Biological and molecular basis of human breast cancer

Abstract

2. Introduction. 3. Human Breast Epithelial Cells (HBEC) in Culture 4. Factors Influencing Susceptibility of HBEC to Cell Transformation 4.1. Lobular differentiation 4.2. Genetic predisposition 4.3. Cell immortalization 5. Molecular Mechanisms of Cell Immortalization 5.1. Activation of telomerase 5.2. Abrogation of cell cycle control 5.3. Genes preferentially expressed during cell immortalization 6. Molecular Mechanisms of Cell Transformation 6.1. Epigenetic mechanisms 6.2. Genetic mechanisms 7. Genomic changes in Immortalization and Transformation of HBEC 7.1. Genomic changes in cell immortalization 7.2. Genomic changes in cell transformation 8. Genomic Changes in Human Breast Lesions 9. Functional Roles of Chromosomes 11 and 17 in Transformed Phenotype Expression of HBEC 10. Summary and Perspectives 11. Acknowledgments 12. References

Histologic changes in the breast with menopausal hormone therapy use

“…This finding may explain why HT increases the susceptibility of the breast to cancer: it increases the number of target cells or structures to be affected, given that ductal carcinoma in situ starts in the ductules of Lob1. 36 , 37 Dual effects of the hormones are observed here. First, activation of cell proliferation in the breast epithelium of the postmenopausal breast results in formation of more branching from the ducts, leading to the formation of Lob1, which therefore explains the higher number of Lob1 in the HT group in association with increased breast density.…”

“…Second, the formation of Lob1 from the ductal structures is associated with the increase in the fibrous stroma because both processes go together. 37 Known concepts about receptor physiology in the normal breast require comment. The content of ERs and PRs in the normal breast tissue, as detected by immunocytochemistry, varies with the degree of lobular development in a linear relationship with the rate of cell proliferation of the same structures.…”

Role of Nf-kB/Rel in the Etiology of Breast Cancer

“…The findings raised the question of whether the loss of responsiveness to TGF-ß1 is associated with a progression to more aggressive breast tumors. Our findings raise the intriguing possibility that resistance to TGF-ß1, which is most often due to the loss of TGF-ß1 receptor (27,(41)(42)(43), can be circumvented inasmuch as the same inhibitory effects on tumor cell proliferation may be achieved via the use of inhibitors of NF-KB. Thus, inhibition of NF-KB may provide a new method to sensitize breast cancer cells to chemotherapeutic treatments.…”

“…Activation of NF-KB involves release from an IKB molecule and transit to the nucleus. Most studies have focused on the predominant IKB species, IKB-OC (43). Several groups have demonstrated a role for CK2 in basal phosphorylation of IKB-OC (3,34); these findings implicate CK2 in constitutive activation of NF-KB levels.…”

Therapeutic Effect of Hydro-Ethanolic Extract of Pothos scandens L on key Carbohydrate Metabolizing Enzymes and Xenobiotic Marker Enzymes in DMBA Induced Experimental Mammary Carcinoma

“…2 Breast cancer is the most common form of cancer and the leading cause of cancer mortality among women worldwide. 3,4 The number of new breast cancer cases in India is about 100,000 per year. 5 It is a major clinical problem that possesses significant social and economic challenges to the health care system.…”