Chapter 11: Biology, Clinical Manifestations, And Treatment Of Cancer Flashcards
Benign tumor
Grow slowly, well-defined capsule, not invasive, well differentiated, low neurotic index, do not metastasize
Cancer
Result of cells losing normal control over their proliferation and form a tumor that serves no biological purpose
Malignant tumor
Grow rapidly, not encapsulated, invasive, poorly differentiated, high mitotic index, can spread distantly(metastasis)
Classification and Nomenclature
Malignant tumors
-named according to the tissues from which they arise
–Malignant epithelial tumors=carcinoma
Arise from or form ductal or glandular structures=adenocarcinomas
–Malignant connective tissue tumors=sarcomas
E.g. Chondrosarcoma and osteosarcoma
–cancers of lymphatic tissues=lymphomas
–cancers of blood forming cells=leukemias
–carcinoma in situ(CIS)
Preinvasive epithelial malignant tumors of glandular or epithelial origin that have not broken through the basement membrane or invaded the surrounding stroma
Transformation
Process of accumulating mutations leading to the development of cancer
Autonomy
Cells no longer rely on extracellular signals to control proliferation
Anchorage independence
No longer need to attach to a substratum to proliferate
Immortalization
Acquire an abnormal lifespan with apparently unlimited potential for proliferation
Anaplasia
Lose tissue organization and levels of cell differentiation
Leads to pleomorphism (different types of cells make up tumor)
Genetic basis of cancer
Types of genes affected:
-growth factors/growth factor receptors
Some cancer cells acquire the ability to secrete growth factors that stimulate their own growth, autocrine stimulation
Some cancers have an increase in growth factor receptors E.g. In breast cancer up-regulation of HER2 receptors sends growth signals into the cell
-intracellular signaling proteins
e.g RAS is activated in many types of cancers, stimulating cell growth even when growth factors are missing
-apoptotic proteins
Down regulation leading to increased life span
-tumor suppressor genes
Function normally to suppress proliferation
Mutation and inactivation
Mutation of normal genes into ocogenes
-point mutations: single nucleotide change in DNA e.g RAS gene
-chromosomes translocations; a piece of one chromosome is translocation to another chromosome leading to dysregulation of gene transcription e.g MYC gene in Burkitt lymphoma
-gene amplification
Duplication of a small piece of chromosomes over and over again so that instead of two copies of a gene, tens or hundreds of copies are present e.g N-myc in neuroblastoma
-loss of heterozygosity
Loss of normal allele of a gene(for tumor suppression)
-gene silencing: decreased production of protein through non-mutational DNA modification
DNA methylation to stop transcription of a tumor suppressor gene
Angiogenesis
Growth of new vessels, advanced cancers can secrete angiogenetic factors(growth factors) to promote blood vessel invasion to provide nutrients
Telomeres and Immortality
Body cells are not immortal and can divide only a limited number of times
Telomeres are protective caps on each chromosome and are held in place by telomerase
Telomeres become smaller and smaller with each cell division
Cancer cells can restore telomeres leading to continued division
Inflammation and cancer
Chronic inflammation is an important favor in the development of cancer -causes cellular injury Cytokine release from inflammatory cells Free radicals Mutation promotion Decreased response to DNA damage
Local tissue invasion
Adherence to extracellular matrix protein and then break down of ECM by tumor produced proteases to allow invasion through basement membrane
