Patterns of Resistance and Incomplete Response to Docetaxel by Gene Expression Profiling in Breast Cancer Patients

Chang, Jenny C.; Wooten, Eric C.; Tsimelzon, Anna; Hilsenbeck, Susan G.; Gutierrez, Maya; Tham, Yee Lu; Kalidas, Mamta; Elledge, Richard M.; Mohsin, Syed K.; Osborne, C. Kent; Chamness, Gary C.; Allred, D. Craig; Lewis, Michael T.; Wong, Helen; O’Connell, P.

doi:10.1200/jco.2005.03.156

Cited by 187 publications

(112 citation statements)

References 20 publications

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“…One explanation for these findings is that breast tumors comprise a population of chemoresistant TIC. Indeed recent studies of patient tumors before and after therapy support the contention that breast TIC are chemo-resistant and underscore the need to develop therapies that target these cells (Chang et al, 2005;Li et al, 2008;Creighton et al, 2009). Our findings illustrate that MRK-003 targets breast TIC as well as non-tumorigenic tumor cells without any deleterious consequences for adult stem cells and thus provides proof-of-principle that eliminating these cells can afford long-lasting cancer cures.…”

Section: Mrk-003 Shrinks and Eliminates Tumors In Micesupporting

confidence: 58%

Gamma-secretase inhibitors target tumor-initiating cells in a mouse model of ERBB2 breast cancer

et al. 2011

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Section: Mrk-003 Shrinks and Eliminates Tumors In Micesupporting

confidence: 58%

Gamma-secretase inhibitors target tumor-initiating cells in a mouse model of ERBB2 breast cancer

et al. 2011

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“…This result is therefore in agreement with the Nomograms's design proposed online, which does not take into account the histological type of the tumour when deciding on the therapeutic option (Rouzier et al, 2005b). There is room to better define biological predictive factors of response to neoadjuvant chemotherapy to screen patients who would benefit most from this therapeutic option (Sotiriou et al, 2002;Chang et al, 2005;Gianni et al, 2005;Rouzier et al, 2005a;Pierga et al, 2007). Lobular carcinomas had reduced clinical responses to neoadjuvant chemotherapy, while responses to breast-conserving treatments were fewer, although not significantly (54% (42 out of 78) vs 65% (434 out of 672); P ¼ 0.07).…”

Section: Discussionsupporting

confidence: 79%

High rates of breast conservation for large ductal and lobular invasive carcinomas combining multimodality strategies

et al. 2008

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The literature reports low rates of breast conservation after neoadjuvant chemotherapy for operable breast cancers not amenable to initial breast-conserving surgery. This study aims to compare the outcome of lobular vs ductal carcinomas after neoadjuvant chemotherapy. Between 1989 and 1999, 750 patients with clinical stage II/IIIA ductal (672) or lobular (78) invasive breast carcinomas were treated at the Institut Curie with primary anthracycline-based polychemotherapy followed by either breast conservation (surgery and/or radiotherapy) or mastectomy. Median follow-up was 10 years. Clinical response to primary chemotherapy was significantly worse for lobular than for ductal carcinomas (47 vs 60%; P ¼ 0.04), but only histological grade remained predictive in multivariate analysis. Breast conservation was high for both ductal and lobular carcinomas (65 and 54%; P ¼ 0.07), due, in part, to the use of radiotherapy, either exclusive or preoperative, for respectively 26 and 40% of patients. The lobular type had no adverse effect, neither on locoregional control nor on overall survival, even in the group of patients treated with breast conservation.

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“…This was demonstrated for chemotherapy by Hannemann et al (2005), who observed that tumours that responded to neoadjuvant chemotherapy showed dramatic changes in their expression profiles when compared to the changes observed in non-responders (Hannemann et al, 2005). On the other hand, a comparison between the transcriptomic profiles of tumours subjected to taxane-based neoadjuvant chemotherapy before and 3 months after treatment revealed strikingly different patterns, independent of initial sensitivity or resistance (Chang et al, 2005b). Cell line studies have demonstrated that changes in gene copy numbers may lead to acquired resistance to chemotherapy (Leyland-Jones et al, 1999;Shimizu et al, 2002;Yasui et al, 2004).…”

Section: Discussionmentioning

confidence: 89%

“…Gene 'signatures' or predictors have been devised for several chemotherapy regimens, including paclitaxel followed by fluorouracil, AC, AC/doxorubicindocetaxel and taxane only chemotherapy (Chang et al, 2003(Chang et al, , 2005bAyers et al, 2004;Hannemann et al, 2005;Cleator et al, 2006). Although these results are promising, the exceedingly small sample size and limitations with the current technology and analysis methods have so far precluded definitive conclusions (Brenton et al, 2005;Reis-Filho et al, 2006b).…”

Section: Discussionmentioning

confidence: 99%

Microarray-based comparative genomic hybridisation of breast cancer patients receiving neoadjuvant chemotherapy

et al. 2006

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We analysed the molecular genetic profiles of breast cancer samples before and after neoadjuvant chemotherapy with combination doxorubicin and cyclophosphamide (AC). DNA was obtained from microdissected frozen breast core biopsies from 44 patients before chemotherapy. Additional samples were obtained before the second course of chemotherapy (D21) and after the completion of the treatment (surgical specimens) in 17 and 21 patients, respectively. Microarray-based comparative genome hybridisation was performed using a platform containing B5800 bacterial artificial chromosome clones (genome-wide resolution: 0.9 Mb). Analysis of the 44 pretreatment biopsies revealed that losses of 4p, 4q, 5q, 12q13.11 -12q13.12, 17p11.2 and 17q11.2; and gains of 1p, 2p, 7q, 9p, 11q, 19p and 19q were significantly associated with oestrogen receptor negativity. 16q21 -q22.1 losses were associated with lobular and 8q24 gains with ductal types. Losses of 5q33.3 -q4 and 18p11.31 and gains of 6p25.1 -p25.2 and Xp11.4 were associated with HER2 amplification. No correlations between DNA copy number changes and clinical response to AC were found. Microarray-based comparative genome hybridisation analysis of matched pretreatment and D21 biopsies failed to identify statistically significant differences, whereas a comparison between matched pretreatment and surgical samples revealed a statistically significant acquired copy number gain on 11p15.2 -11p15.5. The modest chemotherapy-driven genomic changes, despite profound loss of cell numbers, suggest that there is little therapeutic selection of resistant non-modal cell lineages.

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Patterns of Resistance and Incomplete Response to Docetaxel by Gene Expression Profiling in Breast Cancer Patients

Abstract: A specific and consistent gene expression pattern was found in residual tumors after docetaxel treatment. These profiles provide therapeutic targets that could lead to improved treatment.

Cited by 187 publications

References 20 publications

Gamma-secretase inhibitors target tumor-initiating cells in a mouse model of ERBB2 breast cancer

Gamma-secretase inhibitors target tumor-initiating cells in a mouse model of ERBB2 breast cancer

High rates of breast conservation for large ductal and lobular invasive carcinomas combining multimodality strategies

Microarray-based comparative genomic hybridisation of breast cancer patients receiving neoadjuvant chemotherapy

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