Tumour-associated oncogenes induce unscheduled proliferation as well as genomic and chromosomal instability. According to current models, therapeutic strategies that block oncogene activity are likely to selectively target tumour cells. However, recent evidences have revealed that oncogenes are only essential for the proliferation of some specific tumour cell types, but not all. Indeed, the lat...

The concept of tumor suppressor networks comes as a logical consequence of the increasing understanding of the biology of tumor suppressor genes and oncogenes. Indeed, it has been gratifying to realize during the past decade that the products of tumor suppressor genes and oncogenes are often involved in the kind of guardian–delinquent relationship, or cat-and-mouse game suggested by the genetic...

TRK oncoproteins are chimeric versions of the NTRK1/NGF receptor and display constitutive tyrosine kinase activity leading to transformation of NIH3T3 cells and neuronal differentiation of PC12 cells. Signal Transducer and Activator of Transcription (STAT) 3 is activated in response to cytokines and growth factors and it has been recently identified as a novel signal transducer for TrkA, mediat...

Viral oncogenes are responsible for oncogenesis resulting from persistent virus infection. Although different human tumor viruses express different viral oncogenes and induce different tumors, their oncoproteins often target similar sets of cellular tumor suppressors or signal pathways to immortalize and/or transform infected cells. Expression of the viral E6 and E7 oncogenes in papillomavirus,...

Synonymous mutations change the sequence of a gene without directly altering the sequence of the encoded protein. Here, we present evidence that these "silent" mutations frequently contribute to human cancer. Selection on synonymous mutations in oncogenes is cancer-type specific, and although the functional consequences of cancer-associated synonymous mutations may be diverse, they recurrently ...

proteins, termed anchorage independence of growth, correlates closely with tumorigenicity in animal models (14). This property of cancer cells presumably reflects the tendency of tumor cells to survive and grow in inappropriate locations in vivo. Such incorrect localization, as occurs in invasion and metastasis, is the characteristic that distinguishes malignant from benign tumors (31). Great p...

Most retroviruses are innocuous to the cells they infect and do not encode transforming genes, yet many are implicated in naturally occurring cancers that arise at high frequency in virus-infected animals. It is now clear that the oncogenic properties of these viruses can be attributed to the stochastic activation of cellular oncogenes by the insertion of proviral DNA. Specific cancers ensue fr...

The cells from plasmacytomas induced in BALB/c and susceptible BALB/c congenic strains of mice by pristane (2,6,10,14-tetramethylpentadecane) (1) have non-random chromosomal translocations, rcpt (6;15) or rcpt(12;15) (2, 3). To date, the karyotypes of 27 early transfer generation or primary pristine-induced plasmacytomas have determined, and 26 of the tumors have either rcpt(6; 15) or rcpt(12;1...

Although cancer is a disease that will afflict one out of three people in the Western world, when considered at a cellular level, it is a rare clonal event. Long-lived organisms, such as humans, have evolved strategies to restrict the development of potentially malignant cells, and one such mechanism is the coupling of proliferative and apoptotic pathways. Multiple oncogenes have the ability to...