Cancer

activation of oncogenes, inactivate tumor suppressor, or alter genes that regulate apoptosis

activation of oncogenes, inactivate tumor suppressor, or alter genes that regulate apoptosis

how do tumor cells gain self-sufficiency in growth

neoplastic cells

abnormal cells that can lead to tumors or cancer

limitless replicative potential, rate of growth is longer, resistance to apoptosis, telomerase activation, angiogenesis

how does the replicative potential of neoplastic cells outcompete normal cells

oncogene

dominant genes that encode protein that becomes neoplastic when ACTIVATED

erb-B2

oncogene, epidermal growth factor receptorassociated with breast and ovarian cancere

ras

oncogene, signal transduction (GTP-binding) molecule associated with lung, colon, and pancreatic cancers

myc

oncogene, nuclear regulatory protein associated with burkitt lymphoma

cyclin D

oncogene, cell cycle regulator associated with mantle cell lymphoma, breast and esophageal cancers

erb-B2,ras,myc,cyclin D

examples of oncogene

tumor supressor

recessive genes that encodes protein that becomes neoplastic with both genes are INACTIVATED

APC,Rb, p53, BRCA-1

example of tumor supressor genes

APC

tumor supressor, functions for inhibition of signal transduction associated with colon,stomach,and pancreatic carcinomas

Rb

tumor supressor, functions for cell cycle regulation associated with retinoblastoma,osteosarcoma,breast,colon, and lung carcinoma

p53

tumor supressor, functions in reegulation of cell cycle and apoptosis associated with most human cancers

BRCA-1

tumor suppressor, functions in DNA repair associated with breast and ovarian carcinomas

activating mutation in one gene

cancer causing mutation of oncogene

inactivating mutation in both genes

cancer causing mutation in tumor supressor gene

cyclin protein

oncogene that binds CDK and drives cell through cell cycle

cylin dependent kinase (CDK) complex

active complex phosphorylates target proteins and drive cell proliferation

cyclin expression increases when cell is dividing

cyclin levels in normal cell growth

CDK inhibitor

shut off cyclin proteins when cell is not dividing

cell cycle constantly driven forward

result of cyclin d overexpression

tumor supressor genes

associated with anti-growth and death of cells

oncogenes

associated with growth and replication of cells

translocation

method of oncogene activation in which one part of chromosome is cut off and moved to another chromosome

t(9;22)

fusion of Bcr and Abl creating oncogenic protein

CML

example of t(9;22)

t(14;18)

Bcl2 gene translocation from chromosome 18 to 14, leads to over expression of Bcl2 (too much anti-apoptosis, cells not killed off).

follicular lymphoma

example of t(14;18) translocation

mutation of one gene copy is inherited and mutation of second gene copy occurs in somatic cell leading to cancer

how does the two hit hypothesis work

adenomatous poluposis coli (APC)

tumor suppressor protein that normally suppresses cell division, inactivation leads to familial adenomatous polyposis

process by which cancer cells stimulate the growth of new blood vessels enabling them to grow and survive

what is an angiogenic switch

angiogenesis

creation of new blood vessels

degrades basement membrane

role of collagenases in tumor stromal interaction

degrading extracellular matrix components, which facilitates tumor invasion and metastasis

role of proteases in tumor stromal interaction

adds telomeres protect end of chromosome from deterioration, not present in most somatic cells

role of telomerase plays in cell replication

activation in cancer cells allows for immortality

role of telomerase in cancer cells

H. pylori

microorganism leads to chronic inflammation and is associated with gastric adenocarcinoma, gastic MALT lymphoma

HPV

common cause of most cervical cancers

Epstein-barr virus

microorganism b-cell lymphoma, hodgin disease, nasopharyngeal carcinoma

hepatitis B and C

linked to heptocellular carcinoma

HTLV-I

human T-cell leukemia virus type I

free radicals and growth factors that drive mutations

how does inflammation lead to cancer