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CMD Block 2 > Neoplasia I (.Doc + .ppt) > Flashcards

Neoplasia I (.Doc + .ppt) Flashcards

1
Q

5 adjectives that describe neoplasms:

in order of importance

A
  1. autonomous
  2. irreversible (once you go autonomous you never go back)
  3. clonal (from a single cell gone baaad)
  4. Benign (or)
  5. Malignant
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2
Q

Benign or Malignant?

Commonly causes destruction of surrounding tissue

A

malignant

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3
Q

Benign or Malignant?

Cohesive, expansile local growth

A

benign

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4
Q

Benign or Malignant?

Progessively infiltrative, local growth

A

Malignant

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5
Q

Benign or Malignant?

Commonly has a fibrous capsule

A

benign

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6
Q

Benign or Malignant?

Rounded margins

A

benign

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7
Q

Benign or Malignant?

Metastasis

A

malignant

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8
Q

What is metastasis?

A

Secondary site of tumor discontinuous with the primary site

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9
Q

3 patterns of metastatic spread:

A

Lymphatic (to regional lymph nodes)
Hematogenous (to lung/liver)
Seeding (body cavities or surfaces)

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10
Q

Type of metastasis that is typical of sarcoma:

A

Hematogenous

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11
Q

Type of metastasis that is typical of ovarian carcinoma:

A

Seeding

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12
Q

Type of metastasis that is typical of carcinomas:

A

Lymphatic

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13
Q

Malignant neoplasm of epithelial cells

A

CARCINOMA

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14
Q

Malignant neoplasm of mesenchyme-derived tissue

A

SARCOMA

mesenchyme = connective tissue, including bone, cartilage, blood vessels, etc.

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15
Q

Mixed germ cell tumor

A

teratoma

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16
Q

Neoplasm containing components of more than one germ cell layer (usually all three)

A

TERATOMA

layers = ectoderm, mesoderm, endoderm

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17
Q

Mass of mature but disorganized tissue indigenous to its site

A

HAMARTOMA

developmental anomaly*

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18
Q

Mass of normal tissue present outside its normal site

A

CHORISTOMA

or an “ectopic rest”

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19
Q

Chondroma

A

cartilaginous hamartoma

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20
Q

Macroscopic projection above mucosal surface

A

POLYP

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21
Q

Term for “on a stalk” (adj)

A

Pedunculated

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22
Q

Term for “flat, like a plateau” (adj)

A

Sessile

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23
Q

Benign epithelial neoplasm forming glands or derived from glands

A

ADENOMA

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24
Q

Lack of visible differentiation of malignant tumor cells

A

ANAPLASIA

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25
Q

What gives cells the appearance of “primitive” cells?

A

anaplasia

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26
Q

Features of anaplastic cells (3)

A
  1. Larger than normal cells
  2. Higher nuclear/cytoplasmic ratio
  3. Pleomorphic
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27
Q

What is different about the nuclear components of anaplastic cells?

A
  1. angulated shape
  2. hyperchromatism
  3. clumped chromatin
  4. mitoses (the mitosis may be abn?)
  5. nucleoli
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28
Q

Tripolar mitosis is characteristic of:

A

anaplasia

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29
Q

The inability to tell what organ you’re looking at (in Nichols’ powerpoint) implies it’s an example of:

A

anaplasia

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30
Q

2 types of dysplasia:

A
  1. congenital embryonically abnormal cell organization

2. acquired cellular atypia (usually premalignant, may/may not be reversible)

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31
Q

Formation of abundant fibrous stroma by some carcinomas

A

DESMOPLASIA

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32
Q

Tissue with all the cytologic (individual cell) features of malignancy without visible invasion

A

CARCINOMA IN SITU

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33
Q

Most common causes of cancer death:

A
  1. Lung
  2. Breast (women), Prostate (men)
  3. Colon
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34
Q

9 most common types of cancer caused by smoking

A
  1. lung (90% of them)
  2. mouth
  3. pharynx
  4. larynx
  5. esophagus
  6. stomach
  7. pancreas
  8. kidneys
  9. bladder
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35
Q

Obesity is the cause of ____% of cancers in men and ____% of cancers in women in the US.

A

14

20

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36
Q

6 Hallmarks of cancer:

A

(1) self-sufficiency in growth signals
(2) insensitivity to anti-growth signals
(3) evasion of apoptosis
(4) sustained angiogenesis
(5) limitless replicative potential
(6) the ability to invade tissue + metastasize

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37
Q

What do tumor suppressor genes do?

A

control cell proliferation

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38
Q

How does the number of tumor suppressor genes relate to defects?

A

One good tumor suppressor gene is sufficient

Thus, it takes defects in both copies to contribute 1 of the many defects necessary for neoplasia

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39
Q

What are oncogenes?

A

Genes that drive autonomous cell growth in cancer cells

40
Q

“Genes that apply brakes to cell proliferation”

A

TUMOR SUPPRESSOR GENES

41
Q

RB genes are a type of ____ ______ genes

A

tumor suppressor

42
Q

How does phosphorylated RB gene affect the cell? What phorphorylates it?

A

releases/allows transcription factor E2F to initiate cell proliferation

Phosphorylated by cyclins

43
Q

How does dephosphorylated RB gene affect the cell?

A

prevents cell proliferation by binding up transcription factor E2F

44
Q

What stage of the cell cycle can be blocked by RB protein (gene product)?

45
Q

What causes retinoblastomas in infants?

A

Retinoblastomas occur when a SECOND gene is defective in an infant who already has one defective copy of RB gene

(the 1st defective copy can be familial or de novo)

46
Q

What is the function of APC tumor suppressor gene?

A

controls intestinal stem cell proliferation by WNT signaling

47
Q

What is the function of APC gene product?

A

Breaks down beta-catenin so it can’t bind TCF (transcription factor that drive cell prolif)

48
Q

APC mutations are present in ____% of colon cancers with familial adenomatous polyposis and ____% of sporadic colon cancers.

49
Q

What is the function of p53?

A

prevents propagation of genetically damaged cells

  1. binds to DNA -> arrests cell cycle for repair
    OR
  2. initiates apoptosis if repair impossible
50
Q

p53 has a (long/short) half life, and its activity is ended by:

A

short (~20 min)

ubiquitin proteolysis

51
Q

p53 resistance is mediated by: (2)

A
  1. increased MDM2 (destroys p53)

2. E6 protein of HPV (degrades p53)

52
Q

In _____% of tumors, biallelic loss of p53 is present

53
Q

T/F: Hypoxia activates p53

54
Q

Mutated NF-1 and -2) gene causes:

A

neurofibromatosis type 1

55
Q

What function does NF-1 gene product serve in cells?

A
  1. activates GTPase, which produces GDP
  2. GDP binds to cell membrane RAS and inactivates it

*RAS is involved in transduction of growth factor signals for cell prolif

56
Q

Von Hippel Lindau (VHL) gene product causes:

A

ubiquitination/degradation of hypoxia inducible transcription factor-1

(TF-1 causes increased PDGF/VEGF and tumor angiogenesis)

57
Q

What does a germline mutation of Von Hippel Lindau (VHL) gene cause?

A
  • kidney cancer
  • pheochromocytoma (adrenal medulla tumor)
  • retinal angioma

(with second hit mutations)

58
Q

HER2, C-MYC, L-MYC and K-RAS are examples of:

59
Q

What function does HER2 serve in cells?

A

EGFR receptor

60
Q

What is the result of HER2 mutations?

A

EGFR receptor overexpressed

61
Q

HER2 mutations are present in ____% breast cancers, and can be treated by:

A

20

blocking with antibodies

62
Q

Diagnosis of a HER2 mutation?

A

Gene product (of HER2 overexpression) can be:

  1. stained
  2. FISH, look for gene amplification (>6)

(both are “on a continuum”)

63
Q

What does K-RAS code for?

A

Cytoplasmic GTPase

GTPase –> GDP, which generates signal transduction proteins in response to growth factor binding EGFR.
(This induces proliferation)

64
Q

What is the result of mutated K-RAS?

A

Increased cell proliferation (K-RAS works without the EGFR signal)

65
Q

Why don’t extracellular therapies work if K-RAS is mutated?

A

The mutation causes proliferation in the ABSENCE of growth factor binding EGFR, which is an upstream signal

66
Q

T?F: A single nucleotide substitution can cause a K-RAS mutation capable of causing cancer.

67
Q

Tissue with all the cytologic (individual cell) features of malignancy without visible invasion

A

Carcinoma in situ

68
Q

This initiates cell repair or suicide.

69
Q

A neoplasm is considered malignant when it is _______ or _______.

A

invading or metastasizing

70
Q

T/F: A polyp will be on a stalk, never against the mucosal/epidermal surface.

A

F
(If a polyp is on a stalk, it is referred to as pedunculated. If it is flat, like a plateau, it is referred to as sessile. )

71
Q

Disordered growth

72
Q

Acquired dysplasia of glandular epithelium

A

“atypical hyperplasia” or “atypical adenomatous hyperplasia”

73
Q

Why have # deaths from cancer been dropping since the 90’s?

A

Improvements in treatment of the 4 most common types

74
Q

Most cancer deaths occur between the ages of __ and __

75
Q

Causes of cancer: (7)

A 
smoking**
obesity*
alcohol
diet
human papilloma virus (HPV)
ultraviolet light
asbestos
76
Q

_____________ mutation or malfunction is like having faulty brakes, but _______ are like having the accelerator stuck to the floor

A
  • Tumor suppressor gene

- oncogenes (mutations?)

77
Q

Neoplasia usually accumulates multiple mutations before becoming:

A

a benign tumor

78
Q

Why do most cancers occur in patients over 55?

A

the mutations needed to create a malignant tumor usually take decades

79
Q

Oncogenes are mutated:

A

proto-oncogenes

80
Q

It takes _____ bad tumor suppressor genes before theres a problem, and takes ______ bad onocogenes before theres a problem.

81
Q

TP53 is one of the most commonly mutated genes in neoplasia. This is a problem because it encodes:

82
Q

T/F: p53 is generated in short bursts.

A

F: continually generated

83
Q

What mediates a tumor’s response to radiation therapy?

84
Q

Tumor suppressor gene important in cancers of the endometrium and brain

85
Q

TGF-beta pathway mutations are important in _________ carcinomas.

A

pancreatic

86
Q

Important in carcinomas of esophagus, colon and other sites

87
Q

KLF6 is influential in ____ cancers

88
Q

Patched (PTCH) is important in:

A

basal cell carcinoma of the skin

89
Q

K-RAS is active in some carcinomas of: (3)

A

colon, lung and pancreas

90
Q

L-MYC is important in some

A

small cell carcinomas of lung

91
Q

C-MYC is present in:

A

Burkitt lymphoma

92
Q

Monoclonal antibody called trastuzumab, lapatinib and pertuzumab treat:

A

HER2-related breast cancers

93
Q

HER2 is on chromosome:

94
Q

A positive FISH is diagnosed by a HER2/CEP17 ratio of:

A

2.2 (sorry, this is stupid-specific)

95
Q

T/F: EGFR blocker cetuximab is an excellent therapy for metastatic colon cancers with KRAS mutation.

A

F: tumors with KRAS mutation are unresponsive

CMD Block 2 (38 decks)

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