Wang analyzed more than ll,000 patients with simple breast hyperplasia excluding atypical hyperplasia and found that the incidence of breast cancer was 1.6 times higher. The risk of malignancy in benign breast hyperplasia is not limited to a particular ethnic group; Worsham et al. in a multi-ethnic study of benign breast disease investigated more than 4500 patients and found that. Patients with benign breast hyperplasia do have an increased risk of developing breast cancer. In the Dupont and Carter study, the risk of malignancy was further increased in cases of atypical hyperplasia, with a 5-6 fold increase in the risk of development. In McLaren’s study, approximately 20% of atypical lobular hyperplasia later became cancerous, and the malignant potential of atypical hyperplasia was also demonstrated by Hamnann et al [31]. Although atypical hyperplasia can significantly increase the incidence of breast cancer. However, its malignant transformation greatly depends on the extent of the lesion. The risk of developing breast cancer increases with the degree of atypical hyperplasia H. Carcinogenesis of the ductal and lobular epithelium of the breast is a long process, and the epidemiological data of the above-mentioned large sample with a follow-up period of more than 10 years and complete follow-up data, blinded diagnosis and reasonable statistical analysis are reliable for the observation of malignant transformation of mammary hyperplasia. Genetic basis Proliferative lesions of breast tissue are actually benign neoplasms whose development also involves inactivation of tumor suppressor genes. Abnormal chromosomal and genetic alterations lead to structural transformation of the mammary epithelium, and loss of heterozygosity (LOH), which is seen in breast cancer, is often present in hyperplastic breast disease. expression. In their study, O’Connell et al. found that most mammary hyperplasia and carcinoma in situ exhibited the same LoH phenotype as some breast cancers, and in common ductal hyperplasia, atypical ductal hyperplasia, ductal carcinoma in situ, and ductal invasive carcinoma, LOH was expressed at each of the 15 loci on the chromosome to varying degrees. Kaneko et al. also concluded that common ductal hyperplasia and atypical ductal hyperplasia have the malignant potential to develop into breast cancer after analyzing LOH. Allelic imbalance (AI) is also a common genetic abnormality, and the appearance of AI in atypical hyperplasia is similar to that of ductal carcinoma in situ and invasive carcinoma, and is significantly higher than that of normal tissue.161 Larson et al. analyzed AI in different breast ductal tissues and found that breast atypical hyperplasia lesions are highly homologous to breast cancer in terms of occurrence, and concluded that atypical ductal hyperplasia is a direct precursor of ductal carcinoma. direct precursor of ductal carcinoma. xu et al.17l showed the same results as L-1st class, whose recent study found an increasing trend of chromosomal deletions in common ductal hyperplasia, atypical ductal hyperplasia, ductal carcinoma in situ and ductal invasive carcinoma. Comparative genomic hybridization (CGH) is a new molecular cytogenetic technique developed on the basis of fluorescence in situ hybridization, which is a major advancement in molecular cytogenetic research methods and has a positive effect on the occurrence, development and prognostic assessment of tumors. Increased genetic instability and chromosomal variation lead to the evolution of epithelial cells from normal morphology and atypical hyperplasia to carcinoma in situ and invasive carcinoma. gong et m tunnel used CGH technique in their study and found that the same or similar chromosomal variation appeared between common ductal hyperplasia, atypical ductal hyperplasia and breast cancer. some scholars used CGH technique and found that lobular atypical hyperplasia was also associated with the formation of lobular invasive carcinoma Schmitt et al. found that the positive expression of CEA gradually increased in simple hyperplasia, atypical hyperplasia, and cancerous tissues, and Aue et al. used immunohistochemistry to detect Cyclin D. The expression of Cyclin Dl in normal breast epithelium, ductal hyperplasia, atypical hyperplasia, and invasive carcinoma showed a gradual increase. The expression of Cyclin Dl was found to be progressively higher in normal breast epithelium, typical and atypical hyperplasia, ductal carcinoma in situ and ductal invasive carcinoma by using proprimm’s hybridization. In a recent study, Visscher et al. used COX-2 in a 15-year follow-up analysis of 235 patients with atypical hyperplasia and found that the risk of breast cancer in patients with atypical hyperplasia was 2.6 times higher than in controls. Genetic studies have concluded that abnormal chromosomal and genetic alterations in some mammary hyperplasia and atypical hyperplasia share many of the same or similarities with breast cancer and are homologous in occurrence, leading to the belief that breast cancer can be transformed from mammary hyperplasia. Although there is much evidence that mastocytosis is at risk for carcinogenesis, there is also evidence to the contrary.Alexiev did not find an association between CEA expression and breast tissue type, which is not consistent with the conclusions reached by Schmitt.Kasami found that most cases of mastocytosis did not show LOH, and only a few patients who showed LOH at the locus were found to have LOH at the locus during a 20-year follow-up. Pur gland hyperplasia is a general term for benign breast disease with a wide range of histologic changes based on extensive proliferation of lobules, ductal epithelial cells, and interrogated cells, and includes a variety of benign breast diseases with different histotypes. Although epidemiological and genetic data do not support an increased risk of carcinogenesis, most scholars believe that benign breast hyperplasia increases the risk of cancer, especially atypical hyperplasia of the lobules and ducts of the breast, which increases the risk of breast cancer. The risk of cancer from simple breast hyperplasia is about 1.5-2.0 times higher than that of the general population, while the risk of cancer from atypical hyperplasia is 5-6 times higher.