Apoptosis and proliferation as predictors of chemotherapy response in patients with breast carcinoma
BACKGROUND Laboratory evidence suggests that many anticancer agents exert their effect by altering the ratio between apoptosis and cellular proliferation. The objective of this clinical study was to examine in vivo changes in apoptotic index (AI), Bcl‐2 expression, proliferation (Ki‐67 and S‐phase f...
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| Veröffentlicht in: | Cancer 2000-12, Vol.89 (11), p.2145-2152 |
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| creator | Chang, J. Ormerod, M. Powles, T. J. Allred, D. C. Ashley, S. E. Dowsett, M. |
| description | BACKGROUND
Laboratory evidence suggests that many anticancer agents exert their effect by altering the ratio between apoptosis and cellular proliferation. The objective of this clinical study was to examine in vivo changes in apoptotic index (AI), Bcl‐2 expression, proliferation (Ki‐67 and S‐phase fraction [SPF]), and ploidy as potential indicators of chemoresponsiveness.
METHODS
Twenty‐eight women with primary operable breast carcinoma received 2M (mitoxantrone 11 mg/m2, methotrexate 35 mg/m2 every 3 weeks) for 4 cycles before surgery/radiotherapy, and an additional 2 cycles were given after surgery. Clinical response was assessed after four cycles of treatment according to World Health Organization criteria. Changes in molecular markers were assessed from biopsies obtained by fine‐needle aspiration performed before treatment, repeated after 24 and/or 72 hours (T1), and on Days 7 and 21 after the first cycle of chemotherapy. Flow cytometric analysis was used to assess SPF, ploidy, and AI (in situ DNA nick end labeling assay) whereas Ki‐67 and Bcl‐2 were evaluated by immunocytochemical analysis.
RESULTS
The overall response rate was 61% (17 of 28 patients), with a 14% (4 of 28 patients) complete response rate. Patients with diploid carcinomas (P = 0.04) with high Ki‐67 (P = 0.0001) and SPF (P = 0.09) were more likely to respond to treatment. Median AI increased by 3.4% with interquartile (IQ) range of 3.2 in responders, compared with only −0.1% (IQ range, 2.2) in nonresponders at T1 (P = 0.03). Median Ki‐67 decreased by −12.0% (IQ range, 22.9) in responders and increased by 18.5% (IQ range, 15.1) in nonresponders on Day 21 (P = 0.003). Median Bcl‐2 scores increased by 1.0 (IQ range, 4.0) in responders and were unchanged at 0.0 (IQ range, 0.5) in nonresponders (P = 0.08). Changes in SPF or ploidy were not significantly predictive of response.
CONCLUSIONS
The results of this preliminary study support evidence that chemotherapy may increase apoptosis, decrease Ki‐67, and increase Bcl‐2 expression in primary breast carcinomas that subsequently respond to therapy. Methodology allowing morphological confirmation of apoptosis would be advantageous. Cancer 2000;89:2145–52. © 2000 American Cancer Society.
This prospective clinical study confirms in vitro observations of increased apoptosis and decreased proliferation in patients with breast carcinoma who respond to chemotherapy. |
| doi_str_mv | 10.1002/1097-0142(20001201)89:11<2145::AID-CNCR1>3.0.CO;2-S |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_72523793</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>72523793</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4651-cbe829d578edaaf0a9c3eb52ac166486f90d6c260d108a5c6bd8e5e4817618ec3</originalsourceid><addsrcrecordid>eNqVkF-LEzEUxYMobnf1K0hAEH2YmptMZjJdEcr4b2GxYBV8C5nMHRqZTmaTKUu__aa21hdffLrcm3NO7v0Rcg1sDozxt8CqMmOQ89ecMQacwRtVLQDeccjlYrG8-ZDVX-tv8F7M2bxeXfNs_YjMzq7HZJZsKpO5-HlBLmP8ldqSS_GUXABAXkolZqRdjn6cfHSRmqGlY_C96zCYyfmBmpgG2Do7-RCp76jd4NZPm_Q-7mnAOPohInUDHZMBhynSezdtaBPQxIlaE6wb_NY8I08600d8fqpX5Menj9_rL9nt6vNNvbzNbF5IyGyDiletLBW2xnTMVFZgI7mxUBS5KrqKtYXlBWuBKSNt0bQKJeYKygIUWnFFXh1z0xl3O4yT3rpose_NgH4Xdbqei7ISSbg-Cm3wMQbs9Bjc1oS9BqYP8PUBoz5g1H_ga1VpAH2Ar3WCr3_D10IzXa801-uU-uL0_a7ZYvs380Q7CV6eBCZa03fBDNbFs07lUlS5ONO5dz3u_3Ozfy12HIgHFHmsNA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>72523793</pqid></control><display><type>article</type><title>Apoptosis and proliferation as predictors of chemotherapy response in patients with breast carcinoma</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><source>Alma/SFX Local Collection</source><creator>Chang, J. ; Ormerod, M. ; Powles, T. J. ; Allred, D. C. ; Ashley, S. E. ; Dowsett, M.</creator><creatorcontrib>Chang, J. ; Ormerod, M. ; Powles, T. J. ; Allred, D. C. ; Ashley, S. E. ; Dowsett, M.</creatorcontrib><description>BACKGROUND
Laboratory evidence suggests that many anticancer agents exert their effect by altering the ratio between apoptosis and cellular proliferation. The objective of this clinical study was to examine in vivo changes in apoptotic index (AI), Bcl‐2 expression, proliferation (Ki‐67 and S‐phase fraction [SPF]), and ploidy as potential indicators of chemoresponsiveness.
METHODS
Twenty‐eight women with primary operable breast carcinoma received 2M (mitoxantrone 11 mg/m2, methotrexate 35 mg/m2 every 3 weeks) for 4 cycles before surgery/radiotherapy, and an additional 2 cycles were given after surgery. Clinical response was assessed after four cycles of treatment according to World Health Organization criteria. Changes in molecular markers were assessed from biopsies obtained by fine‐needle aspiration performed before treatment, repeated after 24 and/or 72 hours (T1), and on Days 7 and 21 after the first cycle of chemotherapy. Flow cytometric analysis was used to assess SPF, ploidy, and AI (in situ DNA nick end labeling assay) whereas Ki‐67 and Bcl‐2 were evaluated by immunocytochemical analysis.
RESULTS
The overall response rate was 61% (17 of 28 patients), with a 14% (4 of 28 patients) complete response rate. Patients with diploid carcinomas (P = 0.04) with high Ki‐67 (P = 0.0001) and SPF (P = 0.09) were more likely to respond to treatment. Median AI increased by 3.4% with interquartile (IQ) range of 3.2 in responders, compared with only −0.1% (IQ range, 2.2) in nonresponders at T1 (P = 0.03). Median Ki‐67 decreased by −12.0% (IQ range, 22.9) in responders and increased by 18.5% (IQ range, 15.1) in nonresponders on Day 21 (P = 0.003). Median Bcl‐2 scores increased by 1.0 (IQ range, 4.0) in responders and were unchanged at 0.0 (IQ range, 0.5) in nonresponders (P = 0.08). Changes in SPF or ploidy were not significantly predictive of response.
CONCLUSIONS
The results of this preliminary study support evidence that chemotherapy may increase apoptosis, decrease Ki‐67, and increase Bcl‐2 expression in primary breast carcinomas that subsequently respond to therapy. Methodology allowing morphological confirmation of apoptosis would be advantageous. Cancer 2000;89:2145–52. © 2000 American Cancer Society.
This prospective clinical study confirms in vitro observations of increased apoptosis and decreased proliferation in patients with breast carcinoma who respond to chemotherapy.</description><identifier>ISSN: 0008-543X</identifier><identifier>EISSN: 1097-0142</identifier><identifier>DOI: 10.1002/1097-0142(20001201)89:11<2145::AID-CNCR1>3.0.CO;2-S</identifier><identifier>PMID: 11147583</identifier><identifier>CODEN: CANCAR</identifier><language>eng</language><publisher>New York: John Wiley & Sons, Inc</publisher><subject>Antineoplastic agents ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Apoptosis - drug effects ; Apoptosis - physiology ; Biological and medical sciences ; Biomarkers, Tumor - metabolism ; Biopsy, Needle ; breast carcinoma ; Breast Neoplasms - drug therapy ; Breast Neoplasms - pathology ; Breast Neoplasms - surgery ; Carcinoma - drug therapy ; Carcinoma - pathology ; Carcinoma - surgery ; Cell Division - drug effects ; Cell Division - physiology ; Chemotherapy ; Female ; Flow Cytometry ; Humans ; Immunohistochemistry ; Ki-67 Antigen - metabolism ; Medical sciences ; Methotrexate - administration & dosage ; Middle Aged ; Mitoxantrone - administration & dosage ; neoadjuvant chemotherapy ; Neoadjuvant Therapy ; Pharmacology. Drug treatments ; Ploidies ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; S Phase - drug effects ; S Phase - physiology ; tumor growth kinetics</subject><ispartof>Cancer, 2000-12, Vol.89 (11), p.2145-2152</ispartof><rights>Copyright © 2000 American Cancer Society</rights><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4651-cbe829d578edaaf0a9c3eb52ac166486f90d6c260d108a5c6bd8e5e4817618ec3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F1097-0142%2820001201%2989%3A11%3C2145%3A%3AAID-CNCR1%3E3.0.CO%3B2-S$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F1097-0142%2820001201%2989%3A11%3C2145%3A%3AAID-CNCR1%3E3.0.CO%3B2-S$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=845394$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11147583$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chang, J.</creatorcontrib><creatorcontrib>Ormerod, M.</creatorcontrib><creatorcontrib>Powles, T. J.</creatorcontrib><creatorcontrib>Allred, D. C.</creatorcontrib><creatorcontrib>Ashley, S. E.</creatorcontrib><creatorcontrib>Dowsett, M.</creatorcontrib><title>Apoptosis and proliferation as predictors of chemotherapy response in patients with breast carcinoma</title><title>Cancer</title><addtitle>Cancer</addtitle><description>BACKGROUND
Laboratory evidence suggests that many anticancer agents exert their effect by altering the ratio between apoptosis and cellular proliferation. The objective of this clinical study was to examine in vivo changes in apoptotic index (AI), Bcl‐2 expression, proliferation (Ki‐67 and S‐phase fraction [SPF]), and ploidy as potential indicators of chemoresponsiveness.
METHODS
Twenty‐eight women with primary operable breast carcinoma received 2M (mitoxantrone 11 mg/m2, methotrexate 35 mg/m2 every 3 weeks) for 4 cycles before surgery/radiotherapy, and an additional 2 cycles were given after surgery. Clinical response was assessed after four cycles of treatment according to World Health Organization criteria. Changes in molecular markers were assessed from biopsies obtained by fine‐needle aspiration performed before treatment, repeated after 24 and/or 72 hours (T1), and on Days 7 and 21 after the first cycle of chemotherapy. Flow cytometric analysis was used to assess SPF, ploidy, and AI (in situ DNA nick end labeling assay) whereas Ki‐67 and Bcl‐2 were evaluated by immunocytochemical analysis.
RESULTS
The overall response rate was 61% (17 of 28 patients), with a 14% (4 of 28 patients) complete response rate. Patients with diploid carcinomas (P = 0.04) with high Ki‐67 (P = 0.0001) and SPF (P = 0.09) were more likely to respond to treatment. Median AI increased by 3.4% with interquartile (IQ) range of 3.2 in responders, compared with only −0.1% (IQ range, 2.2) in nonresponders at T1 (P = 0.03). Median Ki‐67 decreased by −12.0% (IQ range, 22.9) in responders and increased by 18.5% (IQ range, 15.1) in nonresponders on Day 21 (P = 0.003). Median Bcl‐2 scores increased by 1.0 (IQ range, 4.0) in responders and were unchanged at 0.0 (IQ range, 0.5) in nonresponders (P = 0.08). Changes in SPF or ploidy were not significantly predictive of response.
CONCLUSIONS
The results of this preliminary study support evidence that chemotherapy may increase apoptosis, decrease Ki‐67, and increase Bcl‐2 expression in primary breast carcinomas that subsequently respond to therapy. Methodology allowing morphological confirmation of apoptosis would be advantageous. Cancer 2000;89:2145–52. © 2000 American Cancer Society.
This prospective clinical study confirms in vitro observations of increased apoptosis and decreased proliferation in patients with breast carcinoma who respond to chemotherapy.</description><subject>Antineoplastic agents</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Biopsy, Needle</subject><subject>breast carcinoma</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - pathology</subject><subject>Breast Neoplasms - surgery</subject><subject>Carcinoma - drug therapy</subject><subject>Carcinoma - pathology</subject><subject>Carcinoma - surgery</subject><subject>Cell Division - drug effects</subject><subject>Cell Division - physiology</subject><subject>Chemotherapy</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Medical sciences</subject><subject>Methotrexate - administration & dosage</subject><subject>Middle Aged</subject><subject>Mitoxantrone - administration & dosage</subject><subject>neoadjuvant chemotherapy</subject><subject>Neoadjuvant Therapy</subject><subject>Pharmacology. Drug treatments</subject><subject>Ploidies</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>S Phase - drug effects</subject><subject>S Phase - physiology</subject><subject>tumor growth kinetics</subject><issn>0008-543X</issn><issn>1097-0142</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkF-LEzEUxYMobnf1K0hAEH2YmptMZjJdEcr4b2GxYBV8C5nMHRqZTmaTKUu__aa21hdffLrcm3NO7v0Rcg1sDozxt8CqMmOQ89ecMQacwRtVLQDeccjlYrG8-ZDVX-tv8F7M2bxeXfNs_YjMzq7HZJZsKpO5-HlBLmP8ldqSS_GUXABAXkolZqRdjn6cfHSRmqGlY_C96zCYyfmBmpgG2Do7-RCp76jd4NZPm_Q-7mnAOPohInUDHZMBhynSezdtaBPQxIlaE6wb_NY8I08600d8fqpX5Menj9_rL9nt6vNNvbzNbF5IyGyDiletLBW2xnTMVFZgI7mxUBS5KrqKtYXlBWuBKSNt0bQKJeYKygIUWnFFXh1z0xl3O4yT3rpose_NgH4Xdbqei7ISSbg-Cm3wMQbs9Bjc1oS9BqYP8PUBoz5g1H_ga1VpAH2Ar3WCr3_D10IzXa801-uU-uL0_a7ZYvs380Q7CV6eBCZa03fBDNbFs07lUlS5ONO5dz3u_3Ozfy12HIgHFHmsNA</recordid><startdate>20001201</startdate><enddate>20001201</enddate><creator>Chang, J.</creator><creator>Ormerod, M.</creator><creator>Powles, T. J.</creator><creator>Allred, D. C.</creator><creator>Ashley, S. E.</creator><creator>Dowsett, M.</creator><general>John Wiley & Sons, Inc</general><general>Wiley-Liss</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20001201</creationdate><title>Apoptosis and proliferation as predictors of chemotherapy response in patients with breast carcinoma</title><author>Chang, J. ; Ormerod, M. ; Powles, T. J. ; Allred, D. C. ; Ashley, S. E. ; Dowsett, M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4651-cbe829d578edaaf0a9c3eb52ac166486f90d6c260d108a5c6bd8e5e4817618ec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Antineoplastic agents</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Biopsy, Needle</topic><topic>breast carcinoma</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - pathology</topic><topic>Breast Neoplasms - surgery</topic><topic>Carcinoma - drug therapy</topic><topic>Carcinoma - pathology</topic><topic>Carcinoma - surgery</topic><topic>Cell Division - drug effects</topic><topic>Cell Division - physiology</topic><topic>Chemotherapy</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Medical sciences</topic><topic>Methotrexate - administration & dosage</topic><topic>Middle Aged</topic><topic>Mitoxantrone - administration & dosage</topic><topic>neoadjuvant chemotherapy</topic><topic>Neoadjuvant Therapy</topic><topic>Pharmacology. Drug treatments</topic><topic>Ploidies</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>S Phase - drug effects</topic><topic>S Phase - physiology</topic><topic>tumor growth kinetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, J.</creatorcontrib><creatorcontrib>Ormerod, M.</creatorcontrib><creatorcontrib>Powles, T. J.</creatorcontrib><creatorcontrib>Allred, D. C.</creatorcontrib><creatorcontrib>Ashley, S. E.</creatorcontrib><creatorcontrib>Dowsett, M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chang, J.</au><au>Ormerod, M.</au><au>Powles, T. J.</au><au>Allred, D. C.</au><au>Ashley, S. E.</au><au>Dowsett, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apoptosis and proliferation as predictors of chemotherapy response in patients with breast carcinoma</atitle><jtitle>Cancer</jtitle><addtitle>Cancer</addtitle><date>2000-12-01</date><risdate>2000</risdate><volume>89</volume><issue>11</issue><spage>2145</spage><epage>2152</epage><pages>2145-2152</pages><issn>0008-543X</issn><eissn>1097-0142</eissn><coden>CANCAR</coden><abstract>BACKGROUND
Laboratory evidence suggests that many anticancer agents exert their effect by altering the ratio between apoptosis and cellular proliferation. The objective of this clinical study was to examine in vivo changes in apoptotic index (AI), Bcl‐2 expression, proliferation (Ki‐67 and S‐phase fraction [SPF]), and ploidy as potential indicators of chemoresponsiveness.
METHODS
Twenty‐eight women with primary operable breast carcinoma received 2M (mitoxantrone 11 mg/m2, methotrexate 35 mg/m2 every 3 weeks) for 4 cycles before surgery/radiotherapy, and an additional 2 cycles were given after surgery. Clinical response was assessed after four cycles of treatment according to World Health Organization criteria. Changes in molecular markers were assessed from biopsies obtained by fine‐needle aspiration performed before treatment, repeated after 24 and/or 72 hours (T1), and on Days 7 and 21 after the first cycle of chemotherapy. Flow cytometric analysis was used to assess SPF, ploidy, and AI (in situ DNA nick end labeling assay) whereas Ki‐67 and Bcl‐2 were evaluated by immunocytochemical analysis.
RESULTS
The overall response rate was 61% (17 of 28 patients), with a 14% (4 of 28 patients) complete response rate. Patients with diploid carcinomas (P = 0.04) with high Ki‐67 (P = 0.0001) and SPF (P = 0.09) were more likely to respond to treatment. Median AI increased by 3.4% with interquartile (IQ) range of 3.2 in responders, compared with only −0.1% (IQ range, 2.2) in nonresponders at T1 (P = 0.03). Median Ki‐67 decreased by −12.0% (IQ range, 22.9) in responders and increased by 18.5% (IQ range, 15.1) in nonresponders on Day 21 (P = 0.003). Median Bcl‐2 scores increased by 1.0 (IQ range, 4.0) in responders and were unchanged at 0.0 (IQ range, 0.5) in nonresponders (P = 0.08). Changes in SPF or ploidy were not significantly predictive of response.
CONCLUSIONS
The results of this preliminary study support evidence that chemotherapy may increase apoptosis, decrease Ki‐67, and increase Bcl‐2 expression in primary breast carcinomas that subsequently respond to therapy. Methodology allowing morphological confirmation of apoptosis would be advantageous. Cancer 2000;89:2145–52. © 2000 American Cancer Society.
This prospective clinical study confirms in vitro observations of increased apoptosis and decreased proliferation in patients with breast carcinoma who respond to chemotherapy.</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><pmid>11147583</pmid><doi>10.1002/1097-0142(20001201)89:11<2145::AID-CNCR1>3.0.CO;2-S</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Access via Wiley Online Library; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); Alma/SFX Local Collection |
| subjects | Antineoplastic agents Antineoplastic Combined Chemotherapy Protocols - therapeutic use Apoptosis - drug effects Apoptosis - physiology Biological and medical sciences Biomarkers, Tumor - metabolism Biopsy, Needle breast carcinoma Breast Neoplasms - drug therapy Breast Neoplasms - pathology Breast Neoplasms - surgery Carcinoma - drug therapy Carcinoma - pathology Carcinoma - surgery Cell Division - drug effects Cell Division - physiology Chemotherapy Female Flow Cytometry Humans Immunohistochemistry Ki-67 Antigen - metabolism Medical sciences Methotrexate - administration & dosage Middle Aged Mitoxantrone - administration & dosage neoadjuvant chemotherapy Neoadjuvant Therapy Pharmacology. Drug treatments Ploidies Proto-Oncogene Proteins c-bcl-2 - metabolism S Phase - drug effects S Phase - physiology tumor growth kinetics |
| title | Apoptosis and proliferation as predictors of chemotherapy response in patients with breast carcinoma |
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