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Breast carcinogenesis. Transition from hyperplasia to invasive lesions.
Saudi Med J. 2005 Dec; 26(12):1889-96.SM

Abstract

OBJECTIVES

To examine the balance loss between proliferation and apoptosis that play a role in breast cancer development, and to explore the places of various genes and molecules within this process in this supposed multistep process.

METHODS

We obtained the specimens from 40 patients between 2002 and 2004 at the Department of Pathology, Medical Faculty, Adnan Menderes University, Aydin, Turkey. We categorized the lesions ductal hyperplasia (DH), atypical ductal hyperplasia (ADH), in situ ductal carcinoma (DCIS), and invasive ductal carcinoma (IDC). We determined the tumor size, histological grade and lymph node status of invasive cases and we used nottingham prognostic index (NPI). We applied ER, PR, c-erbB2, p53, Ki-67, bcl-2, dUTP nick end labeling (TUNEL), breast cancer gene-1, matrix metalloproteinases-1 and tissue inhibitor matrix metalloproteinases-1 stains to each lesion using the immunohistochemical method.

RESULTS

We observed that ER and PR decreased in ADH when compared with DH (p=0.0001 and p=0.019). However, we determined that in DCIS as c-erbB2 (p=0.005) and Ki-67 (p=0.004) increase, TUNEL (p=0.04) and bcl-2 (p=0.005) decrease, when compared with ADH. When compared with DCIS lesions, we observed the existence of a higher c-erbB2 (p=0.003) and a lower TUNEL (p=0.012) in invasive tumors. Furthermore, we found that there is a higher MMP-1 (p=0.04) in invasive lesions, when compared with non-invasive lesions. We detected higher PR (p=0.049), lower TUNEL and c-erbB2 (p=0.017) in low grade group of NPI, when compared with high grade group of NPI.

CONCLUSION

As a result, it has been shown that together with increase in proliferation, decrease in apoptosis, too, contributes to the proliferation/apoptosis imbalance that occurs in breast carcinogenesis. Increase in proliferation and decrease in apoptosis are parallel with the progression of lesions. We also showed that the changes, beginning with loss of ER and PR in ADH step, can cause malign transformation, which is especially notable both in DCIS step due to Ki-67 and c-erbB2 increase, and also with bcl-2 and TUNEL decrease.

Authors+Show Affiliations

Department of Pathology, Adnan Menderes University, Medical School, Aydin 09100, Turkey. imete69@hotmail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16380768

Citation

Meteoglu, Ibrahim, et al. "Breast Carcinogenesis. Transition From Hyperplasia to Invasive Lesions." Saudi Medical Journal, vol. 26, no. 12, 2005, pp. 1889-96.
Meteoglu I, Dikicioglu E, Erkus M, et al. Breast carcinogenesis. Transition from hyperplasia to invasive lesions. Saudi Med J. 2005;26(12):1889-96.
Meteoglu, I., Dikicioglu, E., Erkus, M., Culhaci, N., Kacar, F., Ozkara, E., & Uyar, M. (2005). Breast carcinogenesis. Transition from hyperplasia to invasive lesions. Saudi Medical Journal, 26(12), 1889-96.
Meteoglu I, et al. Breast Carcinogenesis. Transition From Hyperplasia to Invasive Lesions. Saudi Med J. 2005;26(12):1889-96. PubMed PMID: 16380768.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Breast carcinogenesis. Transition from hyperplasia to invasive lesions. AU - Meteoglu,Ibrahim, AU - Dikicioglu,Emel, AU - Erkus,Muhan, AU - Culhaci,Nil, AU - Kacar,Furuzan, AU - Ozkara,Esra, AU - Uyar,Meral, PY - 2005/12/29/pubmed PY - 2007/9/12/medline PY - 2005/12/29/entrez SP - 1889 EP - 96 JF - Saudi medical journal JO - Saudi Med J VL - 26 IS - 12 N2 - OBJECTIVES: To examine the balance loss between proliferation and apoptosis that play a role in breast cancer development, and to explore the places of various genes and molecules within this process in this supposed multistep process. METHODS: We obtained the specimens from 40 patients between 2002 and 2004 at the Department of Pathology, Medical Faculty, Adnan Menderes University, Aydin, Turkey. We categorized the lesions ductal hyperplasia (DH), atypical ductal hyperplasia (ADH), in situ ductal carcinoma (DCIS), and invasive ductal carcinoma (IDC). We determined the tumor size, histological grade and lymph node status of invasive cases and we used nottingham prognostic index (NPI). We applied ER, PR, c-erbB2, p53, Ki-67, bcl-2, dUTP nick end labeling (TUNEL), breast cancer gene-1, matrix metalloproteinases-1 and tissue inhibitor matrix metalloproteinases-1 stains to each lesion using the immunohistochemical method. RESULTS: We observed that ER and PR decreased in ADH when compared with DH (p=0.0001 and p=0.019). However, we determined that in DCIS as c-erbB2 (p=0.005) and Ki-67 (p=0.004) increase, TUNEL (p=0.04) and bcl-2 (p=0.005) decrease, when compared with ADH. When compared with DCIS lesions, we observed the existence of a higher c-erbB2 (p=0.003) and a lower TUNEL (p=0.012) in invasive tumors. Furthermore, we found that there is a higher MMP-1 (p=0.04) in invasive lesions, when compared with non-invasive lesions. We detected higher PR (p=0.049), lower TUNEL and c-erbB2 (p=0.017) in low grade group of NPI, when compared with high grade group of NPI. CONCLUSION: As a result, it has been shown that together with increase in proliferation, decrease in apoptosis, too, contributes to the proliferation/apoptosis imbalance that occurs in breast carcinogenesis. Increase in proliferation and decrease in apoptosis are parallel with the progression of lesions. We also showed that the changes, beginning with loss of ER and PR in ADH step, can cause malign transformation, which is especially notable both in DCIS step due to Ki-67 and c-erbB2 increase, and also with bcl-2 and TUNEL decrease. SN - 0379-5284 UR - https://www.unboundmedicine.com/medline/citation/16380768/Breast_carcinogenesis__Transition_from_hyperplasia_to_invasive_lesions_ L2 - https://medlineplus.gov/breastcancer.html DB - PRIME DP - Unbound Medicine ER -