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  2. Carcinogenesis - Wikipedia

    en.wikipedia.org/wiki/Carcinogenesis

    Proto-oncogenes are genes that promote cell growth and mitosis, whereas tumor suppressor genes discourage cell growth, or temporarily halt cell division to carry out DNA repair. Typically, a series of several mutations to these genes is required before a normal cell transforms into a cancer cell. [10] This concept is sometimes termed ...

  3. Oncogene - Wikipedia

    en.wikipedia.org/wiki/Oncogene

    From proto-oncogene to oncogene. The proto-oncogene can become an oncogene by a relatively small modification of its original function. There are three basic methods of activation: A mutation within a proto-oncogene, or within a regulatory region (for example the promoter region), can cause a change in the protein structure, causing

  4. Oncogenomics - Wikipedia

    en.wikipedia.org/wiki/Oncogenomics

    Oncogenomics is a sub-field of genomics that characterizes cancer-associated genes.It focuses on genomic, epigenomic and transcript alterations in cancer. Cancer is a genetic disease caused by accumulation of DNA mutations and epigenetic alterations leading to unrestrained cell proliferation and neoplasm formation.

  5. DNA methylation in cancer - Wikipedia

    en.wikipedia.org/wiki/DNA_methylation_in_cancer

    DNA methylation in cancer plays a variety of roles, helping to change the healthy cells by regulation of gene expression to a cancer cells or a diseased cells disease pattern. One of the most widely studied DNA methylation dysregulation is the promoter hypermethylation where the CPGs islands in the promoter regions are methylated contributing ...

  6. Two-hit hypothesis - Wikipedia

    en.wikipedia.org/wiki/Two-hit_hypothesis

    It was later found that carcinogenesis (the development of cancer) depended both on the mutation of proto-oncogenes (genes that stimulate cell proliferation) and on the inactivation of tumor suppressor genes, that keep proliferation in check. Knudson's hypothesis refers specifically, however, to the heterozygosity of tumor suppressor genes.

  7. Anticancer gene - Wikipedia

    en.wikipedia.org/wiki/Anticancer_gene

    E4orf4 may inhibit these pathways, causing cell death in cancer cells, but not normal cells. 3) E4orf4 may use oncogenes that have been activated in cancer cells, including Src, to cause cell death. 4) Cancer cells have disrupted cell cycle checkpoints and E4orf4 can take

  8. Retrovirus - Wikipedia

    en.wikipedia.org/wiki/Retrovirus

    The retrovirus DNA is inserted at random into the host genome. Because of this, it can be inserted into oncogenes. In this way some retroviruses can convert normal cells into cancer cells. Some provirus remains latent in the cell for a long period of time before it is activated by the change in cell environment. [citation needed]

  9. Myc - Wikipedia

    en.wikipedia.org/wiki/Myc

    c-Myc also plays an important role in stem cell biology and was one of the original Yamanaka factors used to reprogram somatic cells into induced pluripotent stem cells. [ 6 ] In the human genome , C-myc is located on chromosome 8 and is believed to regulate expression of 15% of all genes [ 7 ] through binding on enhancer box sequences ( E-boxes ).