1. Breast cancer (malignantbreast neoplasm) is canceroriginating from breasttissue, most commonlyfrom the inner lining of milkducts or the lobules thatsupply the ducts with milk.

2. The breast is a glandularorgan. It is made up of a networkof mammary ducts. Each breast has about 15-20 mammary ducts thatlead to lobes that are madeup of lobules. The lobules contain cellsthat secrete milk that arestimulated by estrogen andprogesterone which areovarian hormone. 3. A. Breast Duct System B. Lobules C. Breast Duct System D. Nipple E. Fat F. Chest Muscle G. Ribs A. Cells lining duct B. Basement membrane C. Open central duct 4. A. Breast Duct System B. Lobules C. Breast Duct System D. Nipple E. Fat F. Chest Muscle G. Ribs A. Cells lining duct B. Extra cancer like cells C. Intact basementmembrane D. Open central duct 5. histopathological grade Stag Receptor statuse 6. Although breast cancer has many different histologies, theconsiderable majority of breast cancers are derived from theepithelium lining the ducts or lobules, and are classified asmammary ductal carcinoma. Invasive ductal carcinoma Ductal carcinoma in situ Invasive lobular carcinoma 7. Grading focuses on the appearance of the breastcancer cells compared to the appearance of normalbreast tissue. Normal cells in an organ like thebreast become differentiated, meaning that theytake on specific shapes and forms that reflect theirfunction as part of that organ. Cancerous cells losethat differentiation. 8. Stage 0 is a pre-cancerous or marker condition, either ductalcarcinoma in situ (DCIS) or lobular carcinoma in situ (LCIS). Stages 13 are within the breast or regional lymph nodes. Stage 4 is metastatic cancer that has a less favorableprognosis. 9. Breast cancer cells may or may not have many different types ofreceptors. estrogen receptor (ER) progesterone receptor (PR) human epidermal growth factor receptor 2 (HER2) HER2/neu 10. Cells with or without these receptors are called ER positive(ER+), ER negative (ER-), PR positive (PR+), PR negative (PR-),HER2 positive (HER2+), and HER2 negative (HER2-).Cells with none of these receptors are called basal-like ortriple negative. 11. ER receptors belong to a super-family of nuclear hormoneReceptors.The main function of the estrogen receptor is as a DNA-bindingtranscription factor that regulates gene expression when theyare bound to estrogens. ER is generally expressed at low levels in normal breastepithelial cells. ER interactions with a number of other DNA-boundtranscription factors, such as the AP-1 complex or the SP-1family of transcription factors. 12. The progesterone receptor (PR) also known as NR3C3(nuclear receptor subfamily 3, group C, member 3), is anintracellular steroid receptor that specifically bindsprogesterone. 13. HER2/neu stands for "Human Epidermal growth factorReceptor 2" and is a protein giving higher aggressiveness inbreast cancers. It is a member of the ErbB protein family,more commonly known as the epidermal growth factorreceptor family. 14. Inherited Risk Factors Environmental Factors 15. Only 5-10% of breast cancers are inherited. Families that do have genetic defects in one of two genes,breast cancer gene 1 (BRCA1) or breast cancer gene 2(BRCA2), have a much greater risk of developing both breastand ovarian cancer. Other inherited mutations including the ataxia-telangiectasia mutation gene, the cell-cycle checkpoint kinase2 (CHEK-2) gene and the p53 tumor suppressor gene alsomake it more likely that will develop breast cancer. 16. BRCA1 (Breast Cancer 1) BRCA2 (Breast Cancer 2) TP53 gene ATM gene 17. BRCA1 is a human caretaker gene that produces a proteincalled breast cancer type 1 susceptibility protein, responsiblefor repairing DNA. 18. BRCA2 (Breast Cancer 2 susceptibility protein) is a proteinthat in humans is encoded by the BRCA2 gene and belongs tothe tumor suppressor gene family. The BRCA2 gene is located on the long (q) arm ofchromosome 13 at position 12.3 (13q12.3). 19. BRCA1 and BRCA2 proteins are involved in control ofhomologous recombination and double-strand break repairin response to DNA damage . Modulation of chromatin and DNA structure Activation of DNA damage checkpoints. 20. p53 (also known as protein 53 or tumor protein 53), is atumor suppressor protein that in humans is encoded by theTP53 gene. p53 is crucial in multicellular organisms, where itregulates the cell cycle and, thus, functions as a tumorsuppressor that is involved in preventing cancer. 21. Cell Cycle Regulation Cell Senescence Apoptosis Autophagy Mitotic Catastrophe Angiogenesis 22. Ataxia telangiectasia mutated (ATM) is a serine/threonineprotein kinase that is recruited and activated by DNA double-strand breaks. It phosphorylates several key proteins thatinitiate activation of the DNA damage checkpoint, leading tocell cycle arrest, DNA repair or apoptosis. 23. Factors that Cannot be Lifestyle RisksPrevented Oral Contraceptive Use GenderNot Having Children AgingHormone Replacement Genetic Risk Factors Therapy (inherited)Not Breast Feeding Family History Alcohol Use Personal HistoryObesityRace High Fat Diets Menstrual CyclePhysical Inactivity Estrogen Smoking 24. Exposure to Estrogen Radiation Electromagnetic Fields Xenoestrogens Exposure to Chemicals 25. definitive surgery adjuvant chemotherapyadjuvant radiotherapyadjuvant hormonal therapy 26. Surgery is usually the first line of attack against breast cancer. Lumpectomy Mastectomy Lymph node removal Prophylactic mastectomy Prophylactic ovary removal Cryotherapy 27. Chemotherapy treatment uses medicine to weaken and destroycancer cells in the body, including cells at the original cancersite and any cancer cells that may have spread to another partof the body.Chemotherapy is used to treat: early-stage invasive breast cancer to get rid of any cancer cellsthat may be left behind after surgery and to reduce the risk ofthe cancer coming back. advanced-stage breast cancer to destroy or damage thecancer cells as much as possible. 28. Radiation therapy (radiotherapy) is a highly targeted, highlyeffective way to destroy cancer cells in the breast. 29. Hormonal therapy medicines treat hormone-receptor-positive breast cancers in two ways: by lowering the amount of the hormone estrogen in the body by blocking the action of estrogen on breast cancer cells 30. There are several types of hormonal therapy medicines,including: aromatase inhibitors selective estrogen receptor modulators estrogen receptor downregulators. 31. Aromatase inhibitors stop the production of estrogen in post-menopausal womenThere are three aromatase inhibitors: Arimidex (chemical name: anastrozole) Aromasin (chemical name: exemestane) Femara (chemical name: letrozole) 32. SERMs work by sitting in the estrogen receptors in breast cells.There are three SERMs: tamoxifen (also called tamoxifen citrate; brand name:Nolvadex) Evista (chemical name: raloxifene) Fareston (chemical name: toremifene) 33. ERDs work in a similar way to SERMs.ERDs also: reduce the number of estrogen receptors. change the shape of breast cell estrogen receptors so theydont work as well.There is one ERD available to treat hormone-receptor positivebreast cancer:Faslodex (chemical name: fulvestrant) 34. 1)Roles of BRCA1 and BRCA2 in homologous recombination, DNA replication fidelity and the cellular response to ionizing radiation.Simon N Powell*,1 and Lisa A Kachnic22)Pathology of hereditary breast cancer.Leonard Da Silva and Sunil R Lakhani.3)TP53 Status and Response to Treatment in Breast Cancers.Mariana Varna,1, 2 Guilhem Bousquet,1, 2 Louis-Francois Plassa,3 Philippe Bertheau,1, 2, 4and Anne Janin1, 2, 4.4)The Role of Estrogen Receptors in Breast Cancer Metastasis.Suzanne A.W. Fuqua1.5)New Molecular Classifications of Breast Cancer.Mary Cianfrocca, DO1 and William Gradishar.