In addition, loss of HSF2 expression across many human malignancies indicates a fundamental role in tumorigenesis, which deserves future exploration.
D-type Cyclins are upregulated in many human malignancies including breast cancer to promote an uncontrolled proliferation of cancer cells.
Multidrug resistance (MDR) is a major obstacle that hinders the efficacy of chemotherapy in many human malignancies.
Amplification, overexpression, and elevated activation of Akt have been detected in many human malignancies making it an important target for cancer therapy.
Germline tumor antigens, such as WT1, Wilms' tumor gene 1, are overexpressed in many human malignancies but have low expression in somatic tissues.
The c-Myc transcription factor is pathologically activated in many human malignancies [1].
Persistent JAK/STAT activation is oncogenic and characteristic of many human malignancies and thereby provides an attractive point of intervention for molecularly targeted therapeutics.
The MAPK pathway is deregulated in many human malignancies through aberrant signaling upstream of the protein and by activating mutations of the protein itself, both of which induce a proliferative advantage.
Overexpression of the c-MYC proto-oncogene is associated with many human malignancies, including colon, breast, prostate, cervical, and lung carcinomas, osteosarcomas, lymphomas, and leukemias [4], [5], [6], [7], [8], [9], [10], [11], [12].
In the past few months, new findings using genome-wide mutational analysis have placed central importance on protein pathway deregulation as the principal driving force in many human malignancies [2], [3].
Identifying among nephroblastoma those with a high propensity for distant metastases using cell cycle markers: cyclin E as a regulator of progression through the cell cycle and Ki-67 as a tumor proliferation marker, since both are often deregulated in many human malignancies.
