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Articles

  1. Normal and Malignant Cell Growth
  2. Cancer and the Cell Cycle
  3. Cancer cell - Wikipedia
  4. Can We Make Cancer Cells Normal Again?

Table Open in new tab. The application of microarray technology to the analysis of the cancer genome.

Normal and Malignant Cell Growth

Search ADS. Integrative analysis of transcriptomic and proteomic data: challenges, solutions and applications.


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Evaluation of quality-control criteria for microarray gene expression analysis. In silico microdissection of microarray data from heterogeneous cell populations. Systematic variation in gene expression patterns in human cancer cell lines. Distinctive gene expression patterns in human mammary epithelial cells and breast cancers. Immortalization of human bronchial epithelial cells in the absence of viral oncoproteins. Proteomic analysis for the assessment of different lots of fetal bovine serum as a raw material for cell culture. Part IV. Application of Proteomics to the Manufacture of Biological Drugs.

Induction of squamous differentiation of normal human bronchial epithelial cells by small amounts of serum.

Cancer and the Cell Cycle

Type beta transforming growth factor is the primary differentiation-inducing serum factor for normal human bronchial epithelial cells. Clonal growth of normal adult human bronchial epithelial cells in a serum-free medium.


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Serum-free growth of human mammary epithelial cells: rapid clonal growth in defined medium and extended serial passage with pituitary extract. Keratinocyte serum-free medium maintains long-term liver gene expression and function in cultured rat hepatocytes by preventing the loss of liver-enriched transcription factors.

Unique gene expression signature by human embryonic stem cells cultured under serum-free conditions correlates with their enhanced and prolonged growth in an undifferentiated stage. Serum response factor: discovery, biochemistry, biological roles and implications for tissue injury healing. Establishment and expression profiling of new lung cancer cell lines from Chinese smokers and lifetime never-smokers. Gene expression profiling of cultured human bronchial epithelial and lung carcinoma cells.

Integrative genomics revealed RAI3 is a cell growth-promoting gene and a novel P53 transcriptional target. Gene expression profiling in a renal cell carcinoma cell line: dissecting VHL and hypoxia-dependent pathways. Retinoic acid increases expression of the calcium-binding protein SP in human gastric cancer cells. Retinoic acid can induce markers of endocrine transdifferentiation in pancreatic ductal adenocarcinoma: preliminary observations from an in vitro cell line model.

Identification of retinoid-modulated proteins in squamous carcinoma cells using high-throughput immunoblotting. Microarray analysis uncovers retinoid targets in human bronchial epithelial cells. Cloning and characterization of a novel retinoid-inducible gene 1 RIG1 deriving from human gastric cancer cells. Molecular cloning and characterization of a novel retinoic acid-inducible gene that encodes a putative G protein-coupled receptor. Interaction of Myc-associated zinc finger protein with DCC, the product of a tumor-suppressor gene, during the neural differentiation of P19 EC cells.

Retinoids all-trans and 9-cis retinoic acid stimulate production of macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor by human bone marrow stromal cells. Retinoic acid upregulates beta 1 -integrin in vascular smooth muscle cells and alters adhesion to fibronectin. All-trans-retinoic acid increases transforming growth factor-beta2 and insulin-like growth factor binding protein-3 expression through a retinoic acid receptor-alpha-dependent signaling pathway.

Spermatogenesis in the vitamin A-deficient rat: possible interplay between retinoic acid receptors, androgen receptor and inhibin alpha-subunit. A role of N-cadherin in neuronal differentiation of embryonic carcinoma P19 cells. Retinoic acid and serum modulation of thymosin beta gene expression in rat neuroblastoma cells.

Cancer cell - Wikipedia

Retinoic acid regulates thymosin beta 10 levels in rat neuroblastoma cells. Bone morphogenetic protein-2 and retinoic acid induce neurotrophin-3 responsiveness in developing rat sympathetic neurons. Constitutive expression of the Wilms tumor suppressor gene WT1 in F9 embryonal carcinoma cells induces apoptotic cell death in response to retinoic acid.

Cytochrome PRAI CYP26 promoter: a distinct composite retinoic acid response element underlies the complex regulation of retinoic acid metabolism. Retinoic acid enhances leukemia inhibitory factor expression in OLN oligodendrocytes. Erythropoietin in mouse avascular yolk sacs is increased by retinoic acid. Retinoid-induced epidermal hyperplasia is mediated by epidermal growth factor receptor activation via specific induction of its ligands heparin-binding EGF and amphiregulin in human skin in vivo. Modulation of alpha 1 beta 1, alpha 2 beta 1 and alpha 3 beta 1 integrin heterodimers during human neuroblastoma cell differentiation.

Identification of the retinoic acid-inducible Gprc5a as a new lung tumor suppressor gene. Retinoid refractoriness occurs during lung carcinogenesis despite functional retinoid receptors. All-trans retinoic acid enhances differentiation and influences permeability of intestinal Caco-2 cells under serum-free conditions. AGN is a highly effective antagonist of retinoid action in human ectocervical epithelial cells. Published by Oxford University Press. All rights reserved. For permissions, please email: journals. Issue Section:.


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Can We Make Cancer Cells Normal Again?

Email alerts New issue alert. Advance article alerts. Article activity alert. Receive exclusive offers and updates from Oxford Academic. Related articles in Google Scholar. Citing articles via Google Scholar. Eventually, the pace of the cell cycle speeds up as the effectiveness of the control and repair mechanisms decreases. The genes that code for the positive cell cycle regulators are called proto-oncogenes. Proto-oncogenes are normal genes that, when mutated in certain ways, become oncogenes, genes that cause a cell to become cancerous.

Consider what might happen to the cell cycle in a cell with a recently acquired oncogene. In most instances, the alteration of the DNA sequence will result in a less functional or non-functional protein. The result is detrimental to the cell and will likely prevent the cell from completing the cell cycle; however, the organism is not harmed because the mutation will not be carried forward. If a cell cannot reproduce, the mutation is not propagated and the damage is minimal. Occasionally, however, a gene mutation causes a change that increases the activity of a positive regulator.

For example, a mutation that allows Cdk to be activated without being partnered with cyclin could push the cell cycle past a checkpoint before all of the required conditions are met. If the resulting daughter cells are too damaged to undergo further cell divisions, the mutation would not be propagated and no harm would come to the organism.

However, if the atypical daughter cells are able to undergo further cell divisions, subsequent generations of cells will probably accumulate even more mutations, some possibly in additional genes that regulate the cell cycle.