While multiple lines of experimental evidence support the assertion that malfunctions in fragile mechanisms are implicated in solid and hematological cancers, some evidence is contradictory.
HS proteoglycans are implicated in solid tumor development[ 70, 71].
Vascular endothelial growth factor (VEGF) and its receptors have been implicated in promoting solid tumor growth and metastasis via stimulating tumor-associated angiogenesis.
Epigenetic alterations have been implicated in the pathogenesis of solid tumors, however, proto-oncogenes activated by promoter demethylation have been sporadically reported.
We believe that mechanistic insight into MMSET-mediated gene expression changes will provide significant avenues for potential therapeutic strategies, as MMSET overexpression has been implicated in myeloma and other solid tumors.
Members of the OncomiR-1 family, miR-106a, −18b, −20b, −19b, −92-2, and −363 have been implicated in hematopoietic malignancies and solid tumors of the breast, colon, lung, pancreas, prostate, and stomach among others [ 16, 53, 55– 55].
Cytokines have been implicated in the acute rejection of solid organ transplantation.
The actin binding protein Mammalian enabled (Mena), has been implicated in the metastatic progression of solid tumors in humans.
CAF have recently been implicated in important aspects of epithelial solid tumor biology, such as progression, growth, angiogenesis and metastasis.
One of these genes, β1-integrin, has been implicated in therapeutic resistance in multiple solid cancer models [ 20, 21].
