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Flashcards in Neopalsms- Nelson Deck (15):
1

Define neoplasia, and state the underlying pathogenic mechanism of neoplasia. Describe the key difference between benign and malignant neoplasms.

Neoplasia = abnormal mass of tissue, new growth

Mechanism
i. Stimulus causes genetic alterations in single cells
ii. Alterations passed onto progeny & subsequent cells
iii. Allows excessive and unregulated proliferation that becomes autonomous

Benign = cannot spread to other tissues

Malignant = capability to metastasize

2

List the four types of genes typically mutated in cancer

Growth-promoting proto-oncogenes

Growth-inhibiting tumor suppressor genes

Genes that regulate programmed cell death

Genes involved in DNA repair

3

Define proto-oncogene, oncogene, and oncoprotein

Proto-oncogene → un-mutated normal

Oncogene → mutated or overexpressed version of proto-oncogenes

Oncoprotein → results of oncogene

4

For a given proto-oncogene, how many alleles are typically mutated in order to generate an activating mutation?

Only one allele needs to become mutant to create an effect

5

Explain the rationale of performing Her2/neu testing in breast cancer

Her2/neu → over expression of cell membrane epidermal growth factor receptor, can treat with monoclonal antibody to that receptor

6

Explain the rationale of performing KRAS mutation analysis in colon cancer.

presence in colon cancer can be predictive of lack of response to certain forms of chemotherapy

7

Define tumor suppressor gene, and list some of the functions of tumor suppressor genes.

Tumor suppressor gene → products of these genes inhibit cell proliferation, preventing uncontrolled growth

Functions:
Regulation of cell cycle
Regulation of nuclear transcription
Regulation of cell differentiation

8

Explain the “two hit” hypothesis for suppressor gene defects

Two hit hypothesis → both alleles of tumor suppressor genes need to be damaged for loss of growth inhibition

9

State the malignancies associated with inheritance of BRCA1/2 and APC mutations.

BRAC1/2 mutation → regulates DNA repair, implicated in break ovary and prostate carcinomas

APC mutation → prevents nuclear transcription, implicated in colorectal carcinoma

10

Describe how over expression of BCL-2 can lead to follicular lymphoma.

BCL-2 → gene products regulate and prevent apoptosis by limiting the release of cytochrome C

11

Describe how overexpression of telomerase can lead to limitless replication

Shortening of telomeres is a way to signal cell age, and when it gets old, p53 recognizes that and induces apoptosis, up regulation of telomerase prevents this from happening

12

Describe how cancer cells can initiate neoangiogenesis. What cytokine is typically involved?

VEG-F

13

Describe the number of alleles that need to be mutated for dysfunction of DNA repair. Describe the defect in Hereditary Nonpolyposis Colon Cancer Syndrome (HNPCC).

DNA repair genes themselves are NOT oncogenic, but abnormalities greatly enhance occurrence of mutations in other genes

HNPCC → increased risk for carcinomas of the colon-Inactivation of genes involved in DNA mismatch repair

14

Explain the Warburg effect, and how this effect is used in the imaging of cancer.

Even with ample oxygen, cancer cells have increased coercion of glucose to lactose (fermentation) via the glycolytic pathway.

15

In just a few words, describe the evolving, new classification system of cancer.

“Molecular classification of cancer”

Classification according to therapeutic targets rather than cell of origin and morphology