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Background: Gene fusions arising from chromosomal translocations have been implicated in cancer.
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Individually, MT-SP1 and RON overexpression have been implicated in cancer progression and metastasis.
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Among these are genes directly implicated in cancer, schizophrenia, autoimmunity and many other diseases.
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These lipid mediators, collectively referred to as eicosanoids, have recently been implicated in cancer.
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CMA activation has been implicated in cancer growth, but the exact mechanisms are unclear.
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They play key roles in numerous diseases and are implicated in cancer progression and chemoresistance.
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NF-kB is implicated in cancer cell growth and chemoresistance.
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The genes that enable our brains and blood cells to develop are implicated in cancer.
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Mutations in T-box genes are the cause of several congenital diseases and are implicated in cancer.
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Recently, it was reported that Wnt5a is also implicated in cancer cell proliferation, but the mechanism was not clear.
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This review will focus on the current knowledge regarding developmental EMT pathways that have been implicated in cancer progression.
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Connective tissue growth factor (CTGF) has been previously implicated in cancer metastasis and invasion in various tumors.
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The G protein-coupled chemokine receptor CXCR4 is specifically implicated in cancer metastasis and HIV-1 infection.
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Furthermore, lipoproteins can be targeted to their endogenous receptors, when those are implicated in cancer, or to other cancer receptors.
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In addition to cancer of the cervix, HPV has been implicated in cancers of the vulva, penis, anus and throat.
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The WASF3 gene has been implicated in cancer cell movement, invasion, and metastasis by regulating genetic pathways important in these processes.