chapter 19: cancer and regulation of the cell cycle – Flashcards
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APC (adenomatous polyposis) gene
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acts as a tumor suppressor controlling cell-cell contact and growth inhibition
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FAP results from
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one mutant copy of the APC gene (chromosome 5, deletions frameshift and point mutations)
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Heterozygous APC mutation causes
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formation of hundreds to thousands of rectal polyps or adenomas in early life
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Most animal viruses that cause cancer are
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retroviruses
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acute transforming retroviruses
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viruses that cause cancer in animals, because they transform cells into cancer cells.
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V-ONCs
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viral oncogenes
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C-ONCs
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cellular oncogene
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how to retroviruses work?
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Retroviruses integrate into the host genome as a provirus that is replicated with the host's DNA during the normal cell cycle
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generally, how does a retrovirus cause cancer?
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cancer by integrating near a proto-oncogene or by integrating a copy of a host proto-oncogene into its genome. Viral RNA genome is copied into DNA via reverse transcriptase brought into the cell by the infecting virus.
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The integrated DNA copy is called a
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provirus and gets replicated along with the host DNA
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1/3 ways that a retrovirus can cause cancer
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1. The proviral DNA may integrate by chance near one of the normal proto-oncogenes and stimulate high levels or inappropriate timing of transcription of the proto-oncogenes
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2/3 ways that a retrovirus can cause cancer
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Acute transforming retroviruses pick up a copy of a host proto-oncogene and integrate it into its genome. This may be mutated during viral transfer and transform normal cells into tumor cells
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3/3 ways that a retrovirus can cause cancer
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A normal retrovirus with normal viral gene products can stimulate inappropriate cell growth
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several retroviruses associated with human cancers
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HIV, HTLV-1
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The most significant contributors to virus-induced cancers are
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papillomaviruses (HPV 16 and 18), human T-cell leukemia virus (HTLV-1), hepatitis B virus, human herpesvirus 8, and Epstein Barr virus
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carcinogenic substances
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any agent that damages DNA if it causes mutations in proto-oncogenes, or tumor suppressor genes.
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example of carcinogens
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include chemicals, radiation, some viruses, and chronic infections
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The most significant environmental carcinogen is
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tobacco smoke
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natural carcinogens
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aflatoxin, nitrosamines.
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what is cancer
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genetic disease at the somatic level resulting from gene products from mutated or abnormally expressed genes
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2 fundamental properties of cancer
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1. unregulated cell proliferation 2. metastatic spread
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Genomic alterations that are associated with cancer
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single-nucleotide substitutions to large-scale chromosomal rearrangements, amplifications, and deletions
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cancers arise from
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an accumulation of mutations in many genes,
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What cellular functions does cancer affect
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DNA repair, Cell division, apoptosis, cellular differentiation, migratory behavior, and cell-to-cell contact.
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Malignant tumors
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metastasized cells invading other tissue and causing life-threatening problems
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benigns tumors
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unregulated cell growth forming a multicellular mass that can be removed by surgery, causing no serious harm
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clonal
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originated from a common ancestral cell that accumulated numerous specific mutations
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______________ are characteristic of many cancers
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reciprocal translocation
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Burkitt's lymphoma
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reciprocal translocations between chromosome 8 and chromosomes 2, 14, or 22.
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X-chromosome inactivation occurs
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early in development and occurs at random. All cancer cells within a tumor, both primary and metastatic, within one female individual contain the same inactivated X chromosome
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cancer stem cell hypothesis
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states that the tumor cells that do proliferate give rise to cancer stem cells that have the capacity for self-renewal
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Cancer is a _________ process
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multistep, associated with multiple mutations.
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why is age-related cancer an indication that cancer develops from accumulation of several mutagenic events?
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1. The incidence of most cancers rises exponentially with age. 2. Many independent mutations, occurring randomly and with a low probability, are necessary before a cell becomes malignant
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tumorigenesis
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appears to be the result of one or more genetic alterations that progressively release the cell from the normal controls on cell proliferation and malignancy
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driver mutations
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give growth advatage to tumor cells
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passenger mutations
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have no direct contribution to the cancer phenotype
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The high level of genomic instability in cancer cells is known as the
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mutator phenotype
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Cancer cells show higher than normal rates of
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mutation chromosomal abnormalities genomic instability
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The genomic instability in cancer cells manifests itself in gross defects such as
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translocations aneuploidy chromosome loss DNA amplification chromosomal deletions
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specific chromosomal defects that are used to diagnose the type and stage of the cancer
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Chronic myelogenous leukemia (CML)
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Xeroderma pigmentosum (XP)
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Defective nucleotide excision repair leading to skin cancer
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Hereditary nonpolyposis colorectal cancer (HNPCC)
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Autosomal dominant syndrome (200/1000 affected) Increased risk of colon, ovary, uterine, and kidney cancers Eight genes implicated, with four involved in DNA mismatch repair
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epigenetics:
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the study of factors that affect gene expression, but do not alter nucleotide sequence of DNA
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