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Synovial Sarcoma, X Breakpoint 1 (SSX1) is a member of a family of highly homologous synovial sarcoma X (SSX) breakpoint proteins. SSX proteins are localized to the nucleus and expressed in testis and some types of cancers and, hence, they are classified as C/T (cancer/testis) antigens. These proteins may serve as transcriptional repressors. SSX1 genes are involved in the t (X;18) translocation typically found in all synovial sarcomas. This translocation leads to the fusion of the synovial sarcoma translocation gene on chromosome 18 to one of the SSX genes on chromosome X. These hybrid proteins are most likely responsible for transforming activity.

Synovial Sarcoma, X Breakpoint 2 (SSX2) is a part of the family of highly homologous synovial sarcoma X breakpoint proteins which play a role as transcriptional repressors. Homologous synovial sarcoma X breakpoint proteins are also able to bring out spontaneous humoral and cellular immune responses in cancer patients, and are effective targets in cancer vaccine-based immunotherapy.

Alveolar Soft Part Sarcoma Chromosome Region, Candidate 1 (ASPSCR1) contains a UBX domain and interacts with glucose transporter type 4 (GLUT4). ASPSCR1 is a tether, which sequesters the GLUT4 in intracellular vesicles in muscle and fat cells, and redistributes the GLUT4 to the plasma membrane. Translocation t(X;17)(p11;q25) of this ASPSCR1 with transcription factor TFE3 gene ends with a ASPSCR1-TFE3 fusion protein in alveolar soft part sarcoma and in renal cell carcinomas.

Kirsten Rat Sarcoma Viral Oncogene, Isoform 2A (KRAS-2A) belongs to the small GTPase superfamily. The KRAS-2A protein is involved in a variety of malignancies, including lung adenocarcinoma, mucinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma. Ras family members impact cell growth and differentiation events in a subcellular membrane compartmentalization-based signaling system under normal conditions. Oncogenic Ras can deregulate processes which control both cell proliferation and apoptosis.

Crk-like protein (CRKL) is a protein kinase containing SH2 and SH3 (src homology) domains which activates the RAS and JUN kinase signaling pathways and transforms fibroblasts in a RAS-dependent manner. CRKL is a substitute of the BCR-ABL tyrosine kinase, it also has a role in fibroblast transformation by BCR-ABL, and has oncogenic potential.

CRK belongs to the signaling adapter protein family which binds to several tyrosine-phosphorylated proteins. CRK is involved in many cellular processes such as apoptosis, proliferation, and differentiation. CRK has a modular domain architecture consisting of an SH2 followed by two SH3 domains (src-homology domains). The N-terminal SH2 domain of the CRK protein functions as a positive regulator of transformation whereas the C-terminal SH3 domain functions as a negative regulator of transformation.

Retinoblastoma (RB) is an embryonic malignant neoplasm of retinal origin. It almost always presents in early childhood and is often bilateral. Spontaneous regression ('cure') occurs in some cases. Retinoblastoma acts as a regulator of other genes and forms a complex with adenovirus e1a and with sv40 large t antigen. Retinoblastoma acts as a tumor suppressor and modulats functionally certain cellular proteins with which t and e1a compete for pocket binding. Retinoblastoma is potent inhibitor of e2f-mediated trans-activation, recruits and targets histone methyltransferase suv39h1 leading to epigenetic transcriptional repression, inhibits the intrinsic kinase activity of taf1.

ORF73 protein of human herpesvirus 8 is a Kaposi''s sarcoma-associated herpesvirus latent protein that is suspected of playing a critical role in modulating viral and cellular gene expression. ORF73 is linked to cellular chromatin and stays on the chromosomes during cell division. ORF73 maintains the viral genomes during cell division by tethering the viral episomes to the chromosomes. ORF73 binds directly to replication origin recognition complexes which are primarily connected with the terminal repeat region of the HHV8 genome.

C-JUN is a gene which, in combination with c-Fos, forms the AP-1early response transcription factor. C-JUN is activated by the JNKpathway. C-JUN is the putative transforming gene of avian sarcoma virus 17. C-JUN is a protein which is highly similar to the viral protein, and which interacts directly with specific target DNA sequences to regulate gene expression. The C-JUN gene is intronless and is mapped to 1p32-p31, a chromosomal region involved in both translocations and deletions in human malignancies.