Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
46 Cards in this Set
- Front
- Back
|
Unregulated proliferation of Cancer Cells
|
fundamental abnormality that results in development of cancer. Net result of accumulated abnormalities in multiple cell regulatory systems.
|
|
|
Tumor
|
any abnormal proliferation of cells, either benign or malignant
|
|
|
Benign Tumor
|
remains confined to its original location, doesn’t invade surrounding normal tissue or spread to distant body sites
|
|
|
Malignant Tumor
|
capable of both invading surrounding normal tissue and spreading throughout body through circulatory or lymphatic systems
|
|
|
Metastasis
|
spread of cancer cells through the blood or lymphatic system to other organ sites
|
|
|
Carcinomas
|
malignancies of epithelial cells
|
|
|
Sarcomas
|
solid tumors of connective tissues, such as muscle, bone, cartilage, and fibrous tissue
|
|
|
Leukemia
|
cancer arising from precursors of circulating blood cells
|
|
|
Lymphomas
|
arise from the cells of the immune system
|
|
|
Prostate Cancer
|
most common cancer in men
|
|
|
Breast Cancer
|
most common cancer in women
|
|
|
Lung Cancer
|
most lethal cancer |
|
|
Tumor Clonality
|
development of tumors from single cells that begin to proliferate abnormally. Does not imply that original cell that gives rise to tumor initially acquired all characteristics of cancer cells
|
|
|
Normal Tissues
|
mosaic in which different X chromosomes (X1 and X2) have been inactivated
|
|
|
Single Initially Altered Cell
|
origin of tumors, each tumor will have same pattern of X inactivation of this cell
|
|
|
Development of Cancer
|
multistep process, involves mutation and selection for cells with progressively increasing capacity for proliferation, survival, invasion, and metastasis. Single mutation → proliferation → progression → increasingly rapid growth and malignancy
|
|
|
Genetic Alteration
|
the cause of tumor initiation, leads to abnormal proliferation of a single cell
|
|
|
Adenoma
|
polyp, small benign neoplasm, arises from glandular epithelium.
|
|
|
Carcinogens
|
substances that cause cancer, identified by studies in experimental animals and by epidemiological analysis of cancer frequencies in human populations. Ex. Radiation and chemical carcinogens damage DNA inducing mutations
|
|
|
Tumor Promoters
|
contribute to cancer development by stimulating cell proliferation rather than by inducing mutations
|
|
|
Density-dependent inhibition
|
cessation of the proliferation of normal cells in culture at a finite cell density.
|
|
|
Growth Factor Requirements of Tumor Cells
|
reduced compared to normal counterparts, contributes to unregulated proliferation of tumor cells both in vitro and in vivo
|
|
|
Autocrine Growth Stimulation
|
stimulation of cell proliferation as a result of growth factor production by a responsibe cell
|
|
|
Contact Inhibition
|
process in which normal fibroblasts migrate across the surface of a culture dish until they make contact with neighboring cells
|
|
|
Secretion of Proteases
|
leads to digestion of extracellular matrix components, allowing cancer cells to invade adjacent normal tissue
|
|
|
Secretion of Growth Factors
|
done by Cancer cells, results in the formation of blood vessels (angiogenesis), which is needed to support growth of tumor beyond 1 million cells, supply oxygen and nutrients to tumor cells
|
|
|
Failure to Differentiate Normally and Undergo Apoptosis
|
closely coupled to abnormal proliferation, since most fully differentiated cells cease cell division
|
|
|
Leukemias
|
good example of relationship between defective differentiation and malignancy
|
|
|
Tumor Viruses
|
capable of directly causing cancer in either experimental animals or humans. Play critical role in cancer research – serve as models for cellular and molecular studies of cell transformation. Hep B and C – principal causes of liver cancer
|
|
|
Oncogenes
|
capable of inducing cell transformation, cancer results from alteration in critical regulatory genes such as these that control cell proliferation, differentiation, and survival. Frequently encode proteins that differ in structure and function from those encoded by their normal homologs. Strategy for more selective cancer treatment is targeting oncogenes that drive tumor growth.
|
|
|
Rous Sarcoma Virus (RSV)
|
virus in which viral oncogenes were first defined, induced cancer transformation of chicken embryo fibroblasts in cultures. Related to ALV – replicates in same cells without inducing transformation.
|
|
|
Proto-Oncogenes
|
normal cell genes that can be converted into oncogenes.
|
|
|
Non-Virus Induced Tumors
|
contain cellular oncogenes that were generated from proto-oncogenes by mutations.
|
|
|
Ras Oncogenes
|
not present in normal cells, generated in tumor cells as a consequence of mutations that occur during tumor development.
|
|
|
C-myc
|
proto-oncogene that encodes a transcription factor and is frequently activated by chromosome translocation or gene amplification in tumors
|
|
|
Protein-Tyrosine Kinases
|
most of what is coded for by a large group of oncogenes, growth factor receptors which can be converted to oncogene proteins by alteration of extracellular domains, which normally bind growth factors.
|
|
|
PML/RARa
|
mutated form of the retinoic acid receptor in human acute promyrlocytic leukemia
|
|
|
Tumor Suppressor Genes
|
act to inhibit cell proliferation and tumor development. In tumors, these genes are lost or inactivated, thereby removing the negative regulators of cell proliferation.
|
|
|
Retinoblastoma
|
rare childhood eye tumor, studies of this identified first tumor suppressor gene
|
|
|
Rb gene
|
negative regulator of tumorigenesis, tumor suppressor gene, present in normal diploid ells. Involved in more common tumors of adults, prototype for ID of other t.s genes.
|
|
|
P53 Gene
|
regulates cell cycle progression and apoptosis, loss of this results in failure to undergo apoptosis and prevents damage-induced cell cycle arrest. Contribute to resistance of many tumors to chemotherapy.
|
|
|
BRACA-1 and BRACA-2 Genes
|
mutated in some inherited breast and ovarian cancers, appear to be involved in checkpoint control of cell cycle progression, similar to ATM and ATR.
|
|
|
Stability Genes
|
Act to maintain the integrity of the genome. Mutations in these genes lead to development of cancer due to high frequency of mutations.
|
|
|
Most Effective Way to Deal with Cancer
|
prevent development of the disease.
|
|
|
Angiogenesis
|
the disruption of tumor blood vessels, rather than acting against cancer cells, way to inhibit tumor growth.
|
|
|
Small Molecule Inhibitor of EGF
|
shown striking activity against subset of lung cancers in which EGF receptor is activated by point mutations (EGF receptors overexpressed in many lung cancers.)
|
