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Cancer Powered By Docstoc
       Genetic disease requiring a series of mutations, each contributing to the
       development of a tumor
       Alteration in a gene due to a change in DNA composition
       An accumulation of cancer cells that no longer function properly
Characteristics of normal v. cancer cells
       Normal cells- are specialized
                Specific form to perform specific function
       Cancer cells- non-specific
                Look distinctly abnormal
Life span
       Normal cells- undergo division about 50 times, then die
       Cancer cells- immortal
       Normal cells- well defined, normal # of chromosomes
       Cancer cells- enlarged, with abnormal # of chromosomes
                May be mutated [portions duplicated, deleted, extra copies may be present]
Tumor Formation
       Normal cells- exhibit contact inhibition
                When they come in contact to a neighboring cell, they stop dividing
       Cancer cells- grow in multiple layers
       Normal cells- need growth factors to stimulate growth and division
       Cancer cells- do not respond to growth factors
       Formation of new blood vessels to supply needed oxygen and nutrients
       Normal cells- no
       Cancer cells- tumors secrete angiogenic proteins
                Stimulate nearby vessels to branch and infiltrate tumor
       Spread of cancer from place of origin throughout body
       Benign tumor- disorganized, encapsulated mass; non-invasive to adjacent tissue
       Cancer in situ- tumor located in place of origin, before invasion of adjacent tissue
       Malignancy- present when metastasis establishes new tumors distant from primary tumor
Origin of Cancer
       Mutations in at least four classes of genes are associated with cancer
                Genes which code for DNA repair enzymes
                Genes which code for chromatin structure regulating enzymes
                Proto-oncogenes and tumor suppressor genes
                Genes which code for telomerase
DNA Repair Enzymes
       Present in nucleus
       aid in repairing mistakes made during DNA replication
                Sequencing of nucleotide pairs
       Mutations in genes that code for these enzymes may lead to carcinogenesis
Chromatin Structure Regulating Enzymes
       Chromosomes decondense before transcription
                Process governed by structure-regulating enzymes
       Mutations in genes that code for these enzymes may lead to carcinogenesis
Cell Cycle Regulating Enzymes
                Code for proteins that stimulate the cell cycle
       Tumor suppressor genes
                Code for proteins that inhibit the cell cycle
       DNA segments found at ends of chromosomes
                Protect from damage
                Become shorter with every chromosome replication
                After about 50 divisions, cell enters senescence
                Enzyme present in cancer cells
                Keeps telomeres at constant length
Cell Cycle
       Series of stages in which cell prepares for division
       G1- organelles begin to double in number
       S- replication of DNA
       G2- synthesis of protein
       M- mitosis occurs
       Genes that code for proteins which stimulate the cell cycle
       May become oncogenes [cancer-causing genes] with a mutation
                May code for faulty receptor in stimulatory pathway
                May code for abnormal protein product
                May code for abnormally large amounts of normal protein product
       About 100 identified
       Most common in human cancers belong to ras gene family
                Alteration in a single nucleotide pair produces oncogene
Tumor Suppressor Genes
       Code for proteins that inhibit the cell cycle
       Part of normal regulatory mechanism
       Mutation inactivates inhibitory proteins and therefore balance shifts in favor
       of cell cycle stimulation
RB Gene
       one of about half dozen known tumor suppressor genes
       malfunction leads to cancers of breast, prostate, bladder
       linked to retinoblastoma
                Eye tumors by age three
       tumor suppressor gene
       more frequently mutated in human cancers than any other
       codes for protein that acts as transcription factor to “turn on” genes which code
       for cell cycle inhibitors
       can also stimulate apoptosis [programmed cell death]
Causes of Cancer
       Blend of heredity and environmental factors
                some types of cancers seem to run in families
                a number of environmental agents act as carcinogens
       mutated tumor suppressor gene- breast cancer gene #1
       runs in certain families and can be used to predict development of cancer
                risk increases by 2 to 3-fold when close relatives have had cancers
                [breast, lung, colon]
Mutagenic Carcinogens
       environmental agents which increase the chances of mutation and therefore
       contribute to the development of cancer
       organic chemicals
       UV radiation
                sunlight and tanning lamps
                radon gas
                emission from nuclear power plants
Organic Chemicals
       tobacco smoke- tar
       foods- red dye #2
       certain hormones- HRT
       pollutants- benzene, CCl4, dioxin
       Hepatitis B- liver cancer
       Epstein-Barr- nasopharyngeal cancer
       human papillomavirus- cervical cancer
Diagnosis of Cancer
Routine Screening Tests
       need to be relatively easy to do, inexpensive and accurate
       cervical cancer- PAP test
       breast cancer- self-exam, physician’s exam, mammography
       colon cancer- physician’s exam, sigmoidoscopy, stool blood sample, colonoscopy
Tumor Marker Tests
       blood tests for tumor antigens/antibodies
       used in conjunction with other tests
              CEA- relapses in colon cancer
              PSA- prostate specific antigen
              CA-125- detection of ovarian cancer
              AFP- alpha-fetoprotein- liver cancer
Genetic Tests
       determine likelihood of cancer development
       test for genetic mutations
                ex. – BRAC1
                ex. presence of telomerase
Treatment of Cancer

       Cancer in situ
       used in combination with surgery to attack stray cells that might not have been removed
       mutagenic, therefore cancerous cells which are dividing at a increased rate are highly
               cause apoptosis
       used when cancer has spread
       use of drugs to catch cancer cells by damaging their DNA or interfering with synthesis
               ex. TAXOL- interferes with microtubules needed for cell division
       sometimes fails because cancer cells become resistant
Bone Marrow
       contains large numbers of dividing cells- prone to destruction by chemotherapeutic drugs
       removal of bone marrow tissue prior to treatment and subsequent reintroduction after
       short-term, but high dose radiation/ chemotherapy
       stem cells migrate to bone marrow cavities and initiate blood cell formation

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