Basic Oncology Handouts

Melanoma Sq. Cell Carcinoma Basal cell carcinoma (abundant of all but not fatal )

Mutations cell cycle M-G1-S-G2 cdk regulates the cell cycle

if repair in abnormal can not proceed to Apoptosis Rb+P53 tumor supressor genes Transition G1-S if mutations of Rb inhibit transition (G1-S) Proto-oncogenes – mutated oncogenes

Keep dividing does not need growth factor

Apoptosis regulator Complex tight control t triggers the nxt

Eliminate signaling or key enzymes Stop apoptosis cell growth .DNA Repair genes Cells more susceptible mutation required on both alleles Paternal +Maternal

Multiple mutations ---Malignant Tumor Progresses --- Metastasis

Loss of funtion in both of tumor supressor genes as long as 1 is working cell cyle is regulated

Retinoblastoma 1 allele is inherited other sporadic

P53 dins the DNA and halts the cell cycle . Cell is either repaired or apoptized

P53 is called the guardian of the genome .

Other tumor suppressor genes

Only 3% breast cancer have BRCA mutations .

NF1- Chromosome 17 NF2- Chromosome 22

Proto oncogenes Regulate Growth factor Receptors

or Tyrosine Kinase

Oncogenes :RAS P53 most common mutations

RAS in active form because GTP does not hydrolize keep active MAP kinase cell Proliferate BCR-ALB can not be switched on/off always ON.

BCR-ALB gene codes for Non-receptors T-K Cytoplasm same T-K Associated with Specific recoptors .Insulin Various Growth Factors

ret- neurotrophic growth factor receptor Proteins . Receptor outside the cel TK-inside G.F Binds out cell -TK switch on inside .

But when ret mutated T-K always switch on cells than constantly keep growing

Assoc w/ MEN 2A/2B normal ret is Exp in (adrenal medulla),Parafollicular cells of thyroid this causes Pheochromocytoma

Medullary thyroid Cancer assoc w/ Papillary carcinoma of thyroid

cancer drugs transtrezimab ????Antibody targets mutated T.Kina for breast cancer +ve for mutation

Neuroblastoma (Tumor of adrenal medulla) .