death, and repair of double-stranded dna breaks yesbreast/ovarian cancer nf1 cell differentiation, division, development, ras signal transduction no nerve tumors, neuroblastoma ptch hedgehog signaling no medulloblastoma, basal cell carcinoma retinoblastoma protein (prb). prb was the first tumor-suppressor protein discovered in human retinoblastoma; however, recent evidence has also implicated prb as a tumor-survival factor. rb1 gene is a gatekeeper gene that blocks cell proliferation, regulates cell division and cell death. specifically prb prevents the cell cycle progression from g1 phase into the s phase by binding to e2f and repressing the necessary gene transcription. this prevents the cell from replicating its dna if there is damage. p53. tp53, a caretaker gene, encodes the protein p53, which is nicknamed "the guardian of the genome". p53 has many different functions in the cell including dna repair, inducing apoptosis, transcription, and regulating the cell cycle. mutated p53 is involved in many human cancers, of the 6.5 million cancer diagnoses each year about 37% are connected to p53 mutations. this makes it a popular target for new cancer therapies. homozygous loss of p53 is found in 65% of colon cancers, 30–50% of breast cancers, and 50% of lung cancers. mutated p53 is also involved in the pathophysiology of leukemias, lymphomas, sarcomas, and neurogenic tumors. abnormalities of the p53 gene can be inherited in li-fraumeni syndrome (lfs), which increases the risk of developing various types of cancers. bcl2. bcl2 is a family of proteins that are involved in either inducing or inhibiting apoptosis. the main function is involved in maintaining the composition of the mitochondria membrane, and preventing cytochrome c release into the cytosol. when cytochrome c is released from the mitochondria it starts a signaling cascade to begin apoptosis. swi/snf. swi/snf is a chromatin remodeling complex, which is lost in about 20% of tumors. the complex consists of 10-15 subunits encoded by 20 different genes. mutations in the individual complexes can lead to misfolding, which compromises the ability of the complex to work together as a whole. swi/snf has the ability move nucleosomes, which condenses dna, allowing for transcription or block transcription from occurring for certain genes. mutating this ability could cause genes to be turned on or off at the wrong times. as the cost of dna sequencing continues to diminish, more cancers can be sequenced. this allows for the discovery of novel tumor suppressors and can give insight on how to treat and cure different cancers in the future. other examples of tumor suppressors include pvhl, apc, cd95, st5, ypel3, st7, and st14, p16, brca2.