self-sufficiency in growth signals
insensitivity to anti-growth signals ( because they don’t have receptors)
evading apoptosis( telomeres)
sustained angiogenesis
limitless replicative potential
invasion and metastasis
escaping immune surveillance (checkpoint inhibitors)
variation in population of cells
heritable: Mutations in DNA, chromosomes, methylation pattern
carcinoma → epithelial cells
sarcoma → connective tissue
leukemia → circulatory or lymphatic
adenomatous cells → ductal or glandular cells
squamous cells → flat cells
myeloid → blood cells
Lymphoid → lymphocytes or macrophages
Tumor markers are biological markers produced by cancer cells
enzymes
genes
Antigens ( PSA -prostate-specific antigen are associated with prostate cancer)
antibodies
hepatitis B → liver cancer
EBV → kissing disease ( mononucleosis) + Burkitt lymphoma
HIV → cervical cancer, caner of mouth, throat, anus
genetic abnormality that is commonly found in myeloid leukemia → translocation between chromosomes 9 and 22, leading to the fusion of the BCR (breakpoint cluster region) gene on chromosome 22 and the ABL1 (Abelson tyrosine kinase 1) gene on chromosome 9.
what does it cause?: produces a constitutively active tyrosine kinase that promotes uncontrolled cell growth and proliferation
RAS gene is a family of genes that encode proteins involved in cell signaling pathways that regulate cell growth, differentiation, and survival
mutation causes: constitutively active, leading to uncontrolled cell growth and proliferation. This can result in the formation of tumors and the spread of cancer to other parts of the body.
Metastasis → cancer cells spread from the primary tumor to other parts of the body through the bloodstream or lymphatic system.
Seeding within body cavities → A direct seeding of body cavities and surfaces
Lymphatic spread→ They enter the lymphatic
Hematogenous spread → the transfer of tumor cells from the primary tumor with the bloodstream.