The AP-1 complex has been implicated in transformation and progression of cancer. In osteosarcoma and endometrial carcinoma,<unk>  overexpression was associated with high-grade lesions and poor prognosis. Also, in a comparison between precancerous lesion of the cervix uteri and invasive cervical cancer,<unk>  expression was significantly lower in precancerous lesions.<unk>  has also been identified as independent predictor of decreased survival in breast cancer. It was found that overexpression of<unk>  from class I MHC promoter in transgenic mice leads to the formation of osteosarcomas due to increased proliferation of osteoblasts whereas ectopic expression of the other Jun and<unk>  proteins does not induce any malignant tumors. Activation of the<unk>  transgene in mice results in overexpression of cyclin D1, A and E in osteoblasts and chondrocytes, both in vitro and in vivo, which might contribute to the uncontrolled growth leading to tumor. Human osteosarcomas analyzed for<unk>  expression have given positive results in more than half the cases and<unk>  expression has been associated with higher frequency of relapse and poor response to chemotherapy. Several studies have raised the idea that<unk>  may also have tumor-suppressor activity, that it might be able to promote as well as suppress tumorigenesis. Supporting this is the observation that in ovarian carcinomas, loss of<unk>  expression correlates with disease progression. This double action could be enabled by differential protein composition of tumour cells and their environment, for example, dimerisation partners, co-activators and promoter architecture. It is possible that the tumor suppressing activity is due to a proapoptotic function. The exact mechanism by which<unk>  contributes to apoptosis is not clearly understood, but observations in human hepatocellular carcinoma cells indicate that<unk>  is a mediator of c-myc-induced cell death and might induce apoptosis through the p38 MAP kinase pathway. Fas ligand (FASLG or FasL) and the tumour necrosis factor-related apoptosis-inducing ligand (TNFSF10 or TRAIL) might reflect an additional apoptotic mechanism induced by<unk> , as observed in a human T-cell leukaemia cell line. Another possible mechanism of<unk>  involvement in tumour suppression could be the direct regulation of BRCA1, a well established factor in familial breast and ovarian cancer. In addition, the role of<unk>  and other<unk>  family proteins has also been studied in endometrial carcinoma, cervical cancer, mesotheliomas, colorectal cancer, lung cancer, melanomas, thyroid carcinomas, esophageal cancer, hepatocellular carcinomas, etc. Cocaine, methamphetamine, morphine, and other psychoactive drugs have been shown to increase<unk>  production in the mesocortical pathway (prefrontal cortex) as well as in the mesolimbic reward pathway (nucleus accumbens), as well as display variability depending on prior sensitization.<unk>  repression by ΔFosB's AP-1 complex within the D1-type medium spiny neurons of the nucleus accumbens acts as a molecular switch that enables the chronic induction of ΔFosB, thus allowing it to accumulate more rapidly. As such, the<unk>  promoter finds utilization in drug addiction research in general, as well as with context-induced relapse to drug-seeking and other behavioral changes associated with chronic drug taking. An increase in<unk>  production in androgen receptor-containing neurons has been observed in rats after mating.
C-Fos
Orf 
Bcl-2
BIM-1
AP-7 
HER2/neu
COVAX-19
Mad2