ReviewJournal of mammary gland biology and neoplasia2001
Genes, chromatin, and breast cancer: an epigenetic tale.
Review in Journal of mammary gland biology and neoplasia, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 44 citations in OpenAlex.
- A proof-of-principle study of epigenetic therapy added to neoadjuvant doxorubicin cyclophosphamide for locally advanced breast cancer.PloS one · 2006Trial
- Mechanisms of Cell Adhesion Molecules in Endocrine-Related Cancers: A Concise Outlook.Frontiers in endocrinology · 2022Review
- E-cadherin deregulation in breast cancer.Journal of cellular and molecular medicine · 2020Review
- Cross-species functional genomic analysis identifies resistance genes of the histone deacetylase inhibitor valproic acid.PloS one · 2012Article
- Interactions between the actin filament capping and severing protein gelsolin and the molecular chaperone CCT: evidence for nonclassical substrate interactions.Cell stress & chaperones · 2011Article
- Promoter hypermethylation in sentinel lymph nodes as a marker for breast cancer recurrence.Breast cancer research and treatment · 2009Article
- Increased shedding of soluble fragments of P-cadherin in nipple aspirate fluids from women with breast cancer.Cancer science · 2008Article
- BMP-6 promotes E-cadherin expression through repressing deltaEF1 in breast cancer cells.BMC cancer · 2007Article
- Rapid cycling bipolar disease: new concepts and treatments.Current psychiatry reports · 2001Review
- Role of DNA methylation and histone acetylation in steroid receptor expression in breast cancer.Journal of mammary gland biology and neoplasia · 2001Review
- Epigenetic downregulation of the retinoic acid receptor-beta2 gene in breast cancer.Journal of mammary gland biology and neoplasia · 2001Review
- The contribution of epigenetic changes to abnormal centrosomes and genomic instability in breast cancer.Journal of mammary gland biology and neoplasia · 2001Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The production of heritable changes in gene expression is the driving force in the development and progression of breast cancer. Such changes can result from mutations or from epigenetic events such as hypermethylation of DNA and hypoacetylation of histones. Histone acetylation and DNA methylation are major determinants of chromatin structure, and chromatin structure is a primary regulator of gene transcription. Cancer cells frequently contain both mutated genes and genes with altered expression due to one or more epigenetic mechanisms. This review describes the epigenetic changes that disrupt normal chromatin architecture and modify the expression of key genes in breast cancer cells. The structural integrity of the latter genes is usually intact, but their expression has been substantially altered due to methylation in their promoter region or deacetylation of histones that interact with their promoter region or both mechanisms. Genes affected by epigenetic changes in breast cancers include HoxA5, p21WAF, gelsolin, BRCA1, BRCA2, E-cadherin, steroid hormone receptors, and retinoic acid receptor II. Because these epigenetic modifications are usually reversible by treatment with certain drugs, they represent vulnerabilities in the cancer cell that can be exploited as novel targets for new prevention and therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.