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Transcription profiling of human sequential breast cancer biopsies during letrozole treatment

ABSTRACT: In the present investigation, we have exploited the opportunity provided by neoadjuvant treatment of a group of postmenopausal women with large operable or locally advanced breast cancer (in which therapy is given with the primary tumour remaining within the breast) to take sequential biopsies of the same cancers before and after 10-14 days treatment with letrozole. RNA extracted from the biopsies has been subjected to Affymetrix microarray analysis and the data from paired biopsies interrogated to discover genes whose expression is most influenced by oestrogen deprivation. Experiment Overall Design: biopsies were taken from the same subjects both pretreatment and after 10-14 days Letrozol, 2.5 mg/day, oral

ORGANISM(S): Homo sapiens

SUBMITTER: Miller WR

PROVIDER: S-ECPF-GEOD-5462 | biostudies-other | 2007 Oct

REPOSITORIES: biostudies-other

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Transcription profiling of human sequential breast cancer biopsies during letrozole treatment

Project description:In the present investigation, we have exploited the opportunity provided by neoadjuvant treatment of a group of postmenopausal women with large operable or locally advanced breast cancer (in which therapy is given with the primary tumour remaining within the breast) to take sequential biopsies of the same cancers before and after 10-14 days treatment with letrozole. RNA extracted from the biopsies has been subjected to Affymetrix microarray analysis and the data from paired biopsies interrogated to discover genes whose expression is most influenced by oestrogen deprivation. Experiment Overall Design: biopsies were taken from the same subjects both pretreatment and after 10-14 days Letrozol, 2.5 mg/day, oral

2008-06-13 | E-GEOD-5462 | biostudies-arrayexpress

Transcription profiling of human breast cancer patients treated with Letrozole (Femara) early response to treatment

Project description:Tumorigenic breast cancer cells characterized by high CD44 and low or undetectable CD24 levels (CD44+/CD24-/low) may be resistant to conventional therapies and responsible for cancer relapse. We defined a “signature” expression pattern of hundreds of genes associated with CD44+/CD24-/low, mammosphere-forming cells. In a panel of patient breast tumors, this tumorigenic gene signature was found exclusively manifested in tumors of the recently identified “claudin-low” molecular profile subtype characterized by overexpression of many mesenchymal-associated genes, suggesting that these tumors have pre-existing higher levels of tumorigenic cells. Furthermore, when comparing the expression profiles of paired breast cancer core biopsies before versus after hormone therapy or chemotherapy, both the tumorigenic and “claudin-low” signatures were more active in about half of tumors after treatment, indicative of a greater enrichment of tumorigenic cells as a result of treatments targeting the bulk tumor cells. Experiment Overall Design: Biopsies were taken from the same subjects both pretreatment and after 10-14 days Letrozol, 2.5 mg/day, oral.

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Transcription profiling of human formalin-fixed paraffin-embedded breast cancer core biopsies

Project description:The routine workflow for invasive cancer diagnostics is based on biopsy processing by formalin fixation and subsequent paraffin embedding. Formalin-fixed paraffin-embedded (FFPE) tissue samples are easy to handle, stable and particularly suitable for morphologic evaluation, immunohistochemistry and in situ hybridization. However, it has become a paradigm that these samples cannot be used for genome-wide expression analysis with microarrays. To oppose this view, we present a pilot microarray study using FFPE core needle biopsies from breast cancers as RNA source. We found that microarray probes interrogating sequences near the poly-A-tail of the transcribed genes were well suitable to measure RNA levels in FFPE core needle biopsies. For the ER and the HER2 gene, we observed strong correlations between RNA levels measured in these probe sets and protein expression determined by immunohistochemistry (p = 0.000003 and p = 0.0022). Further, we have identified a signature of 364 genes that correlated with ER protein status and a signature of 528 genes that correlated with HER2 protein status. Many of these genes (ER: 60%) could be confirmed by analysis of an independent publicly available data set. Finally, a hierarchical clustering of the biopsies with respect to three recently reported gene expression grade signatures resulted in widely stable low and high expression grade clusters that correlated with the pathological tumor grade. These findings support the notion that clinically relevant information can be gained from microarray based gene expression profiling of FFPE cancer biopsies. This opens new opportunities for the integration of gene expression analysis into the workflow of invasive cancer diagnostics as well as translational research in the setting of clinical studies. Experiment Overall Design: RNA from 24 breast cancer biopsies extracted with kit A, RNA from 6 breast cancer biopsies extracted with kit B

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Gene expression profiling of sequential metastatic biopsies for biomarker discovery in breast cancer.

Project description:The feasibility of longitudinal metastatic biopsies for gene expression profiling in breast cancer is unexplored. Dynamic changes in gene expression can potentially predict efficacy of targeted cancer drugs. Patients enrolled in a phase III trial of metastatic breast cancer with docetaxel monotherapy versus combination of docetaxel + sunitinib were offered to participate in a translational substudy comprising longitudinal fine needle aspiration biopsies and Positron Emission Tomography imaging before (T1) and two weeks after start of treatment (T2). Aspirated tumor material was used for microarray analysis, and treatment-induced changes (T2 versus T1) in gene expression and standardized uptake values (SUV) were investigated and correlated to clinical outcome measures. Gene expression profiling yielded high-quality data at both time points in 14/18 patients. Unsupervised clustering revealed specific patterns of changes caused by monotherapy vs. combination therapy (p = 0.021, Fisher's exact test). A therapy-induced reduction of known proliferation and hypoxia metagene scores was prominent in the combination arm. Changes in a previously reported hypoxia metagene score were strongly correlated to the objective responses seen by conventional radiology assessments after 6 weeks in the combination arm, Spearman's ρ = 1 (p = 0.017) but not in monotherapy, ρ = -0.029 (p = 1). Similarly, the Predictor Analysis of Microarrays 50 (PAM50) proliferation metagene correlated to tumor changes merely in the combination arm at 6 and 12 weeks (ρ = 0.900, p = 0.083 and ρ = 1, p = 0.017 respectively). Reductions in mean SUV were a reliable early predictor of objective response in monotherapy, ρ = 0.833 (p = 0.008), but not in the combination arm ρ = -0.029 (p = 1). Gene expression profiling of longitudinal metastatic aspiration biopsies was feasible, demonstrated biological validity and provided predictive information.

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