Immunohistochemical expression of the mutant p53 protein and nuclear DNA content during the transition from benign to malignant breast disease

Eriksson, Ejnar; Schimmelpenning, H.; Aspenblad, Ulla; Zetterberg, Anders; Auer, Gert

doi:10.1016/0046-8177(94)90040-x

Cited by 47 publications

(26 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…P53 im- munoreactivity was generally not detected immunohistochemically before the carcinoma in situ phase throughout the course of possible breast carcinoma development (12). Results from our study revealed that there was a difference in the patterns of p53 immunoreactivity between apocrine and nonapocrine carcinomas.…”

Section: Discussioncontrasting

confidence: 52%

See 1 more Smart Citation

Immunohistochemical Analysis of Ki-67, p53, p21, and p27 in Benign and Malignant Apocrine Lesions of the Breast: Its Correlation to Histologic Findings in 43 Cases

et al. 2000

View full text Add to dashboard Cite

show abstract

Section: Discussioncontrasting

confidence: 52%

“…None of the benign or borderline cases examined in our study was associated with p53 immunoreactivity. These results suggest that the Ki-67 and/or p53 immunohistochemistry can be an auxiliary method for determining the possible biologic behavior of lesions, as reported in other nonapocrine breast ductal proliferative disorders (11,12).…”

Section: Discussionsupporting

confidence: 52%

Immunohistochemical Analysis of Ki-67, p53, p21, and p27 in Benign and Malignant Apocrine Lesions of the Breast: Its Correlation to Histologic Findings in 43 Cases

et al. 2000

View full text Add to dashboard Cite

show abstract

“…9 Interestingly, none of the BPBD showed nuclear p53 protein expression. This lack of nuclear reactivity not only concurs the findings of other groups, 9,20,21,22,23 but also suggests that p53 alterations are associated with the promotion and progression, rather than initiation stage of mammary carcinogenesis. Also, the difference in p53 protein expression among the BPBD and ductal carcinomas may be a plausible explanation for the differences in their biological behavior.…”

Section: Discussionsupporting

confidence: 90%

Alterations of p53, Bcl-2, and hMSH2 protein expression in the normal breast, benign proliferative breast disease, in situ and infiltrating ductal breast carcinomas in the upper egypt

Hussein¹,

Hassan²

2004

Cancer Biology & Therapy

View full text Add to dashboard Cite

Background: Tumorigenesis involves alterations in the tumor suppressor genes (p53), protooncogenes (Bcl-2) and housekeeping genes [human MutS homologue-2 (hMSH2)]. We hypothesized that mammary carcinogenesis involves interactions among p53, Bcl-2 and hMSh2 proteins. In the Upper Egypt, the clinicopathologic features and genetic changes during mammary carcinogenesis are unknown.Methods: To test our hypothesis and to examine these issues, 53 mastectomy specimens, each entailing normal breast, benign proliferative breast disease (BPBD), duct carcinoma in situ (DCIS) and infiltrating ductal carcinoma (IDC) were immunostained for p53, Bcl-2 and hMSH2 protein expression.Results: The average age incidence of ductal carcinomas was 43.2 ± 7.06 years. The tumors were common in the left than right side (1.2:1, respectively, p > 0.05). Infiltrating ductal carcinoma of non-specific type was the most common histologic type. Examination of the average weighted scores in the normal breast, BPBD, DCIS and IDC, respectively, showed: (1) significant upregulation of p53 proteins (0.00 ± 0.00, 0.00 ± 0.00, 6.25 ± 2.42, 6.62 ± 2.15, p = 0.001), (2) insignificant downregulation of Bcl-2 (6.67 ± 1.33, 5.17 ± 2.20, 4.79 ± 2.27 and 4.42 ± 2.83, p = 0.37), and (3) significant downregulation of hMSH2 (11.3 ± 0.75, 10.70 ± 1.27, 7.11 ± 1.50 and 7.0 ± 1.33, p = 0.0006). There were insignificant negative correlations between p53 and both Bcl-2 (r = -0.20, p > 0.05) and hMSH2 (r = -0.15, p > 0.05) protein expression.Conclusions: In the Upper Egypt: (1) breast cancer had similar clinicopathologic features to those in the high risk regions, and (2) alterations of the p53, Bcl-2 and hMSH2 proteins occur during mammary carcinogenesis.

show abstract

“…There are few investigations of AH lesions in the literature (24)(25)(26)(27)(28)(29)(30). It is noteworthy that most studies have examined AH lesions present in an already cancerous breast; such lesions may not be directly comparable with the AH lesions we have studied, which occurred in breasts lacking coincident or previous malignancies.…”

Section: Discussionmentioning

confidence: 99%

Detection of monoclonal microsatellite alterations in atypical breast hyperplasia.

Rosenberg

Morenas²,

Huang³

et al. 1996

J. Clin. Invest.

View full text Add to dashboard Cite

Atypical hyperplastic (AH) breast lesions are currently classified and treated as benign proliferative disorders, but their presence is associated with a four-to fivefold increased risk of developing breast cancer. Currently, it is not known if an AH lesion is a marker of increased risk, or is itself a premalignant lesion. To investigate this question, we used a series of 15 microsatellite loci to analyze 15 separate AH lesions microdissected from the archived pathology specimens of subjects with no coincident or previous breast malignancy. We found that a significant subset (6/15, or 40%) of these AH lesions demonstrated evidence of monoclonal microsatellite alterations, both length variation and allele loss. These monoclonal alterations suggest that the AH lesion has already undergone genetic changes conferring a growth advantage. Thus, these AH lesions may actually be early neoplasms. We also noted that monoclonality characterized AH lesions in younger as compared with older women (44 vs. 59 yrs, P Ͻ 0.05) and that a subset of monoclonal lesions (4/6) demonstrated microsatellite alterations at more than one locus, suggesting that an undetermined type of genetic instability may play a role early in the development of abnormal breast proliferations. These findings contribute to our un-

show abstract

Immunohistochemical expression of the mutant p53 protein and nuclear DNA content during the transition from benign to malignant breast disease

Cited by 47 publications

References 27 publications

Immunohistochemical Analysis of Ki-67, p53, p21, and p27 in Benign and Malignant Apocrine Lesions of the Breast: Its Correlation to Histologic Findings in 43 Cases

Immunohistochemical Analysis of Ki-67, p53, p21, and p27 in Benign and Malignant Apocrine Lesions of the Breast: Its Correlation to Histologic Findings in 43 Cases

Alterations of p53, Bcl-2, and hMSH2 protein expression in the normal breast, benign proliferative breast disease, in situ and infiltrating ductal breast carcinomas in the upper egypt

Detection of monoclonal microsatellite alterations in atypical breast hyperplasia.

Contact Info

Product

Resources

About