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However, many oncogenes and oncogenic pathways (e.g., c-Myc, EGFR, Akt, mTORC1, Ras/Raf, and others), which regulate normal growth, are valid targets for cancer therapy.
Many oncogenes and tumor suppressors mediate their effects by interfering with or inducing apoptotic signaling.
Many oncogenes and tumor suppressor genes, previously reported to exhibit particular breast cancer mutations, e.g. ERBB2 and TP53, are typically not detected through analysis of differential expression but can play a central role in signalling networks by interconnecting many expression-responsive genes [74].
Many oncogenes and oncosuppressors regulate autophagy [ 42].
Many oncogenes and tumor suppressor genes responsible for cancer are linked to mutations [ 2].
Many oncogenes and tumor suppressor genes have been discovered and implicated in the regulation of apoptosis.
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During the regulation of EMT, many oncogene and tumor suppressor genes play crucial roles.
It is well known that many oncogenes are hyperactivated and suppressor genes are inactivated when non-tumor tissue progressed to invasive carcinoma.
Many oncogenes, tumor suppressor genes and DNA repair genes are all likely to be involved.
Recently, biological researchers have shown that some diseases like cancer are closely related to the breakdown of regulatory networks, and many oncogenes (i.e., genes closely related to cancer) have been shown enrichment in this regulation mechanism [ 2].
PXN is an adaptor protein and a target of many oncogenes such as BCR/ABL, v-Src, and human papillomavirus E6 protein.
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