Name the cell-types that define carcinomas, sarcomas, lymphomas, and leukemia’s. Which type is most common? Carcinomas- glands, organs and tissues, arise from epithelial cell lining external and internal body surfaces; most common cancer Sarcomas- connective tissues (fat, bone, muscle) Lymphomas- lymph nodes Leukemias- bloodstream. Describe and identify normal tissues, tissues undergoing hyperplasia, dysplasia, and carcinoma in situ. What is the general progression of cancer at this tissue level? Hyperplasia- more cells than normal but still organized Dysplasia- more cells that normal but not organized Carcinoma in situ- severe dysplasia.it is still pre-cancer, benign tumor.
Use the car analogy to describe the basic differences between oncogenes and tumor suppressor gene mutations in the development of cancer. 1. Turning on oncogens (go signals, step on gas, gas petal is stuck, stuck accelerator) 2. Losing tumor suppressor (cutting the brakes) 3. Becoming immortal/immortalization (endless tank of gas) 4. Loss of apoptosis- loss of cell destruction, cells don’t die 5. angiogenesis- growth of new blood cells 6. invasion/metastasis- spread of cancer to distant sites What is telomerase and how does it relate to the development of cancer/cell immortality?
Allows cell growth What is angiogenesis and how does it relate to cancer progression? Cancer cells promote new blood supply to feed growing tumor What is apoptosis and how does it relate to cancer progression? Normal cell death Mutations in cancer cells enable cell to bypass cellular safeguard mechanisms that normally eliminate damaged or unwanted cells What is metastasis and how does it relate to cancer progression? Cancer cells acquire the capability to invade surrounding tissues, migrate to distant sites, and grow secondary cancerous lesions. How are tumors graded and staged?
How does the stage and grade related to prognosis? Tumor grade refers to histological appearance (abnormality of cell and tissue structure). Low grades (I and II) cells and tissues have fewer abnormalities compared to grade III and IV) Tumor stage refers to tumor progression i. Has tumor invaded surrounding tissue? ii. Has tumor invaded local lymph nodes? iii. Has cancer spread to distant body regions? iv. High stage decreases survival chances. Describe the differences between a retrospective and prospective study. Retrospective studies: Look at past exposures and the occurrence of disease Rely on medical histories and participant recall Compare factors of people with the disease with those without disease (control group).
Advantage: Quick,data already exists Disadvantage: Data subject to recall bias and hard to identify all confounding factors Prospective studies (cohort studies) Study populations prior to onset of disease Divide into those exposed to potential carcinogen (experimental group) and those not exposed (control group) Monitor the relative onset of cancer between groups Advantage: Easier to control variables Disadvantage: Large sample sizes and time needed for studies.
What is random fluctuation and how does it relate to sample size and P values when setting up an experiment? Random Fluctuation: Data could be explained by chance Need large sample size Statistical significance: Real difference not due to random fluctuation P value: The probability that the observed difference is due to chance. Want P values to be low Ex. A p value of 0. 05 means that there is a 5% chance that the observed result is due to chance….. 95% chance that it is a reliable difference Explain experimental bias and how to set up a “blinded” and “double-blinded” experiment. Experimental bias.
Expectations of scientist influence gathering or interpretation of data Scientist should be “blinded” to sources of data Subjects/participants don’t know which group they are in Scientists don’t know which data set they are analyzing Does correlation establish cause and effect? If not, what further tests are necessary? No epidemiological study shows cause and effect. Need: 1. Epidemiological correlation agent: human 2. Animal/lab subjects carcinogen can correlate Describe the basic components and structure of DNA and RNA. 17. Differences between DNA and RNA: Sugar Group Nucleotide Bases.
Base pairings DNA Double-stranded Deoxyribose Adenine (A) Guanine(G) Cytosine(C) Thymine(T) A:T C:G RNA Single-stranded Ribose Adenine (A) Guanine(G) Cytosine(C) Uracil(U) A:U C:G Describe the complementary base pairs that occur between strands of DNA. A:T, C:G (Adenine:Thymine) (Cytosine:Guanine) Describe DNA replication. Why is DNA replication termed “semi-conservative”? DNA Replication Each strand of the double-stranded DNA molecule serves as a template for construction of a new complementary strand Step 1: The two strand of DNA unwind and separate DNA helicase important for these functions.
Step 2: The enzyme DNA polymerase binds to each strand of DNA Step 3: DNA polymerase catalyzes the addition of complementary bases to each strand The Result: Two identical DNA double stranded molecules Template DNA (Parental…old) Strands: Original unreplicated strands Complementary Strands (Daughter…new)Strands : Newly made strands Each new double stranded DNA molecule has one Old strand and one new strand Semi-Conservative Replication: For each double-stranded DNA molecule made: 1 strand original parental DNA 1 strand newly made DNA Describe some events that may lead to DNA damage DNA mutations: Changes in the DNA sequence.
Can arise spontaneously Can be created by environmental mutagens Base mismatches: Wrong base inserted during replication Can generally be repaired by DNA polymerase proofreading function or mismatch repair enzymes People lacking mismatch repair enzymes (e. g. those who inherit hereditary nonpolyposis colon cancer (HNPCC) have higher likelihood of developing cancer Other types of DNA Damage Some chemicals can induce the loss of bases Some chemicals can induce the modification of bases: Note: Conversion of C to U will result in a C:G to A:T mutation after replication UV radiation induced pyrimidine (Mostly T) dimer formation.
Explain the difference between the two classes of carcinogens: promoters and mutagens, and how they sometimes work together to increase the risk of cancer development. What is a complete carcinogen? How is the Ames test used? Carcinogens: Substances known to promote cancer development 2 types: mutagenic: They directly cause DNA mutation promoters: Epigenetic: They do not cause DNA mutation They increase likelihood of acquiring DNA mutations Epigenetic: They do not cause DNA mutation Many mechanisms: Increase cell proliferation Decrease cell death Decrease DNA repair Alter transcription or translation of a gene.
*Mutagenic and Promoters can work together (synergistically) ((Smoking (mutagenic) and Alcohol(promoter)) they can be called a complete a (COMPLETE CARCINOGEN) Ames test: Rapid screening of suspected carcinogens using bacteria. Tests for mutagenic carcinogens Suspected carcinogens are added to bacteria Many carcinogens are activated by enzymes contained in liver; liver extracts are added Substances that result in bacterial DNA mutation can be detected. Strong mutagens are generally strong carcinogens. About what % of cancer incidences are considered caused by hereditary factors? Genetics (heredity) contribute 10-20%.