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ORIGINAL ARTICLE

Separation and identification of differentially expressed nuclear matrix proteins in breast carcinoma forming

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Pages 76-84 | Received 12 Apr 2009, Accepted 25 Aug 2009, Published online: 02 Nov 2009

Figures & data

Figure 1. Western blot analysis of DNA topoisomerase II (A) and histone (B). Lane 1, nuclear protein of normal breast. Lane 2, nuclear matrix protein of normal breast. Lane 3, nuclear protein of breast carcinoma. Lane 4, nuclear matrix protein of breast carcinoma. β-actin as used as an internal loading control.

Figure 1. Western blot analysis of DNA topoisomerase II (A) and histone (B). Lane 1, nuclear protein of normal breast. Lane 2, nuclear matrix protein of normal breast. Lane 3, nuclear protein of breast carcinoma. Lane 4, nuclear matrix protein of breast carcinoma. β-actin as used as an internal loading control.

Figure 2. Representative 2-D gel analyses of NMPs from (A) normal breast, (B) hyperplastic mammary, (C) atypical epithelial hyperplasia and (D) breast carcinoma.

Figure 2. Representative 2-D gel analyses of NMPs from (A) normal breast, (B) hyperplastic mammary, (C) atypical epithelial hyperplasia and (D) breast carcinoma.

Figure 3. MALDI-TOF mass spectrum maps of Hsp27 (A), prohibitin (B) and laminA/C (C).

Figure 3. MALDI-TOF mass spectrum maps of Hsp27 (A), prohibitin (B) and laminA/C (C).

Table I. Differentially-expressed proteins in the different groups.

Figure 4. Western blot analysis of the Hsp27 (A), prohibitin (B) and laminA/C (C) in normal breast (Lane 1) and breast carcinoma (Lane 2). β-actin was used as an internal loading control.

Figure 4. Western blot analysis of the Hsp27 (A), prohibitin (B) and laminA/C (C) in normal breast (Lane 1) and breast carcinoma (Lane 2). β-actin was used as an internal loading control.

Figure 5. Representative immunohistologic features of Hsp27 (A), prohibitin (B) and laminA/C (C) in normal breast and breast carcinoma (original magnification 200).

Figure 5. Representative immunohistologic features of Hsp27 (A), prohibitin (B) and laminA/C (C) in normal breast and breast carcinoma (original magnification 200).

Figure 6. Correlation analysis of prohibitin expression with clinicalpathological characteristics. (A and B) The expression of prohibitin was increased from normal breast (lane 1–2), hyperplastic mammary (HM) (lane 3), to breast carcinoma (BC) lanes 4–6). However, prohibitin expression was not correlated with the differentiation status of breast carcinoma (lanes 4–6 are low-, medium-, and high-differentiated breast carcinoma, respectively).

Figure 6. Correlation analysis of prohibitin expression with clinicalpathological characteristics. (A and B) The expression of prohibitin was increased from normal breast (lane 1–2), hyperplastic mammary (HM) (lane 3), to breast carcinoma (BC) lanes 4–6). However, prohibitin expression was not correlated with the differentiation status of breast carcinoma (lanes 4–6 are low-, medium-, and high-differentiated breast carcinoma, respectively).

Table II. The correlation of prohibitin with clinicalpathological features.

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