📝 摘要
Decades of hypothesis-driven research have led to the discovery of oncogenes and tumor suppressors that affect carcinogenesis. With the advent of powerful genomic and proteomic microarray techniques, a different scientific paradigm is emerging—one in which hypotheses are generated based on the evaluation of global gene expression in cells or tissues. Tissue microarrays are also useful to interrogate expression, at the mRNA or protein level, of a single or small set of gene products in normal, preneoplastic, or malignant tissues. In this issue of the Journal, Gurrieri et al. (1) used tissue microarrays to analyze comprehensively the mRNA and protein expression profiles of the tumor suppressor PML in diverse cancers of hematopoietic and solid tumor origin. They found frequent loss of PML protein but not of PML mRNA in cancers from multiple histopathologic sites. In a few cases, PML mutations or polymorphisms were identified. However, neither these changes nor loss of heterozygosity (LOH) could account for the loss of PML protein. These findings and those obtained after treatment with a proteasome inhibitor, point to a post-transcriptional mechanism for this PML regulation.
🧾 论文要素
| 作者 | Ethan Dmitrovsky |
|---|---|
| 期刊 | JNCI Journal of the National Cancer Institute |
| 出版机构 | https://openalex.org/P4310311648 |
| 年份 | 2004 |
| 归属类 | 血液肿瘤 |
| 平台 | OpenAlex |
| 被引数 | 2 |
| 阅读量 | 18 |
| DOI | 10.1093/jnci/djh068 ↗ |
| 关键词 | Computational biology; Biology; DNA microarray; Tissue microarray; Genetics |