Neoplasia 2 Flashcards

1
Q

_________ is the development of secondary deposits of a tumor in a distant site.

A

Metastasis

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2
Q

True or False: Metastasis is considered the hallmark of malignancy although it is not always seen.

A

True

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3
Q

True or False: All types of cancer metastasize at a similarly fast speed.

A

False, some more rapid than others

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4
Q

____% of newly diagnosed patients with solid tumors will already have obvious metastasis.

A

30

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5
Q

What is “occult metastasis?”

A

hidden; so small that they’re difficult to detect

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6
Q

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

A
larger
more anaplastic (less differentiated)
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7
Q

What are the three pathways for metastasis?

A
  1. seeding within body cavities
  2. lymphatic spread
  3. hematogenous spread
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8
Q

Mesothelioma is a cancer that metastasizes through which pathway?

A

seeding within the body cavity (lungs)

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9
Q

Which type of metastasis is common for carcinomas?

A

lymphatic spread (the lymph nodes are involved)

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10
Q

Which type of metastasis is common for sarcomas?

A

hematogenous spread (most often affects the liver and lungs)

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11
Q

In regards to metastasis, why is melanoma so dangerous?

A

it is not restricted to one pathway. Spread occurs through lymph, blood, or both

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12
Q

________ is a field of study that will often provide clues as to the etiology of or contributing factors to cancer development.

A

epidemiology

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13
Q

Cigarettes and alcohol are ______ in the development of oral cancer.

A

synergistic

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14
Q

What is the #1 cause of cancerous death in both men and women?

A

lung

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15
Q

Which type of cancer seemed to rise in women over the last forty years?

A

lung

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16
Q

True or False: The prevalence of uterine cancer is decreasing.

A

True (thanks, pap smear and cervical screenings)

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17
Q

What proportion of cancer risk is attributable to ENVIRONMENTAL sources?

A

2/3rds (65%)

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18
Q

What type of cancer is 7 times more frequent in Japan than in the U.S?

A

stomach

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19
Q

What types of cancer are 5 times less common in Japan than in the U.S?

A

breast and prostate

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20
Q

Why is age associated with an increased frequency of cancer (two reasons)?

A
  1. accumulation of somatic mutations

2. decreased immune competence

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21
Q

True or False: Between 1962 and 2008 there was a dramatic increase in 5-year survival rate for child cancers.

A

True

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22
Q

Cancer occurs in every 1 of ____ people.

A

5

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23
Q

True or False: Cancer is a hereditary disease.

A

False, it is a predisposing factor for some cancers but well-defined genetic influences only occur in a few types

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24
Q

What are the three broad categories of genetic predisposition to cancer?

A
  1. Inherited cancer syndromes
  2. Familial cancers
  3. Defective DNA repair
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25
Q

Inherited cancer syndromes are usually due to ______ mutation and generally show _______ ______ transmission.

A

a single gene

autosomal dominant

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26
Q

True or False: Inherited cancer syndromes are usually due to autosomal recessive transmission.

A

false,

  • usually autosomal DOMINANT
  • *however: Xeroderma pigmentosum is autosomal recessive and causes defective repair of DNA
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27
Q

What are the characteristics of “familial cancers?”

A
  • early age at onset
  • tumors in two or more close relatives of the index
  • multiple or bilateral tumors
28
Q

_____, ______, ______, and ______ malignancies have been reported to occur in familial patterns.

A

colon, breast, ovary, brain

29
Q

Xeroderma Pigmentosum is an autosomal recessive syndrome that results from defective _______.

A

DNA Repair

-ultraviolet induced dimerization does not repair itself

30
Q

True or False: 50% of human cancers have an identifiable heritable basis.

A

False, only 5-10%

31
Q

What are acquired preneoplastic disorders?

A

conditions that are associated with a significantly increased cancer risk.

32
Q

Persistent regenerative cell replication (liver), villous adenomas of the colon (polyps), and ______ of the oral or genital mucosa are examples of acquired preneoplastic disorders.

A

leukoplakia

33
Q

True or False: Leukoplakia can be a carcinoma or a callus, but either one is considered fertile soil.

A

True, the “abnormal mass of tissue” is fertile ground for production of carcinoma

34
Q

Nonlethal genetic damage, often due to _____, ______, viruses, or inherited mutations, is central to all cancers.

A

chemicals

radiation

35
Q

What are the three classes of normal regulatory genes that are often affected in carcinogenesis?

A
  1. protooncogenes (growth promoting)
  2. cancer suppressor genes (growth inhibiting)
  3. apoptosis genes
36
Q

________ genes will indirectly contribute to cancer development because acquired mutation are maintained

A

DNA repair

37
Q

Carcinogenesis is a multi-step process at both the ____ and _____ levels.

A

phenotypic

genetic

38
Q

________ are normal functional components of the cell that are transformed into oncogenes.

A

protooncogenes

39
Q

What type of proteins do oncogenes encode for?

A

oncoproteins (duh!)

40
Q

How do oncogenes differ from the protooncogene?

A

they are similar (or identical) to the normal gene but they LACK REGULATION

41
Q

In what two ways are protooncogenes transformed to oncogenes?

A
  1. Structural mutation of a gene = abnormal product

2. Altered regulation of expression = increased production of growth-promoting proteins

42
Q

All normal cells require ____ ____ stimulation to undergo proliferation.

A

growth factor

43
Q

Glioblastoma (brain tumor) results from the over expression of _______.

A

Platelet derived growth factor

44
Q

Some sarcomas are associated with the over expression of ______.

A

TGF alpha

45
Q

What is the effect of the overexpression of growth factor receptors?

A

makes cancer cells hyperresponsive to even normal levels of Growth Factor

46
Q

What are two commonly documented mutations associated with overexpression of GF Receptors?

A

ERB B1 and B2 (epidermal growth factor receptors)

47
Q

What is a common Signal Transducing Protein that is associated with 30% of human tumors?

A

RAS

48
Q

Mutant RAS remains in its _______ form.

A

active (stimulating constant cell proliferation)

49
Q

True or False: Normal (non-mutated) RAS is inactivated quickly.

A

True

50
Q

Which Nuclear Transcription Factor gene is most commonly affected?

A

MYC gene

51
Q

The over-expression of MYC gene leads to continuous activation of __________ which drives the cell to divide.

A

Cyclin-Dependent Kinases

52
Q

_______ is associated with an over-expression of MYC gene.

A

Burkitt’s Lymphoma

53
Q

Orderly progression of the cell cycle is orchestrated by _____ binding to _____.

A

CDK to cyclins

54
Q

Activity of CDK’s is regulated by ____ families of CDK inhibitors.

A

two

55
Q

Dysregulation of CDK activity will favor ______.

A

cell proliferation

56
Q

__________ inhibit cell proliferation.

A

tumor suppressor genes

57
Q

What was the first discovered tumor supporessor gene?

A

RB

58
Q

What is Knudson’s “Two Hit Hypothesis?”

A

two mutations are required to induce retinoblastoma

  • both normal RB alleles must be inactivated
  • if inherit one defective copy, the other must undergo mutation for the tumor to develop
59
Q

What do tumor suppressor genes do?

A
  • regulate cell cycle
  • regulate cell adhesion
  • regulate signal transduction
60
Q

What is the most common of all tumor suppressor genes that is associated with cancers/tumors?

A

TP53 (p53)

61
Q

True or False: Heterozygous loss of p53 is found in virtually every type of cancer.

A

False: homozygous loss of TP53 (p53) is found in virtually all forms of cancer

62
Q

What does the TP53 product normally do for the cell?

A

acts in the nucleus to inhibit cell cycle progression

63
Q

Normally, when TP53 accumulates (after DNA damage), the ________ is inhibited to allow time to repair DNA.

A

cell proliferation

64
Q

What does TP53 cause in the case of failed repair mechanisms?

A

apoptosis

65
Q

True or False: With a homozygous loss of p53, DNA damage goes unrepaired.

A

True

66
Q

In Li-Fraumeni Syndrome, one allele defect of TP53 is inherited. What influence does this have?

A

25 times increased risk for malignancy before age 50!