Vol. 1(2) SEP 2011 - SAVAP International

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Academic Research International ISSN: 2223-9553 Volume 1, Issue 2, September 2011 Phase 3A In this sub phase the greatest dimension of cancer not more than 5 cm and not less than 2 cm (Lugo et al., 1990). • with homolateral region but some time lacking. Phase 3B Describes invasive breast cancer in which Phase 4 • cancer size of up to and more than 5 cm in diameter • cancer may have broaden to lymph nodes near the breastbone • this stage is considered as inflammatory breast cancer It is also invasive in which Cancer of any size may spread to any organ of body. This stage is considered as metastatic cancer (Baccarani et al., 2006; Baccarani et al., 2009). ALCOHOLISM AND BREAST CANCER Alcohol enhances the level of hormones such as estrogen in our body. A high level of estrogen causes breast cancer. In our body, acetaldehyde is formed by the conversion of alcohol. Acetaldehyde is loom that causes cancer by damaging DNA and averting it from being mended. Acetaldehyde is found in large amount in the saliva of people who drink heavily and smoke. It is found by various observations that every alcohol unit drunk a day enhances the possibility of breast cancer about 7- 11%. The chances of breast cancer in teenage girls is 25% elevated than as compare to women because of early menarche (Hochhaus et al., 2008; Shah et al., 2008). GENES INVOLVED Breast cancer genes (BRCA) BRCA1 and BRCA2 genes are found in human chromosomes. Breast cancer is developed by its altered form. But several studies have shown that breast cancer is not developed by only an altered form BRCA-1 gene. It is also observed that 10% of such cancer originated by abnormal form of these genes (Shah et al., 2010). p53 The p53 involves in protein construction which use in the growth of cell. Abnormal p53 gene causes Li-Fraumeni syndrome (soft tissue cancer), it enhances the threat feature of breast cancer (Druker et al., 2006; de Lavallade et al., 2008). Other genes ATM: Dented DNA are repaired by the ATM gene But brain development is affected by inherit two abnormal copies of ATM gene. In some families, inherit abnormal ATM gene enhances the risk of breast cancer because it stops renovation of cells of breast tissue. Copyright © 2011 SAVAP International www.savap.org.pk www.journals.savap.org.pk 384
Academic Research International ISSN: 2223-9553 Volume 1, Issue 2, September 2011 CONCLUSION It is serious inflammatory disease which leads to death in women. Various risk factors are responsible for it. Different gene that control the breast tissue’s cell cycle, when they are in abnormal form they may cause breast cancer. REFERENCES Baccarani et al., (2006). Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet. Blood, 108:1809-1820. Baccarani et al., (2009). Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet. J Clin Oncol, 27:6041-6051. de Lavallade et al., (2008). Imatinib for newly diagnosed patients with chronic myeloid leukemia: incidence of sustained responses in an intention-to-treat analysis. J Clin Oncol, 26:3358-3363. DeBoer et al., (2010). Breast cancer prognosis and occult lymph node metastases, isolated tumor cells, and micrometastases. J Natl Cancer Inst, 102:410-425. Dowlatshahi et al., (1997). Lymph node micrometastases from breast carcinoma: reviewing the dilemma. Cancer, 80:1188-1197. Druker et al., (2006). Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med, 355:2408-2417. Faderl et al., (1999). The biology of chronic myeloid leukemia. N Engl J Med, 341:164-172. Greene et al., (2002). AJCC cancer staging manual. 6th ed. New York: Springer. Hochhaus et al., (2008). Dasatinib induces durable cytogenetic responses in patients with chronic myelogenous leukemia in chronic phase with resistance or intolerance to imatinib. Leukemia, 22:1200- 1206. Krag et al., (2007). Technical outcomes of sentinel-lymph-node resection and conventional axillarylymph-node dissection in patients with clinically node-negative breast cancer. Lancet Oncol, 8:881-888. Lugo et al., (1990). Tyrosine kinase activity and transformation potency of bcr-abl oncogene products. Science, 247:1079-1082. Shah et al., (2008). Intermittent target inhibition with dasatinib 100 mg once daily preserves efficacy and improves tolerability in imatinib-resistant and -intolerant chronic-phase chronic myeloid leukemia. J Clin Oncol, 26:3204-3212. Shah et al., (2010). Potent, transient inhibition of BCR-ABL with dasatinib 100 mg daily achieves rapid and durable cytogenetic responses and high transformation-free survival rates in chronic phase chronic myeloid leukemia patients with resistance, suboptimal response or intolerance to imatinib. Haematologica, 95:232-240. Weaver et al., (2000). Pathologic analysis of sentinel and nonsentinel lymph nodes in breast carcinoma: a multicenter study. Cancer, 88:1099-1107. Weaver et al., (2009). Metastasis detection in sentinel lymph nodes: comparison of a limited widely spaced (NSABP protocol B-32) and a comprehensive narrowly spaced paraffin block sectioning strategy. Am J Surg Pathol, 33:1583-1589. Weaver, D. L. (2003). Sentinel lymph nodes and breast carcinoma: which micrometastases are clinically significant. Am J Surg Pathol, 27:842-845. Zhu et al., (2011). Perspectives of breast cancer etiology: synergistic interaction between smoking and exogenous hormone use. Chin J Cancer, 30(7):433-41. Copyright © 2011 SAVAP International www.savap.org.pk www.journals.savap.org.pk 385
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