Transcription profiling of human atypical ductal hyperplasia tissue from women with or without a history of breast cancer
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Poola I
PROVIDER: S-ECPF-GEOD-2429 | biostudies-other | 2005 May
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Fresh Atypical ductal hyperplasia (ADH) tissue collected from breast of a women who either (1) had no prior history of breast cancer and had not developed breast cancer in five years after diagnosis, (2) had cancer before ADH, or had cancer at the time as ADH or developed cancer after ADH diagnosis
2007-08-25 | E-GEOD-2429 | biostudies-arrayexpress
Project description:Fresh Atypical ductal hyperplasia (ADH) tissue collected from breast of a women who either (1) had no prior history of breast cancer and had not developed breast cancer in five years after diagnosis, (2) had cancer before ADH, or had cancer at the time as ADH or developed cancer after ADH diagnosis Keywords: other
2005-04-06 | GSE2429 | GEO
Project description:Women with atypical hyperplasia and lobular or ductal carcinoma in situ (LCIS/DCIS) are at increased risk of developing invasive breast cancer. Chemoprevention with selective estrogen receptor modulators or aromatase inhibitors can reduce breast cancer risk; however, uptake is estimated to be less than 15% in these populations. We sought to determine which factors are associated with chemoprevention uptake in a population of women with atypical hyperplasia, LCIS, and DCIS. Women diagnosed with atypical hyperplasia/LCIS/DCIS between 2007 and 2015 without a history of invasive breast cancer were identified (N = 1,719). A subset of women (n = 73) completed questionnaires on breast cancer and chemoprevention knowledge, risk perception, and behavioral intentions. Descriptive statistics were generated and univariate and multivariable log-binomial regression were used to estimate the association between sociodemographic and clinical factors and chemoprevention uptake. In our sample, 29.3% had atypical hyperplasia, 23.3% had LCIS, and 47.4% had DCIS; 29.4% used chemoprevention. Compared with women with atypical hyperplasia, LCIS [RR, 1.43; 95% confidence interval (CI), 1.16-1.76] and DCIS (RR, 1.54; 95% CI, 1.28-1.86) were significantly associated with chemoprevention uptake, as was medical oncology referral (RR, 5.79; 95% CI, 4.80-6.98). Younger women were less likely to take chemoprevention (RR, 0.61; 95% CI, 0.42-0.87), and there was a trend toward increased uptake in Hispanic compared with non-Hispanic white women. The survey data revealed a strong interest in learning about chemoprevention, but there were misperceptions in personal breast cancer risk and side effects of chemoprevention. Improving communication about breast cancer risk and chemoprevention may allow clinicians to facilitate informed decision-making about preventative therapy. Cancer Prev Res; 10(8); 434-41. ©2017 AACR.
| S-EPMC5540777 | biostudies-literature
Project description:A Cartes d'Identite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net) | 74 samples on Affymetrix HG-U133 Plus 2.0 GeneChips arrays for 74 patients. 5 samples on CGH CIT v7 | Breast carcinoma is the main malignant tumor occurring in patients with Cowden disease, a cancer prone syndrome caused by germline mutation of the tumor suppressor gene PTEN. To better understand this disease, we have performed a transcriptomic study of three Cowden disease breast carcinomas included in a panel of 74 familial breast cancers. Unsupervised clustering of these 74 tumors followed the intrinsic gene classification of breast cancer except for a group of five tumors that included the three Cowden tumors. The gene expression profile of the Cowden tumors shows considerable overlap with that of a breast cancer subgroup known as molecular apocrine breast carcinoma, which is suspected to have increased androgenic signaling and shows frequent ERBB2 amplification. A histological and immunohistochemical study performed on 13 additional cases of Cowden disease breast carcinomas, for which RNA was not available, showed that they have apocrine histological features and express GGT1, a marker of molecular apocrine breast carcinoma. These data suggest that activation of the ERBB2-PI3K-AKT pathway by loss of PTEN at early stages of tumorigenesis promotes the formation of breast tumors with apocrine features. | Submitter : Renaud Schiappa schiappar@ligue-cancer.net | Project leader : Michel Longy longy@bergonie.org
| S-ECPF-TABM-854 | biostudies-other
Project description:BackgroundWomen with atypical hyperplasia (AH) on breast biopsy have a substantially increased risk of breast cancer (BC). Here the BC risk for the extent and subtype of AH is reported for 2 separate cohorts.MethodsAll samples containing AH were included from 2 cohorts of women with benign breast disease (Mayo Clinic and Nashville). Histology review quantified the number of foci of atypical ductal hyperplasia (ADH) and atypical lobular hyperplasia (ALH). The BC risk was stratified for the number of AH foci within AH subtypes.ResultsThe study included 708 Mayo AH subjects and 466 Nashville AH subjects. In the Mayo cohort, an increasing number of foci of AH was associated with a significant increase in the risk of BC both for ADH (relative risks of 2.61, 5.21, and 6.36 for 1, 2, and ≥3 foci, respectively; P for linear trend = .006) and for ALH (relative risks of 2.56, 3.50, and 6.79 for 1, 2, and ≥3 foci, respectively; P for linear trend = .001). In the Nashville cohort, the relative risks of BC for ADH were 2.70, 5.17, and 15.06 for 1, 2, and ≥3 foci, respectively (P for linear trend < .001); for ALH, the relative risks also increased but not significantly (2.61, 3.48, and 4.02, respectively; P = .148). When the Mayo and Nashville samples were combined, the risk increased significantly for 1, 2, and ≥3 foci: the relative risks were 2.65, 5.19, and 8.94, respectively, for ADH (P < .001) and 2.58, 3.49, and 4.97, respectively, for ALH (P = .001).ConclusionsIn 2 independent cohort studies of benign breast disease, the extent of atypia stratified the long-term BC risk for ADH and ALH. Cancer 2016;122:2971-2978. © 2016 American Cancer Society.
| S-EPMC5030128 | biostudies-literature
Project description:Gene expression analysis of meduallary breast cancer vs ductal breast cancer
| S-ECPF-MEXP-441 | biostudies-other
Project description:Breast cancer tumors of ductal (D) and lobular (L) type. Not all lobular tumors are "classical lobular" tumors. Experiment "BC2_Jeffrey_minus_G50_1" was denoted as BC-D-002.
| S-ECPF-SMDB-3962 | biostudies-other
Project description: Not available
| S-ECPF-TABM-657 | biostudies-other
Project description:To gain insights into the transcriptional differences between subgroups of grade III invasive ductal breast cancers, we performed gene expression profiling of a series of RNA extracted from microdissected frozen tissue from patients with breast cancer
| S-ECPF-TABM-543 | biostudies-other
Project description:Introduction: A major challenge in the interpretation of genomic profiling data generated from breast cancer samples is the identification of driver genes as distinct from bystander genes which do not impact tumorigenesis. One way to assess the relative importance of alterations in the transcriptome profile is to combine complementary analyses that assess changes in the copy number alterations (CNAs). This integrated analysis permits the identification of genes with altered expression that map within specific chromosomal regions that demonstrate copy number alterations, providing a mechanistic approach to identify the 'driver genes’. Methods: We have performed whole genome analysis of CNAs using the Affymetrix 250K Mapping array on 22 infiltrating ductal carcinoma samples (IDCs). Analysis of transcript expression alterations was performed using the Affymetrix U133 Plus2.0 array on 16 IDC samples. Twelve IDC samples were analyzed using both platforms and the data integrated. We also incorporated data from LOH analysis to identify genes showing loss of expression in LOH regions. Results: Copy number analysis results demarcated smaller boundaries for many previously reported CNAs, and in some cases, the CNAs were defined as more than a single contiguous event. Additionally, we were able to assign driver genes to these commonly reported regions using a rigorous methodology. For example, RAB25 showed a large increased expression in the tumors and mapped to the commonly reported amplification at 1q22. We also identified 5 genes in the 8q24 amplicon and TSEN4 in the 17q25 amplified region. LOH analysis confirmed some previously reported regions, and integration with copy number data determined that the detected LOH were copy neutral events. Finally, we have identified several RXR pathways that demonstrated down-regulation in IDC whose members may represent further targets of therapeutic intervention. Conclusion: We have demonstrated the utility of the application of integrated analysis using high-resolution CGH and whole genome transcript analysis for detecting driver genes in IDC. The high resolution platform allowed a refined demarcation of CNAs, and gene expression profiling provided a mechanism to detect genes directly impacted by the CNA. This is the first report of LOH in IDC using a high resolution platform. 16 IDC samples analyzed with the U133 Plus 2.0 array compared to 4 normal control samples.
| S-ECPF-GEOD-22544 | biostudies-other