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gen path- exam 1 > Neoplasia 2- Metastasis > Flashcards

Neoplasia 2- Metastasis Flashcards

1
Q

what is metastasis?

A

Metastasis is the development of secondary deposits of a tumor in a distant site

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2
Q

___________ is the “hallmark of malignancy”

A

metastasis

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3
Q

T/F: Some types of cancer metastasize more readily than others

A

true

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4
Q

In general, the ________ and more _______ a tumor is, the more likely it is to metastasize

A

larger and more anaplastic (less differentiated)

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5
Q

what are the 3 mechanisms for metastasis?

A
  • Seeding within body cavities
  • Lymphatic spread
  • Hematogenous spread
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6
Q

carcinomas usually metastasize through what mechanism?

A

lymphatic spread

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7
Q

how do most sarcomas metastasize?

A

Hematogenous spread

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8
Q

what organs are most effected by hematogenous spread?

A

Liver and lungs most often affected.

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9
Q

___________ Often provides clues as to the etiology (cause) of or contributing factors to cancer development

A

epidemiology

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10
Q

Proportion of cancer risk attributable to environmental sources estimated to be roughly _______

A

2/3rds (65%)

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11
Q

most cancer mortality occurs between what ages?

A

55 and 75 years of age

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12
Q

what are the 3 broad categories of genetic predisposition to cancer?

A

a. Inherited cancer syndromes
b. Familial cancers
c. Defective DNA repair

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13
Q

_____________ cancer syndromes are usually due to a single gene mutation

A

Inherited cancer syndromes

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14
Q

what type of genetic transmission is usually seen in inherited cancer syndromes?

A

autosomal dominant

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15
Q

give 3 examples of inherited cancer syndromes

A

1) Retinoblastoma
2) Familial adenomatous polyposis
3) Multiple endocrine neoplasia (MEN)

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16
Q

what are the characteristics of familial cancers?

A

early age at onset

tumors arising in two or more close relatives of the index case

multiple or bilateral tumors

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17
Q

what types of malignancies have been linked to familial inheritance patterns?

A

Colon, breast, ovary and brain malignancies

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18
Q

what inherited trait causes xeroderma pigmentosum?

A

Autosomal recessive syndromes of defective DNA repair

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19
Q

Approximately ____% of newly diagnosed patients with solid tumors will present with metastases, while another ____% will have occult (too small to be detected clinically) metastases at the time of diagnosis.

A

30%

20%

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20
Q

T/F: Probably no more than 20-30% of all human cancers have an identifiable heritable basis

A

FALSE

its 5-10%

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21
Q

Acquired Preneoplastic Disorders (APD’s) will increase the LIKELIHOOD of what forms of cancers?

A
  • Persistent regenerative cell replication
  • Villous adenomas of the colon
  • Leukoplakia of oral or genital mucosa
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22
Q

what does Carcinogenesis refer to?

A

Nonlethal genetic damage (that causes cancer)

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23
Q

what types of cellular damage result in carcinogenesis?

A

chemicals, radiation, viruses or inherited mutations

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24
Q

what 3 classes of normal regulatory genes are often affected by non-lethal genetic damage?

A

1) protooncogenes (growth promoting)
2) cancer suppressor genes (growth inhibiting)
3) apoptosis genes

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25
Q

____________ genes will indirectly contribute to cancer development since acquired mutations can’t be repaired

A

DNA repair genes

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26
Q

Carcinogenesis is a multi-step process at both the ___________ and __________

A

phenotypic and genetic levels

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27
Q

T/F: Protooncogenes are a normal functional component of the cell

A

true

28
Q

Oncogenes encode proteins called ___________

A

oncoproteins

29
Q

what is the difference between the proteins made from protoonconogens, and those of onconogenes?

A

the onconoproteins lack REGULATION

30
Q

Protooncogenes are transformed to oncogenes by what 2 processes?

A

1) Structural mutation of the gene

2) Altered regulation of gene expression

31
Q

__________ mutations of a gene result in an abnormal product

A

structural

32
Q

Altered regulation of gene expression results in what?

A

results in increased production of a normal growth-promoting protein

33
Q

what are 2 examples of growth-factor mutations that can cause cancer?

A

1) Glioblastoma - platelet-derived growth factor (PDGF)

2) some Sarcomas - transforming growth factor-alpha (TGF-α)

34
Q

what class of growth-factor receptor is linked to cancer when mutated?

A

epidermal growth factor receptor family

ERBB-1 and ERBB-2

35
Q

____________ (a receptor) is overexpressed in 80% of Squamous cell carcinomas (SSCa’s) of the lung

A

ERBB-1 (EGF receptor)

36
Q

an elevation of ERBB-2 (HER2/NEU receptor) is amplified in some _______ cancers, which correlates to poorer prognosis

A

breast

37
Q

Mutant receptor proteins deliver continuous ________ signals

A

mitogenic

38
Q

Over-expression of growth factor receptors makes cancer cells hyperresponsive to what?

A

normal levels of growth factors

39
Q

several oncoproteins mimic the functions of normal cytoplasmic ______________ proteins

A

signal-transducing

40
Q

approximately 30% of all human tumors contain what mutated gene?

A

contain mutated RAS oncogene

41
Q

_______ is the most commonly mutated proto-oncogene

A

RAS

42
Q

In the normal situation, activated RAS (resulting from exchange of GDP for GTP) turns on what?

A

downstream regulators of proliferation

43
Q

Normally inactivated quickly, mutant RAS remains in its active form….. what effect does this have?

A

stimulates constant cell proliferation

it is a growth signal transducer that never turns off

44
Q

With mutated ras, the ras proteins bind the ________, but GTPase activity is not accentuated

A

GAP’s (GTPase-activating proteins)

45
Q

how is RAS inactivated?

A

inactivated by hydrolysis of GTP
(this is enhanced by binding of RAS to GAP)

GTP= active
GDP= inactive
46
Q

the ____ gene is the most commonly affected Nuclear transcription factor gene

A

MYC

47
Q

MYC gene dysregulation leads to ____________

A

overexpression

48
Q

mutated MYC, resulting in overexpression, will have what effects in the cell?

A

leads to continuous activation of cyclin-dependent kinases (CDKs)

49
Q

the result of continuously activated CDK’s will cause what cellular response?

A

drives cell to divide indefinitely

50
Q

what is cyclin D1?

A

a gene whose product drives cells into the cell cycle

51
Q

what is a type of cancer linked to MYC onconogenes?

A

Burkitt’s lymphoma

52
Q

along with activating CDK enzymes, MYC will also represses ________

A

CDK inhibitors

53
Q

Orderly progression of cell cycle is orchestrated by CDK’s following activation by binding to ______

A

cyclins

54
Q

Overexpression of _______ is seen in a variety of tumors, including melanoma, lymphoma and esophageal carcinomas

A

CDK’s

55
Q

the products of __________ genes inhibit cell proliferation

A

tumor-supressing genes

56
Q

what is Knudson’s “two-hit” hypothesis?

A

Two mutations (“hits”) in the genome of a cell required to induce retinoblastoma

  • you need BOTH alleles of the RB genome to be mutated
57
Q

T/F: while protooncogenes stimulate cell growth, suppressor genes inhibit cell proliferation

A

true

58
Q

how is Knudson’s “two-hit” hypothesis related to the familial inheritance of retinoblastoma?

A
  • kids inherit ONE mutant allele of the RB gene

- this VASTLY increases likelihood of BOTH RB genes becoming mutated

59
Q

The Rb gene product (pRb) is a ___________ protein that is a key player in the regulation of the cell cycle

A

transcription regulatin protein (DNA-binding)

60
Q

The ___________________ gene is the single most common target for genetic alteration in human tumors

A

The TP53 tumor suppressor gene

61
Q

___________ loss of TP53 is found in virtually every type of cancer

A

Homozygous

62
Q

Li-Fraumeni syndrome is caused by what?

A

the familial inheritance of ONE aberrant TP53 gene

  • they start with 1 mutated copy, making the likelihood of both being mutated much higher
63
Q

how does TP53 normally work?

A

TP53 works to slow down DNA replication when mutations have affected the DNA

  • normally works in the NUCLEUS to inhibit cell cycle progression
64
Q

under normal circumstances, if DNA repair mechanisms fail, TP53 activates _______ genes

A

“cell-suicide” (apoptosis)

65
Q

people suffering from _________ syndrome have a 25x increased risk for malignancy before age 50

A

Li-Fraumeni syndrome

inherited defect of one TP53 allele

gen path- exam 1 (10 decks)

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