Genetics of Cancer – Flashcards
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Single gene changes
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10%, inherited, mutation in every cell, cancer at young age, multiple types of cancer present
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genetic/ environmental changes
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90%, multifactoral, somatic mutations, older age, most people will get one type of cancer
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most common mutagen
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sunlight
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is cancer genetic or inherited?
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yes genetic but not inherited
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carcinogens
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substances that cause cancer, damage DNA
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what's cancer caused by? (when dealing with cell cycle)
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loss of cell cycle control
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tumor
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growth formed if a cell escapes normal control over its division rate
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does cancer stand out when looking through a microscope?
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yes, has different color/shape/size than normal cells
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a tumor is benign if:
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it does not spread or invade surrounding tissue
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a tumor is malignant if:
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it infiltrates nearby tissue
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metastasis
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when a tumor spreads to other parts of the body by blood or lymph
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oncogenes definition
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more than 100, cause cancer when inappropriately activated
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tumor suppressor genes definition
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more than 30 genes, deletion/inactivation causes cancer, control cell cycle check points
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are normal oncogenes turned off or on?
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turned off
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are cancer oncogenes turned off or on?
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turned on, cell divides uncontrollably
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are normal tumor suppressor genes turned off or on?
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turned on
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are cancer tumor suppressor genes turned off or on?
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turned off, lose protection
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timing, rate, and number of cell divisions depend on:
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protein growth factors, signaling molecules from outside cell, transcription factors
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what controls the cell cycle?
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checkpoints
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what are the 3 checkpoints in the cell cycle control?
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apoptosis, spindle assembly, DNA damage
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telomerase
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enzyme that adds telomere sequence to the end of the chromosome
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normal, specialized cells have telomerase turned:
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off to limit cell division
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cancer cells have to: (telomerase)
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express telomerase to divide infinitely
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somatic mutations
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sporadic cancer, 90%, result from single dominant mutation or 2 recessive mutations in same gene, not inherited
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germline mutations
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inherited cancer, 10%, requires 2nd somatic mutation, rare but results in early onset of the cancer
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what is the origin of cancer?
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begins at the genetic and cellular levels
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characteristics of cancer cells
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divide continually and quicker than normal cells, contain heritable mutations, transplantable, dedifferentiated
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angiogenesis
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formation of local blood vessels
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invasive
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squeeze into any space available
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metastasize
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move to new location in body
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VGEF
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stimulates blood vessel to give Oxygen and food to continue growing the tumor
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4 ways cancer starts
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1. activation of stem cells that produce cancer cells 2. dedifferentiation 3. increase in proportion of a tissue that consists of stem cells or progenitor cells 4. faulty tissue repair
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dediffferentiation reverses what?
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specialization
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proto-oncogens
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normal versions of genes that promote cell division
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expression at the wrong time or in the cell type leads to ____ and ____
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cell division and cancer
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what is the mutated form of proto-oncogenes called?
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oncogenes
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one copy of an oncogenic mutation is sufficient to what?
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promote cell division (cancer)
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what activates oncogenes?
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environmental exposures, chromosomal mutations
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what type of mutations are oncogenes?
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point mutation, translocation, inversion
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proto
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trigger cell cycle when appropriate
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oncogenes
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unchecked cell division
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what virus causes Mono?
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EBV
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how are oncogenes activated?
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when a proto-oncogene moves next to another gene
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overexpression: translocation
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move near antibody
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overexpression: inversion (moves next to...)
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move near hormone
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overexpression: point mutation (moves near...)
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move near viral insertion
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double gene product is what?
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fusion; activates or lifts control of cell cycle
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what causes acute promyelocytic leukemia? (gene, chromosome)
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translocation bt chromosomes 15 and 17, combination of retinioc acid cell surface receptor and an oncogene
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the ____ is transcribed together
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gene pair
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viruses iintegrated next to a proto-oncogene can cause:
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transcription when the virus is transcribed
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moving a proto-oncogene next to a hightly transcribed gene can lead to:
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overexpression of the proto-oncogene
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CML patients have a translocated:
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Philadelphia chromosome (tip of 9 on 22)
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what is the treatment for CML and how was it developed?
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Gleevec, understanding cellular changes allowed development for the drug
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how does gleevec work?
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it has the same structure as the antibody that stimulates transcription, so the CML protiens are never produced
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what is Her-2/neu?
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product of an oncogene, causes breast cancer, too many receptors and signals to divide
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types of tumor suppressor genes
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1. deletions 2. point mutations 3. promotor methylation
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tumor suppressor genes normally stop:
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a cell from dividing
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retinoblastoma (gene, chrome, what happens)
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a rare childhood cancer, RB gene is on chromosome 13 and binds transcription factors so that they cannot activated genes unless carry out mitosis
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two hit hypothesis
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two mutations or deletions are required
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sporadic cases of two-hit hypothesis
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non-inherited, RB is a result of 2 somatic mutations
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familial cases of two-hit hypothesis
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inherited, individuals harbor one mutant allele for the RB gene of their cells, this is followed by a somatic mutation in the normal allele
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p53 gene
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"guardian of the genome"
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two main forms of breast cancer
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1. familial form: a germline mutations is inherited and then a somatic mutation occurs in a breast cell (bcra) 2. sporadic form: two somatic mutations affect the same cell
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what are the two major breast-cancer susceptibility genes? And what do they do?
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BRCA1 AND BRCA2, encode proteins that join two others to form a complex that allows repair of double stranded DNA breaks
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inheriting BRCA mutations increases the risk of:
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other types of cancer (most commonly ovarian cancer)
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microRNAs normally control:
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the expression of proto-oncogenes and tumor suppressor genes (when mutated --> causes cancer)
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gatekeeper genes
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directly control mitosis and apoptosis
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caretaker genes
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control mutation rates and may have an overall effect, when mutant, in destabilizing the genome
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Familia Adenomatous Polyposis (FAP)
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5 % of colon cancer cases are inherited, 1 in 5000 in US has FAP, causes multiple polyps at an early age, several mutations contribute
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the discovery of cancer follows a __ test
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screening
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oldest treatment is ___, which removes the tumor
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surgery
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radiation and cheotherapy non-selectively destroy ___ dividing cells
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rapidly
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other drugs help patients tolerate the ____
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side effects (hair loss, infection, infertility)
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new types of cancer drugs:
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1. anti-antogenesis 2. differentiate cells again 3. inhibitors telomerase 4. apoptosis inducers
