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18 Cards in this Set

  • Front
  • Back

Carcinomas

Epithelial tissue cancers

adenocarcinomas

glandular tissue

sarcomas

connect, muscle, bone tissue



Gliomas

Tissue of brain and spinal cord

melanomas

pigment cell

myelomas

plasma cell

lymphomas

lymphatic tissue

leukocytes

leukemia

erythrocytes

erythroluekemia

CAUTION

Changes in the bowel or bladder habbits


A sore that doesn't heal


Unusual bleeding or discharge


Thickening or lump


Indigestion or difficulty swallowing


Obvious changes in a wart or mole


Nagging cough or hoarseness

Three mechanisms through which cancer cells metastasize

-By directly spreading by diffusion to other body cavities


-By circulation through the blood and lymphatic cells


-By direct transportation of cell from one site to another

Carcinogenesis

Cell's transformation from normal to cancerous

Oncogenes

Mutant genes that in their normal nonmutant state direct synthesis of proteins that positively regulate (accelerate) proliferation.

Tumor-suppressor genes

Encodes proteins that in their normal state negatively regulate (halt, or "put the brakes on") proliferation. Anti-oncogenes.

Proto-oncogene

Normal, non-mutant state of oncogene


ex: growth factor or a growth factor receptor

Point mutations

alteration of one or few nucleotide base pairs; most common one that can activate oncogenes.


ex: pancreatic, colorectal cancers.

Chromosomal translocation

Large changes in chromosomes structure in which a piece of one chromosome is translocated to another chromosome.


Can activate oncogenes two ways: First traslocation can cause excess and inappropriate production of a proliferation factor.


Secondly can lead to production of novel proteins with growth-promoting properties.

Gene amplification

A type of chromosome structural abnormality that can activate oncongenes. Results from duplication of a region of a chromosome over and over again causing tens or hundred of extra copies present.