Cancer - Answers A genetic disorder characterized by uncontrolled cell growth.
Abnormal Differentiation Model - Answers A theory suggesting cancer is due to defects in cell
differentiation, causing cells to deviate from their developmental pathways.
Viral Causation Model - Answers A theory proposing that cancer is caused by viral infections, though it
cannot explain most cancers, especially in the Western world.
Carcinogen-Mutagen Model - Answers A model linking carcinogens, such as radiation and chemicals, to
cancer, with many acting as mutagens that damage genes.
Ames Test - Answers A test developed by Bruce Ames in the 1970s correlating mutagenic compounds
with their carcinogenic potential.
Somatic Mutations - Answers Mutations occurring in non-reproductive cells that are considered a
primary cause of cancer.
Oncogenes - Answers Cancer-causing genes derived from proto-oncogenes that can induce cancerous
growth when mutated.
Proto-oncogenes - Answers Normal genes that can become oncogenes when mutated.
src gene - Answers A gene from the Rous Sarcoma Virus that was found to originate from a normal
chicken gene (c-src).
v-src oncogene - Answers A proto-oncogene from the chicken genome that demonstrates how viruses
can convert normal genes into oncogenes.
Point mutations - Answers A type of mutation that can activate proto-oncogenes, such as the H-ras
oncogene in human cancers.
Gene amplification - Answers A process that can activate proto-oncogenes, exemplified by the myc
oncogene in certain hematopoietic tumors.
Chromosomal translocations - Answers A genetic alteration where the myc gene is fused with
immunoglobulin genes, leading to activation of proto-oncogenes.
Transfection - Answers A laboratory technique used to introduce genes from tumor cells into normal
cells to induce malignant transformation.
ras oncogenes - Answers A family of oncogenes identified as critical drivers of transformation in cells.
Multistep Tumorigenesis - Answers The process of cancer development involving multiple genetic
mutations over time.
,Collaborative Oncogenes - Answers The concept that multiple oncogenes, such as ras and myc, are
needed for full transformation of normal cells.
Transgenic mice - Answers Mice genetically modified to study the direct contribution of oncogenes to
cancer development.
Oncogene - Answers A gene that has the potential to cause cancer due to mutations or overexpression.
Proto-oncogene - Answers A normal gene that can become an oncogene due to mutations or other
genetic changes.
Somatic Mutation - Answers A mutation that occurs in non-reproductive cells, leading to cancer in
specific tissues.
Carcinogen - Answers Any substance or agent that can cause cancer by inducing mutations.
Mutagen - Answers An agent that causes genetic mutations, which can lead to cancer.
Epigenetic - Answers Changes in gene expression or cellular behavior that do not involve changes in the
DNA sequence.
Transfection - Answers A method of introducing DNA into cells, used to identify oncogenes.
Point Mutation - Answers A single nucleotide change in DNA that can lead to oncogene activation.
Gene Amplification - Answers The process by which a gene's copy number increases, often leading to
overexpression of an oncogene.
Chromosomal Translocation - Answers A type of mutation where a part of a chromosome is transferred
to another chromosome, potentially activating oncogenes.
Multistep Tumorigenesis - Answers The idea that cancer develops through a series of genetic mutations
over time, rather than a single event.
Tumor Suppressor Genes (TSGs) - Answers Genes that prevent cancer rather than promoting it.
Cell Hybridization - Answers A method involving fusing tumor cells with normal cells, creating hybrid
cells that contain a mixture of the two cell genomes.
Dominant Normal Alleles - Answers Normal alleles that likely repress tumorigenic behavior of cancer
cells.
Retinoblastoma - Answers A childhood eye tumor that led to the identification of the RB gene.
RB Gene - Answers A critical tumor suppressor gene located in the q14 band of chromosome 13.
Sporadic Retinoblastoma - Answers A form of retinoblastoma characterized by two somatic mutations.
, Familial Retinoblastoma - Answers A form of retinoblastoma characterized by one inherited mutation
and one somatic mutation.
Two-hit Hypothesis - Answers The theory that tumorigenesis occurs only when both alleles of a tumor
suppressor gene like RB are inactivated.
Inactivation of TSGs - Answers Common in tumor genomes, often via null alleles, whereas oncogenes are
often hyperactivated.
Cell-Physiological Mechanisms - Answers The various ways TSGs control cell proliferation.
Inactivation of TSGs - Answers Inactivation of both alleles of a TSG leads to uncontrolled cell division, a
hallmark of cancer.
RB gene - Answers RB gene became a paradigm for TSGs because its inactivation alone could lead to
tumor formation.
Inherited mutations in TSGs - Answers Inherited mutations in TSGs predispose individuals to specific
types of cancers.
RB gene - Answers Retinoblastoma.
APC gene - Answers Adenomatous polyposis coli syndrome (predisposing to colon cancer).
TP53 gene - Answers Li-Fraumeni syndrome (predisposing to various cancers like sarcomas and
carcinomas).
Hereditary cancer syndromes - Answers More than 25 hereditary cancer syndromes are linked to
inherited mutations in TSGs.
Loss of heterozygosity (LOH) - Answers Loss of heterozygosity (LOH) refers to the loss of the normal
(wild-type) allele of a TSG, leaving the cell with two mutated copies of the gene.
Mechanisms of LOH - Answers In premalignant cells, after one copy of a TSG is mutated, the second
functional copy can be lost through mechanisms like chromosomal loss or deletion, or gene duplication
that results in a homozygous mutation.
Indicator of TSGs - Answers LOH is a key indicator for the presence of TSGs in specific chromosomal
regions.
Molecular cloning and genetic techniques - Answers Molecular cloning and genetic techniques like LOH
analysis are used to identify TSGs.
Inactivation of TSGs in tumors - Answers Many human tumors exhibit inactivation of TSGs, with TSGs
often inactivated even more frequently than oncogenes are activated.