Relationship of Fibrocystic Disease to Carcinoma of the Breast

Karpas, Charles M.; Leis, Henry P.; Oppenheim, A. N.; Mersheimer, Walter L.

doi:10.1097/00000658-196507000-00001

Cited by 39 publications

(15 citation statements)

References 5 publications

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“…The nature and site of origin of neoplastic growth in human breast has been the subject of numerous studies based on examination of surgical and autopsy tissues (10, 23, 24, 31,32, 47, 48, 68, 69, 70, 74, 93, 115, 121, 123, 146). …”

Section: Pathogenesismentioning

confidence: 99%

Significance of Rat Mammary Tumors for Human Risk Assessment

Russo

2014

Toxicol Pathol

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We have previously indicated that the ideal animal tumor model should mimic the human disease. This means that the investigator should be able to ascertain the influence of host factors on the initiation of tumorigenesis, mimic the susceptibility of tumor response based on age and reproductive history, and determine the response of the tumors induced to chemotherapy. The utilization of experimental models of mammary carcinogenesis in risk assessment requires that the influence of ovarian, pituitary, and placental hormones, among others, as well as overall reproductive events are taken into consideration, since they are important modifiers of the susceptibility of the organ to neoplastic development. Several species, such as rodents, dogs, cats, and monkeys, have been evaluated for these purposes; however, none of them fulfills all the criteria specified previously. Rodents, however, are the most widely used models; therefore, this work will concentrate on discussing the rat rodent model of mammary carcinogenesis.

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Section: Pathogenesismentioning

confidence: 99%

Significance of Rat Mammary Tumors for Human Risk Assessment

Russo

2014

Toxicol Pathol

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“…In a similar study, Ryan and Coady 8 found that hyperplasia was four times more common in the cancerous breasts. Karpas et al 9 evaluated 645 breast biopsies (226 malig-nant and 419 benign) and found atypical hyperplasia in 62 per cent of malignant biopsies, compared with 4 per cent of benign biopsies. Similarly, Kern and Brooks 10 found a greater incidence of atypical ductal hyperplasia (ADH) in cancer-bearing breasts.…”

Section: Review Of Human Histopathological Materialsmentioning

confidence: 99%

“…[29][30][31][32][33] FISH has also been used to study chromosomal changes in DCIS. Using DNA probes to centromeric sequences on chromosomes 1, 3,4,6,7,8,9,10,11,16,17, and 18, polysomies of chromosomes 3, 10, and 17 were identified and losses of chromosomes 1, 16, and 18 were also seen. 34 The CGH method has been modified for paraffin-embedded material, allowing studies on archival material and, in particular, the study of preinvasive disease.…”

Section: Molecular Genetic Analysismentioning

confidence: 99%

The transition from hyperplasia to invasive carcinoma of the breast

Lakhani

1999

J. Pathol.

132

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“…The most likely cancer precursors include proliferative lesions, particularly atypical ductal hyperplasia (ADH) and perhaps simple ductal hyperplasia (DH). These lesions are considered benign, but they are associated with increased risk of developing breast cancer 4–11; they are found alongside cancers in surgical specimens and are present in greater numbers in breasts at high cancer risk than in controls 12–18. ADH, by definition, can resemble ductal carcinoma in situ (DCIS) 19.…”

Section: Introductionmentioning

confidence: 99%

Quantitative analysis of allele imbalance supports atypical ductal hyperplasia lesions as direct breast cancer precursors

Larson

Morenas

Cerda

et al. 2006

The Journal of Pathology

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It remains unclear whether hyperplastic breast lesions, especially with atypia, are cancer precursors or markers of increased cancer risk. Quantified comparisons of genomic alterations in coexisting lesions could address this question. Therefore, we examined allele imbalance (AI), also known as loss of heterozygosity (LOH), at 20 microsatellite markers on nine chromosome arms, in DNA from 106 samples microdissected from 17 randomly selected cancer-containing breast specimens: 13 simple (DH) and 45 atypical ductal hyperplastic (ADH) lesions, 30 in situ (DCIS) and 18 invasive ductal carcinomas (IDC). Data were analysed using regression models and generalized estimating equations. We found that AI increased as histology became more aberrant and varied with histology across the chromosome arms (p<0.0001). ADH had more AIs on 1q (p=0.03) and 16q (p=0.02) and fewer AIs on 17p (p=0.06) and 17q (p<0.0001) than on other arms. In cancers, AIs remained high on 1q and 16q, and became frequent on 17p and 17q. Concordance between AIs in ADHs and cancers exceeded the 50% expected if the lesions were separate clones in 16/20 (80%) ADHs (p=0.05), from 9/11 (82%) cases (p=0.03), and involved 41/51 (80%) evaluable markers (p=0.05). The occurrence of any AI in ADH predicted greater AI (p=0.009) and possibly lower grade (p=0.05) in coexisting cancers. Nevertheless, ADHs were not genetically identical to cancers or to each other. We found AIs discordant between ADHs and cancers (always on 1q and 16q), AIs unique to ADH (usually on 11q) and some genetic heterogeneity among coexisting ADHs. We conclude that ADH lesions are genetically advanced, with frequent alterations on 1q and 16q, and are often direct cancer precursors. Their global genetic characteristics predict features of cancers in the same breast. Nevertheless, the genetic heterogeneity detected suggests that hyperplasias and cancers may arise on a field at generalized increased cancer risk.

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Relationship of Fibrocystic Disease to Carcinoma of the Breast

Cited by 39 publications

References 5 publications

Significance of Rat Mammary Tumors for Human Risk Assessment

Significance of Rat Mammary Tumors for Human Risk Assessment

The transition from hyperplasia to invasive carcinoma of the breast

Quantitative analysis of allele imbalance supports atypical ductal hyperplasia lesions as direct breast cancer precursors

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