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Treatment of Low-grade versus High-Grade Ductal Carcinoma in situ
ATM mutations and Carcinoma breast
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David L. Page, M.D. Vanderbilt University Department of Pathology, Schuyler, Peggy A.
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david.page{at}vanderbilt.edu David L. Page, et al.
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In their review of premalignant and in situ breast disease(1), Arpino, Laucirica, and Elledge note that “Ductal carcinoma in situ represents a heterogeneous group of preinvasive lesions.” While recognizing this well-established fact, the authors do not go on to recognize any differences in the treatment of DCIS and its potential for subsequent invasive disease based upon heterogeneity. A major barrier to achieving a greater level of understanding among clinicians and patients attempting to make diagnostic and therapeutic decisions is the erroneous idea that DCIS is one disease. DCIS is a spectrum of disease ranging from extensive high-grade lesions, usually requiring mastectomy, to small low- grade lesions, which can be effectively cured by local excision only. Division of DCIS into high-grade categories with necrosis and a high degree of nuclear atypia (comedo) and a low-grade group with orderly nuclei and no necrosis, each group with wide variations in recurrence according to grade are recognized by Lagios, Silverstein, and Page.(2-4) Several studies have assessed the risk of subsequent invasive carcinoma for patients for whom the diagnosis of DCIS was not made at initial biopsy for small non-comedo lesions.(5) Approximately 1/3 of these patients developed invasive disease in the same breast as their original biopsy within 10-18 years, indicating that not all DCIS lesions will progress to invasion, even after a prolonged interval. Short-term outcomes (median follow-up, 5.4 years) from the EORTC trial indicate that patients with high-grade DCIS have the greatest risk of subsequent life-threatening distant metastases after invasive local recurrence.(6) Optimal clinical management decisions are appropriately guided by pathologic assessment of histologic pattern, grade, size, and margin status, knowledge of natural history, and by the likelihood of therapeutic effectiveness. 1. Arpino G, Laucirica R, Elledge RM. Premalignant and in situ breast disease: biology and clinical implications. Ann Intern Med. 2005;143(6):446-57. 2. Lagios MD, Margolin FR, Westdahl PR, Rose MR. Mammographically detected duct carcinoma in situ. Frequency of local recurrence following tylectomy and prognostic effect of nuclear grade on local recurrence. Cancer. 1989;63(4):618-24. 3. Silverstein MJ, Lagios MD, Craig PH, et al. A prognostic index for ductal carcinoma in situ of the breast. Cancer. 1996;77(11):2267-74. 4. Jensen RA, Page, D.L. Ductal carcinoma in situ: Pathology-its role in guiding therapy. In: Singletary SE, Robb, G.L., Hortabgyi G.N., ed. Advanced Therapy of Breast Disease. London: BC Cedker; 2004:281-288. 5. Sanders ME, Schuyler PA, Dupont WD, Page DL. The natural history of low -grade ductal carcinoma in situ of the breast in women treated by biopsy only revealed over 30 years of long-term follow-up. Cancer. 2005;103(12):2481-4. 6. Bijker N, Peterse JL, Duchateau L, et al. Risk factors for recurrence and metastasis after breast-conserving therapy for ductal carcinoma-in- situ: analysis of European Organization for Research and Treatment of Cancer Trial 10853. J Clin Oncol. 2001;19(8):2263-71. Conflict of Interest:None declared |
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Prasanta Padhan, MD Internal Medicine JIPMER,PONDICHERRY,INDIA.605006.
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prasanta.padhan{at}gmail.com Prasanta Padhan
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Dear Editor, Ataxia-telangiectasia is an autosomal-recessive disease that affects neuro-immunological functions, associated with increased susceptibility to malignancy, chromosomal instability and hypersensitivity to ionizing radiation.An increased incidence of breast carcinoma has been reported among relatives of individuals who are affected with this rare autosomal recessive disorder, and those who are heterozygous for mutations in the ataxia- telangiectasia mutated (ATM) gene.The ATM gene located at chromosome 11q22.3 , consists of 66 exons encoding a large protein kinase that orchestrates the recognition and repair of radiation-induced DNA double strand breaks and it regulates several oncoproteins like tumor suppressors p53 and BRCA1.A-T heterozygotes account for about 1% of the general population, and are susceptible to the carcinogenic effect of ionizing radiation because of an increased intrinsic cellular radiosensitivity.This may be important from therapeutic point of view as high dose radiation therapy in A-T heterozygotes with breast carcinoma may increase the risk of cancer in the contralatral breast. Conflict of Interest:None declared |
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