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MOD II > Chapter 7-Neoplasm Learning objectives > Flashcards

Chapter 7-Neoplasm Learning objectives Flashcards

1
Q

Define Cancer, Neoplasia, Tumor, Oncology and Clonal

A

Cancer: Malignant neoplasm

Neoplasia: New growth

Tumor: Neoplasm

Oncology: the study of Tumors/neoplasms

Clonal: Clones

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2
Q

Define Benign and Malignant in common usage and as used by physicians.

A

Benign: Localized

Malignant: spreads

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3
Q

Describe cell and tissue origins in determining the nomenclature of human neoplasms
and characterize the designations -oma, carcinoma and sarcoma.

A
  1. -Oma: Bening tumor
  2. Carcinoma: Malignant tumor from epithelium-any of 3 germ layers. (Adenocarcinoma = glandular)
  3. Sarcoma: From solid mesenchymal tissue (CT)
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4
Q

What are the two basic tissue components of benign and malignant neoplasms?

A
  1. Parenchyma: Neoplastic cells-tumor cells

2. Stroma: supply (CT, BV, Immune system)

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5
Q

Discuss the use of the terms polyp and adenoma in the GI tract

A
  1. Polyp: Benign or Malignant projection from mucosa (colon cancer)
  2. Adenoma: Benign EPITHELIAL neoplasm from GLANDS
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6
Q

List examples of malignant neoplasms that have inappropriate benign terminology.

A
  1. ??
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7
Q

Explain how a mixed tumor of the salivary gland is different from an adenoma of the colon.

A

Mixed Tumors: Contain epithelial components and myxoid stroma => islands of cartilage or bone

Adenoma Parenchyma will be relatively uniform

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8
Q

Explain how a cystic teratoma of ovary fundamentally differs from a mixed tumor of salivary gland.

A

Mixed tumors: generally from 1 germ level (Epi +Myo = pleomorphic)

Teratoma: Multigerm layer (often from ovary(Dermoid Cyst)/testes)

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9
Q

Define differentiated and anaplasia

A

Differentiated:

-The extent to which neoplastic parenchymal cells resemble corresponding normal parenchymal cells.

Anaplasia-Lack of diffentiation

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10
Q

4 Malignant tumors

A
  1. Sarcoma
  2. Carcinoma
  3. Lymphoma
  4. Leukemia
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11
Q

3 Benign Tumors

A
  1. Adenoma (epithelial-glands)
  2. Papilloma: Epithelial finger-like/warty projections
  3. Cystadenoma: Ovarian cysts etc
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12
Q

1 Variable Tumor

A

Polyp

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13
Q

Define desmoplasia

A
  1. Collagenous Stroma
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14
Q

Define Scirrhous

A
  1. Stony/hard Stroma

- Often associated with breast tissue

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15
Q

Explain why benign tumors are generally considered well differentiated.

A

Often keep most of the function of normal parenchyma

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16
Q

List and describe histopathologic criteria used in employing the term anaplasia.

A

Anaplasia: lack of differentiation

-Malignant neoplasms are generally composed of poorly differentiated cells

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17
Q

Compare and contrast metaplasia versus dysplasia.

A

Metaplasia: Change in cell type

Dysplasia: Loss in uniformity of the individual cells as well as loss in architectural orientation

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18
Q

Define carcinoma in situ (CIS) and explain what distinguishes CIS from carcinoma

A

Dysplasia: Considered Carcinoma in situ when it is full thickness but does not invade basal layer

  • Invasive once it crosses this basement membrane
  • Metastatic action results in squamous epithelial carcinoma
  • Does not always progress to cancer
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19
Q

Delineate the most common histopathologic features used to assess rate of growth in a
neoplasm: Neoplastic growth accompanied by progressive…?

A
  1. infiltration
  2. Invasion
  3. Destruction of surrounding tissue
    - Benign: grow as cohesive expansile masses that remain localized
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20
Q

Delineate the most common histopathologic features used to assess rate of growth in a
neoplasm: needed for malignancy

A

Metastases is Key!!!

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21
Q

Delineate the most common histopathologic features used to assess rate of growth in a
neoplasm: second best for malignancy determination

A

Invasiveness

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22
Q

Define Anaplastic

A

Malignant neoplasms composed of poorly diff cells

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23
Q

Nucleus:Cytoplasm

A

norm = 1:4 or 1:6

Abnormal = 1:1

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24
Q

Anaplastic cell growth

A

Anarchy!

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25
Q

Large tumors have what at center?

A

Ischemia

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26
Q

Define Hemangioma

A

Tumor of tangled blood tissue

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27
Q

Tumor supressor genes that inhibit mitogenic signaling pathways (3)

A
  1. APC
  2. NF1
  3. NF2
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28
Q

APC Protein and Fxn

A

Protein: Adenomatous polyposis coli protein

Fxn: Inhibitor of WNT signaling in colon epithelium - degrades B-catenin

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29
Q

APC is considered the…

A

gatekeeper of colonic neoplasia

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30
Q

APC bi-allelic loss

A

results in colon cancer-70%

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31
Q

APC Familial Syndromes

A

Familial colonic polyps and carcinomas

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32
Q

APC sporadic cancers: Carcinomas of (4)

A
  1. Stomach
  2. Colon
  3. Pancreas
  4. Melanoma
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33
Q

NF1 protein and function

A

P: Neurofibromin-1

Fxn: inhibitor of RAS/MAPK

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34
Q

NF1 familial syndromes

A

Neurofibromatosis type 1 (neurofibromas and malignant peripheral nerve sheath tumors)

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35
Q

NF1 sporadic cancers (2)

A
  1. Neuroblastoma

2. Juvenile myeloid leukemia

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36
Q

NF2 P and F

A

P: Merlin

F: Cytoskeletal stability and Hippo pathway signaling

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37
Q

NF2 Familial syndromes

A

Neurofibromatosis type 2 (Acoustic schwannoma and meningioma)

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38
Q

NF2 Sporadic cancers: (2)

A
  1. Schwannoma

2. Meningioma

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39
Q

Inhibitors of cell cycle progression (2)

A
  1. RB

2. P53

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40
Q

RB p and fxn:

A

P: Retinoblastoma Protein

Fxn: Inhibitor of G1/S checkpoint

-Major proponent of 2-hit hypothesis

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41
Q

RB is considered the…?

A

govener of proliferation

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42
Q

Mutation of RB leads to

A
  1. Gene amplification of CDK4/cyclin D

2. Loss of p16/INK4a

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43
Q

Virus-protein that inhibits RB?

A

E7 protein of HPV virus

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44
Q

Phosphorylation of RB… (2)

A
  1. Turns it off

2. Activates E2F xsription factor

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45
Q

RB Familial Syndromes (3)

A

Familial Retinoblastoma Syndrome

  1. Retinoblastoma
  2. Osteosarcoma
  3. Sarcomas
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46
Q

RB sporadic Cancers (3)

A
  1. Retinoblastoma
  2. Osteosarcoma
  3. Carcinomas of breast/colon/lung
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47
Q

Inhb of pro-growth programs of metabolism and angiogenesis (1)

A
  1. VHL
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48
Q

VHL P and F

A

P: Von Hippel Lindau

F: Inhb hypoxia-induced transcription factors (H1F1-alpha)

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49
Q

VHL is a component of what? What does it degrade?

A
  1. Component of ubiquitin ligase

2. Degrades HIFs

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50
Q

What are HIFs?

A

HIFs alter gene expression in response to hypoxia

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51
Q

What type of mutation happens with VHL?

A

Loss of function

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52
Q

VHL: Increased RBC count can be associated with…?

A

-Paraneoplastic Syndrome

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53
Q

Tumors and cancers associated with RBC

A
  1. CNS tumors
  2. Renal Cysts
  3. Neuroendocrine Tumors
  4. Renal Cell Carcinomas
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54
Q

VHL: Familial Syndromes (4)

A

Von Hippel Lindau Syndrome

  1. Renal Cell Carcinoma
  2. Pheochromocytoma
  3. Cerebellar Hamagioblastoma
  4. Retinal Angioma
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55
Q

VHL: Sporadic cancers

A

Renal cell carcinoma

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56
Q

Are angiomas and hemangioblastomas malignant?

A

NO! Dude, just no.

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57
Q

Inhibitors of invasion and metastasis (1)

A

CDH1 (E-cadherin gene)

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58
Q

CDH1 P and F

A

P: E-cadherin

F: Cell adhesion, Inhb of cell motility

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59
Q

What does E-cadherin sequester?

A

B-catenin

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60
Q

What does B-catenin do?

A

Signals the WNT pathway

61
Q

WNT pathway is related to?

A

Metastisis

62
Q

CDH1 Loss of function results in?

A

Sporadic Carcinomas

-Loss of contact inhibition, cohesiveness and increased invasiveness

63
Q

CDH1 Familial syndroms

A

Familial gastric carcinoma

64
Q

CDH1 Sporadic Cancers (2)

A
  1. Gastric Carcinoma

2. Lobular breast carcinoma

65
Q

Enablers of genomic stability?

A

TP53

66
Q

TP53 P and F

A

P: p53

F: Cell cycle arrest and apoptosis in resp to DNA dmg

67
Q

TP53 is considered the guardian of the…?

A

genome

68
Q

What chromosome is p53 on?

A

Chromosome 17

69
Q

What does p53 regulate? (4)

A
  1. G1/s progression
  2. DNA repair
  3. Cell Senescence
  4. Apoptosis
70
Q

DNA damage is sensed by?

A

ATM/ATR kinase family

71
Q

How is P53 activated?

A

p53 is phosphorylated and released from MDM2 (inhibitor)

72
Q

What does p53 do and what are its effects?

A

p53 up-regulates p21 and causes cell arrest

73
Q

P53 is inactivated by what protein of what virus?

A

E6 of HPV

74
Q

Therapeutic Implications of P53?

A
  1. Chemotherapy and irradiation help cure cancer by inducing DNA cell damage to cause apoptosis
75
Q

Pt has 1 inherited TP53 gene mutation. What is the disease and what does it cause?

A
  1. Li-Fraumeni Syndrome

2. 25-fold increase for cancer

76
Q

TP53 bi-allelic is common in what population?

A

Anyone under 40 with 1 sarcoma

77
Q

P53 Familial syndromes

A

Li-Fraumeni syndrome (diverse cancers)

78
Q

Sporadic cancers of p53

A

Most human cancers

79
Q

DNA repair factors?

A

BRCA1/BRCA2

80
Q

BRCA1/BRCA2: P and F

A

P: Breast cancer 1 and 2

F: Repair breaks in dsDNA

81
Q

BRCA1/BRCA2: Familial syndromes

A
  1. Familial breast/ovarian carcinoma

2. Chronic Lymphocytic leukemia (BRCA2)

82
Q

Unknown Mechenisms?

A

WT1

83
Q

WT1 P and F

A

P: Wilms tumor-1

F: Transcription Factor

84
Q

WT1 Familial Syndromes

A

Familial Wilms tumor (pediatric-kidney cancer)

85
Q

WT1 sporadic Cancers: (2)

A
  1. Wilms Tumor

2. Certain Leukemias

86
Q

Upregulation Mechanisms (4)

A
  1. BCR-ABL translocation (philadelphia chromosome)
  2. BCL-2
  3. MYC proto-oncogene
  4. Oncofetal Antigens
87
Q

BCR-ABL translocation (philadelphia chromosome): P and F

A

P: Tyrosine Kinase

F: Upreg cell proliferation

88
Q

BCR-ABL translocation?

A

9 to 22: forms the active BCR-ABL

89
Q

BCR-ABL translocation (philadelphia chromosome): Seen in? (2)

A
  1. CML: Chronic myelogenous leukemia

2. ALL: Acute lymphoblastic leukemias (Most common malignancy in western children)

90
Q

BCL-2 P and F

A

P: BCL2

F: Anti-apoptotic factor

91
Q

BCL-2 translocation?

A

14: 18

- Seen in 85% of B-cell lymphomas

92
Q

BCL-2 translocation results in?

A

Cell unable to undergo apoptosis

93
Q

This member of BCL-2 is seen to increase cell survival and drug resistance in cancers?

A

MCL-1

94
Q

MYC Proto-oncogene P and F

A

P: MYC

F: activates many genes involved in cell growth

95
Q

MYC uses what type of signaling? What does this signaling do?

A
  1. RAS/MAPK signaling

2. follows stim of quiescent cells and upregulates telomerase

96
Q

Oncofetal Antigens Proteins (2)

A

CEA (Carcinoembryonic antigen)

AFP (A-fetoprotein)

97
Q

Oncofetal Antigens Proteins expressed at high levels when?

A

Specifically in cancer and fetal tissues

98
Q

Oncofetal Antigens Proteins can be used as?

A

Marker for cancer

99
Q

Oncogenes created by Translocations:

A
  1. Philly chromosome-ALL and CML (9:22)
  2. AML-Acute myeloid leukemia (15:17 or 8:21)
  3. Burkitt Lymphoma (8:14)
  4. Mantle Cell Lymphoma (11:14)
  5. Follicular Lymphoma (14:18)
100
Q

Philly chromosome is related to?

A

ALL and CML

101
Q

ALL and CML have what translocation?

A

9:22

102
Q

9:22 can also be considered

A

Pre-leukemia

-Myelo-proliferative syndrome

103
Q

Is 9:22 prognosis good?

A

Yes

104
Q

AML (Acute myeloid leukemia) translocations?

A

15:17 and 8:21

105
Q

What can 15:17 translocation cause?

A

Pt can bleed out from DIC (disseminated intravascular coagulation)

106
Q

8:14 translocation is?

A

Burkitt Lymphoma

107
Q

Burkitt Lymphoma is what type of lymphoma?

A

B-cell related to MYC oncogene

108
Q

14:18 translocation is related to?

A

Follicular lymphoma

109
Q

14: 18 is required to diagnose

A

you guessed it… follicular lymphoma! (B-cell lymphoma)

110
Q

11:14 is?

A

Mantle Cell Lymphoma (B-cell lymphoma)

111
Q

Virus/Bacterial Oncogenesis/carcinogenesis (7)

A
  1. HTLV-1
  2. HPV
  3. EBV (Burkitt Lymphoma)
  4. HBV and HCV
  5. Merkel Cell Polyomavirus
  6. HHV-8
  7. H. Pylori
112
Q

HTLV-1 Is found in? (4)

A

Japan, Caribbean and parts of South America and Africa

113
Q

HTLV-1 causes?

A

Adult T-cell leukemia/lymphoma (CD4+ T cell tumor)

114
Q

HTLV-1 encodes what viral protein?

A

Tax

115
Q

What does tax do?

A

Tax activates growth/survival pathways (PI3K/AKT, NF-kB) in T cells

116
Q

This virus causes benign warts, cervical cancer (squamous cell carcinoma) and oropharyngeal cancer?

A

HPV

117
Q

What are 2 HPV viral proteins and what do they do?

A

E6: binds RB

E7: binds p53

Both proteins neutralize their proteins.

118
Q

Ubiquitous herpes virus implicaed in pathogenesis of Burkitt lymphoma and B-cell lymphoma in Pt with T-cell immunosupression

A

EBV

119
Q

70-85% of hepatocellular carcinomas are related to what virus?

A

HBV and HCV

120
Q

Oncogenic effects HBV/HCV are?

A

multifactorial

121
Q

What is the dominant effect of HBV/HCV?

A

Immunologically mediated chronic inflammation and hepatic injury.

122
Q

What are the proteins of HBV and HCV that activate signals, leading to increased carcinogenesis?

A

HBV: HBx protein

HCV: Core protein

123
Q

This virus causes neuro-endocrine skin cancer

A

Merkel Cell Polymomavirus

124
Q

Kaposi sarcoma is caused by what virus?

A

HHV-8

125
Q

Where do you often see Kaposi Sarcoma skin lesions?

A

In AIDS pts

126
Q

What does KS look like?

A

Skin lesions of LE, (genitalia, mouth/gums/hard palate, GI and resp. tract) nodular/blotches. Appear red/purple and usually raised/palpable

127
Q

This bacteria is involved with pathogenic genes like CagA and can stim GF pathways.

A

H. Pylori

128
Q

Chronic infection of H. pylori can lead to?

A

MALT lymphoma of the stomach

-Caused by B-cell proliferations/a monoclonal B-cell tumor.

129
Q

Paraneoplasmic Syndromes: Endocrinopathies (5)

A
  1. Cushings Syndrome
  2. SIADH (Syndrome of inappropriate ADH)
  3. Hypercalcemia
  4. Hypoglycemia
  5. Polycythemia
130
Q

This syndrome causes Intracranial neoplasms and small cell carcinoma of the lung.

What is its mech?

A
  1. SIADH (syndrome of Inappropriate ADH)

2. ADH or ANH (atrial natriuretic hormone)

131
Q

This causes pancreatic carcinoma, Neural tumors and small cell carcinoma?

What is its mech?

A
  1. Cushings Syndrome

2. ACTH or ACTH like things

132
Q

What cancers results in Hypercalcemia? (4)

A
  1. Squamous cell carcinoma of lung
  2. Breast Carcinoma
  3. Renal Carcinoma
  4. Adult T-cell leukemia/lymphoma
133
Q

What is the mech of hypercalcemia?

A

PTH-related protein (PTHRP)

  1. TGF-alpha
  2. TNF
  3. IL-1
134
Q

The mechanism of action for this syndrome involve Insulin/insulin-like substances

A

Hypoglycemia

135
Q

Cancers causing Hypoglycemia? (3)

A
  1. Ovarian Carcinoma
  2. Fibrosarcoma
  3. Other mesenchymal sarcomas
136
Q

These cancers may result in Polycythemia? (3)

A
  1. Renal carcinoma
  2. Cerebellar Hamangioma
  3. Hepatocellular carcinoma
137
Q

What is the mech of Polycythemia?

A

Erythropoietin

138
Q

“other” types of Paraneoplasms? (4)

A
  1. Neuromyopathic (nerve + Muscle)
  2. Acanthosis Nigricans
  3. Hypertrophic Osteoarthropathy (Clubbing of fingers)
  4. Trousseau Syndrome (Migratory Thrombophlebitis)
139
Q

Gastric carcinoma, lung carcinoma, uterine carcinoma can all generate what?

What is the causal Mech?

A
  1. Acanthosis Nigricans

2. Immunologic secretion of EGF (epidermal growth factor)

140
Q

Myasthenia gravis causes?

A

Neuromyopathic (N and M)

141
Q

Myasthenia gravis can be a result of what cancers?

A
  1. Bronchogenic Carcinoma

2. Thymic Neoplasms

142
Q

CNS and PNS disorders are caused by?

A

Breast carcinoma

143
Q

Hypertrophic Osteoarthropathy looks like?

A

Clubbing of fingers

144
Q

What cancers can cause finger clubbing/hypertrophic osteoarthropathy?

A
  1. Bronchogenic carcinoma

2. Thymic neoplasms

145
Q

Pancreatic carcinoma and Bronchogenic carcinoma can cause?

A

Trousseau Syndrome (Migratory Thrombophlebitis)

146
Q
  1. Progressive loss of body fat.
  2. Profound weakness, anorexia and anemia

This is? What causes number 2?

A
  1. Cachexia

2. The release of factors by tumor or host immune cells

147
Q

Tumor grades?

A
  1. Poor
  2. Mild
  3. Moderate
    - Done by pathologists
148
Q

Tumor stages?

A

Metastisis = stage 3

Does the cancer spread?

Number of nodes/size?

-Oncologists do this

MOD II (1 decks)

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