Cancer Flashcards
2nd stage : promotion
Promoting agents:
- single altered cell will not cause cancer but in presence of promoters increase odds
• accelerates the process
-promoters
Obesity, smoking, alcohol consumption , prolonged sever stress, fat in diet, hormones, nutrition, infections.
•reversible if promoters are removed
3 stages of cancer development
Stage 1: Initiation
Mutation in the cells genetic structure.
- activate proto-oncogenes or inactive tumor suppressor genes.
- carcinogens that can alter a cells genes
•chemical carcinogens: > 6 million chemicals
-polycyclic hydrocarbons: cigarette smoke, tars
-industrial agents: vinyl chloride, asbestos, benzene
-food and drugs:anti cancer drugs, smoked food, nitrosamines
(Alcohol modifies metabolism of carcinogens in liver and esophagus.. Enhances effect of cigarette smoke.
-tobacco ( chewing and smoking)
• related to lung cancer (30% of lung ca deaths r/t to tobacco)
• linked also to cancersin : pancreas, kidney, bladder, larynx, esophagus and cervix
• chemicals in smoking are the initiators and act as promoters.
-radiation:damage DNA
-ionizing radiation (atomic bomb) & UV rays
-viruses: DNA and RNA viruses transform the cells they infect
-hormones
-des in 1st trimester and increased vaginal carcinoma in female offspring.
3rd stage: progression
Characterized by: increased growth rate of tumor, increased invasive mess, metastasis
- metastasis: spread from initial site to distant site.
• multistep process
-rapid tumor growth
-tumor angiogenesis
-invasion (local spread into surrounding tissue)
-hematogenous metastasis
Hematogenous metastasis
- Once tumor cells free of primary tumor release enzymes that penetrate basement membrane of blood vessels and lymph
- enter blood vessel and float until adhere to vessel wall.
- secrete enzymes to degrade basement membrane and move into interstitial tissue and proliferate.
- while floating 1/10,000 cells are destroyed by immune resonse.
staging of tumors
Staging
Describes the location, and pattern of spread of a tumor within the host. Factors such as tumor size, extent of local distant metastasis are considered. TNM (tumor, node, metastasis) system is used extensively as a general framework for staging tumors.
Grading
Refers to the histologic characterization of tumor cells and is basically a determination of the degree of anaplasia. Most grading systems classify tumors into 3 or 4 classes of increasing degrees of malignancy. A greater degree of anaplasia indicates a greater malignant potential.
Grading of tumor
Evaluation of the extent to which tumor cells differ from normal precursors.
Grade 1: well-differentiated with minimal deviation from tissue of origin
Grade 2: moderately well differentiated with evidence of structural changes from normal tissue of origin.
Grade 3- poorly differentiated (hardly) looks like original tissue) with extensive structural changes from tissue of orgin.
Grade 4: very anaplastic with no resemblance to tissues of orgin.
Incidence rate
The # of new cases in a give population
Mortality rate
The # of deaths in a total population in specific time period. Helps describe trends.
Prevalence
The # of individuals who have given disease in given population over specific period of time.
% 2010 estimated cancer deaths
Lung cancer is by far the most common fatal cancer in men 29%, followed by prostate 11% and rectum 9%.
In women lung 26%, breast 15%, and colon and rectum 9%
Normal cell vs cancer cell
Normal: large cytoplasm, single nucleus, single nucleolus, fine chromatin
Cancer: small cytoplasm, multiple nuclei, multiple and large nucleoli, coarse chromatin.
Differentiation
Process by which cells attain structure & functional characteristics
All cells derive from ova- have potential to perform all body functions
Then cells differentiate into specialized committed cells: repress all potential functions and express only the genes related to cell’s specific functions.
Proliferation
Process in which cells divide and reproduce
-normally controls prevent excess proliferation: (dynamic equilibrium)
-contact inhibition
-activation only when new cells needed. (Ie infection- WBC s proliferate
–or when cells degenerate
- rate of normal proliferation differs depending on cell type
. Some tissues don’t proliferate at all ( cardiac, neurons)
Some proliferate rapidly -bone marrow and epithelial.
Cancer cells and proliferation
Proliferate indiscriminately and haphazardly
-stem cell theory- mutation of stem cell ( a predetermined undifferentiated cell)
-a stem cell of a certain tissue will become a mature, functioning cell of that tissue of orgin.
Mutated stem cells
- die from the mutation-apoptosis
-recognize damage and repair itself.
-or pass on mutation to daughter cells and become malignant
Rate
: not faster than normal.. Just more cells proliferating
- pyramid effect
- doubling time: time required for tumor mass to double
Cancer -critical genes
Porto-oncogenes & tumor-suppressor genes
Porto-oncogenes- regulate cellular growth -activating pathways.
Become activated oncogenes when mutations alter their activity so that proliferation signals become inappropriate.
Tumor - suppressor genes (cancer-critical genes)
Normally inhibit cellular proliferation
In order for cell to become malignant, cells must devise ways to evade the normal inhibitory mechanisms that keep the brakes applied to cell- division.
Cancer
Disease of disordered growth and differentiation
Patterns of spread
Cancer cells generally spread via circulatory or lymphatic systems.
Tumor markers help identify parent tissue of cancer orgin
-rely on some retention of parent tumor characteristics.
Angiogenesis
Process by which cancer tumor forms new blood vessels in order to grow.
Usually does not develop until late stages of development.
Triggers are not generally understood.
Inhibition of angiogenesis is important therapeutic goal.
