Exam 1; Neoplasia II Flashcards Preview

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Flashcards in Exam 1; Neoplasia II Deck (38):
1

This refers to the process in which portions of a malignant break free and travel to distant sites where they form new tumor masses; establishes a tumor as malignant

metastasis

2

The ability to metastasize depends on what

the type of tumor; some readily metastasize while others rarely do

3

Approximately what percentage of newly diagnosed patients with solid tumors present with metastases

30%

4

In general the greater the what, that greater the tendency to metatasize

anaplasia (less differentiated)

5

What are the three pathways in which malignancies spread

seeding within the body cavities; peritoneal cavity
lymphatic spread
hematogenous spread

6

In the US, there were an estimated how many new cases of cancer and how many deaths

1.66 mil new cases
589K deaths

7

What differs about the rates of lung cancer

lung cancer rates have leveled off for men but have increased in women

8

Overall, what are the stats about cancer deather

substantial increase in death in males, but a slight decrease in females; pap smears

9

What is the proportion of cancer risk attributed to environmental sources

roughly 2/3rds

10

In general, cancer frequency increases with what

Age
most ≥55 years of age
accumulation of mutations and/or decrease of immune competence

11

What percentage of deaths among children does cancer attest for

10%

12

Is cancer a heredity disease?

There are pre-disposing factors for some cancer, but well-defined genetic influences identified in only a few types

13

What are the three broad categories of genetic predisposition to cancer

inherited cancer syndromes
familial cancers
defective DNA repair

14

Inherited cancer syndromes are usually due to what

a single gene mutation and generally show autosomal dominant transmission

15

What are some examples of inherited cancer syndromes

retinoblastoma
familial adenomatous polyposis
multiple endocrine neoplasia

16

Which types of cancers have been shown to occur in familial patterns

colon
breast
ovarian
brain

17

Probably no more than what percentage of all humans cancers have an identifiable heritable basis

5-10%

18

What are some examples of acquired preneoplastic disorders (persistent regenerative cell replication)

squamous metaplasia and dysplasia of bronchial mucosa
endometrial hyperplasia and dysplastic proliferations
leukoplakia of the oral mucosa, vulva, or penis
villous adenomas of the colon

19

This lies at the heart of carcinogenesis; the fact that most cancers are clonal proliferations, suggest s that tumors arise from one genetically altered cel

nonlethal genetic damage

20

What are the three classes of normal regulatory genes that are the principal targets of genetic damage

protoncogenes
cancer suppressor genes
apoptosis regulatory genes

21

These genes are also important in carcinogenesis; if these genes are disabled, the frequency of mutations increases, and the rate of neoplastic transformation increases

DNA repair genes

22

Carcinogenesis is what kind of process

MULTI-STEP both phenotypically and genetically

23

These are proteins that are similar to normal cellular proteins derived from proto-oncogenes, but lack regulation

oncogenes - oncoproteins

24

protooncogenes are transformed to oncogenes via what two mechanisms

structural mutation of the gene, resulting in an abnormal product
altered regulation of gene expression, resulting in increased production of a normal growth-promoting protein

25

Mutations and overexpression of these have been documented; this makes cancer cells hyper responsive to even normal levels

growth factors

26

Overexertion of these have been found in both SCC of the lung and some breast cancers

overexpression of growth factor receptors; particularly the epidermal growth factor receptor family

27

Approx. 30% of all human tumor contain a mutated this

RAS oncogene; signal transduction pathway
mutated to be always on, therefore stimulating constant cell proliferation

28

What is the most commonly affected nuclear transcription factor

MYC

29

MYC gene dysregulation leads to this

overexpression, leading in continuous activation of cyclin dependent kinases, driving the cells to divide
also, repression of CDK inhibitors

30

These are important in determining whether a cell is going to enter the cell cycle, and this dysregulation appears to favor cell proliferation

cyclin dependent kinases (CDK)

31

What is the activity of CDKs regulated by, and if these are dysregulated, what occurs

CDK inhibitors
if dysregulated, proliferation occurs

32

These inhibit cell proliferation, the first one discovered was Rb gene (retinoblastoma)

tumor supressor genes

33

What is the "two-hit" hypothesis

two mutations ("hits") in the (Rb) genome of a cell are required to induce retinoblastoma

34

What occurs most often in familial cases of retinoblastoma

a child that inherits one detective copy of Rb, its very likely that the second mutation will develop

35

What is the mechanism of Rb

Rb is a DNA-binding protein that is a key player in the regulation of the cell cycle. It binds DNA TFs and then released them trigger DNA synthesis, if Rb is mutated the cell cycle "essentially doesn't have any brakes"

36

This is the single most common target for genetic alteration in human tumors, homozygous loss of it is found in virtually every type of cancer

TP53

37

What is the mechanism of TP53

TP53 normally acts in the nucleus to inhibit cell cycle progression, when DNA is damaged, TP53 accumulates, inhibiting cell proliferation and allowing time for DNA repair. If the DNA cannot be repaired, TP53 induces apoptotic genes. Without normal TP53, the cell incorporates mutations in its genome and ultimately cancer forms

38

This is an inherited defect of one TP53 allele

Li-Fraumeni syndrome