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MOD Exam II - Neoplasia > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What are the most common primary tumors/cancers?

A

Skin, Lung, Large Bowel, Breast, Prostate

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2
Q

What is the most common lung cancers?

A

Lung Adenocarcinoma, SCC, Small Cell, Large Cell,

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3
Q

What is the difference between a Mixed Tumor and a Teratoma?

A

Mixed Tumor – is from the same germ line (ie. Ectoderm) – common in salivary glands

Teratoma – all 3 germ layers

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4
Q

Parenchyma (if malignant) is generally associated with what??

A

Carcinomas

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5
Q

The Stroma (if malignant) is generally associated with what??

A

Sarcomas

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6
Q

What characterizes Atypia?

A

Small Cytoplasm, Multiple Nuclei, Multiple and Large Nucleoli, Coarse Chromatin

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7
Q

Where in the histological image do Neoplasia ALWAYS BEGIN?

A

They begin near the basement membrane, from undifferentiated cells (NEVER DE-DIFFERENTIATED ADULT CELLS)

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8
Q

“Differentiation” in Benign vs. Malignant tumors?

A

Benign – well differentiated

Malignant – anaplasia (un-differentiated)

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9
Q

What are the Cavitary Lung Lesions?

A

Fibro-Caseous Cavitary TB

Bronchogenic Carcinoma

Staphyloccocal Pneumonia

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10
Q

What are Fibroma, Lipoma, Chondroma, Osteoma’s all derived from?

A

Connective Tissue dedrivatives

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11
Q

What is a Benign vs Malignant blood vessel tumor?

A

Benign – Hemangioma

Malignant – Angiosarcoma

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12
Q

What is Benign vs Malignant Brain Covering tumor?

A

Benign – Meningioma

Malignant – Invasive Meningioma

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13
Q

What is a Benign vs Malignant mesothelium tumor?

A

Benign – Benign Fibrous Tumor

Malignant – Mesothelioma

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14
Q

What are benign vs malignant epi lining of glands or ducts?

A

Benign – Adenoma, Papilloma, Cystadenoma

Malignant – Adenocarcinoma, Papillary Carcinomas, Cystadenocarcinomas

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15
Q

What are Benign vs Malignant Respiratory Passage tumors?

A

B: Bronchial Adenoma

M: Bronchogenic Carcinomas

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16
Q

What are Benign vs Malignant Liver cell tumors?

A

B: Hepatic Adenoma

M: Hepatocellular Carcinoma

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17
Q

What are Benign vs Malignant Urinary Tract Epi?

A

B: Transitional Cell Papilloma

M: Trasitional Cell Carcinoma

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18
Q

What are Benign vs Malignant tumors of melanocytes

A

B: Nevus

M: Melanoma

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19
Q

What are Benign vs Malignant Placental Epi?

A

B: Hydatidiform Mole

M: Choriocarcinoma

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20
Q

What are Malignant Testicular Epi?

A

Seminoma

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21
Q

What are Benign vs Malignant Salivary Glands?

A

B: Pleomorphic Adenoma

M: Malignant Mixed Tumor of Salivary Gland Origin

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22
Q

What are Malignant Renal Anlage tumors?

A

Wilms Tumor

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23
Q

What are Benign vs Malignant Totipotential Cells in gonads?

A

B: Mature Teratoma (dermoid cyst)

M: Immature Teratoma (Teratocarcinoma)

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24
Q

What is the pathway of spread (Metastasis)?

A

1) Loosening of Intercellular Inteactions
2) Degradation of ECM
3) Migration down
4) INVASION!?!?

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25
Q

What are the most common cancers of Women vs Men?

A

Women – Breast, Lung, Colon

Men – Prostate, Lung, Colon

In developing world:

W: Breast, Cervix, Lung

M: Lung, Stomach, Liver

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26
Q

What type of cells are most at risk for accumulating the genetic leasions that lead to carcinogenesis?

A

Proliferating Cells

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27
Q

What is the difference between Morbidity and Mortality?

A

Morbididty – is how many people get the diease (are affected)

Mortality – is how many people die from the disease

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28
Q

What infectious Agents are the most epidemologically attributed to cancer?

A

HPV and EBV

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29
Q

What is the most common cancer in adults vs children?

A

Adults: Carcinomas (most common)

Children: Leukemia (most common), Neuroblastomas, Retinoblastomas

(A nice little review of chapter 10 . . . youre welcome)

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30
Q

What is the development of Cancer (stepwise)?

A

1) An Initiating Mutation
2) Acquire Genomic Instability
3) Acquire your Cancer Hallmarks
4) Than Further Genetic Evolution

(the last two steps can take years to develop)

over time tumors become more aggresive.

as tumors progess you get a tumor cell population that expands, but more of them leave the replicating pool (think about the darwian comparison)

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31
Q

What are the 4 classes of regulatory genes? (the principal targets of cancer causing mutations)

A

1) Proto-oncogenes
2) Tumor Suppresors
3) DNA Repair Mechs
4) Genes that regulate Apoptosis

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32
Q

Complementary Mutations occur in a stepwise fashion and result in 3 things?

A

1) Cancer Hallmarks
2) Driver Mutations
3) LOF mutations

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33
Q

Conversion of 1 of the 2 alleses from a proto-oncogene to an oncogene is sufficient to promote neoplasia – but it requires loss of ___?

A

Both Tumor Suppressor alleles to promote neoplasia (as one of the two protein products made is sufficient to inhibit neoplasia

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34
Q

What do MiR’s do?

A

They inhibit translation of SELECT specific sequences of mRNA

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35
Q

What are some RNA-mediated Modifications?

A

RNA directed DNA Methylation

RNA interference mediated chromatin remodeling

miRNA (MiR’s) etc

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36
Q

What are the Hallmarks of Cancer?

A

1) Self-sufficiency
2) Insesitivity to growth inhibitory signals
3) Altered Cell Met
4) Evasion of Apoptosis
5) Limitless Replication
6) Sustained Angiogenesis
7) Ability to invade and metastasize
8) Ability to evade host defense mechs

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37
Q

What tends to accerelarte the features of Hallmarks of Cancer?

A

Genomic Instability

Cancer Promoting Inflammation

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38
Q

How do cancer cells have limitless replicative potential?

A

1) inactivate senescence
2) reactivate telomerase

(Some of the cells must be able to be stem-cell like – or this can’t occur)

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39
Q

What is a Proto-Oncogene?

A

A normal cell gene whose products promote cell proliferation

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40
Q

What is an Oncogene?

A

is a mutated or overexpressed version of a proto-oncogene that fxns autonomously – it has lost dep. on normal growth promotion signals

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41
Q

What is an Oncoprotein?

A

Is a protein encoded by an oncogene

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42
Q

What are the Fxns of the following?

CDK4/C-D

P21/P27

Rb

P53

A

CDK4/C-D – complex that Phosp, RB – progreses through G1

P21/P27 – blocks cell cycle, by binding to CDK4/C-D complex

Rb – binds to E2F in its hypophosp. state – prevents G1-S transition

P53 – causes cell cycle arrest – to fix damage, or to promote apoptosis

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43
Q

What negatively inhibits p53?

A

MDM2

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44
Q

What is cancers are implicated in the following?

EGF Recp TK

HER2 Receptor

Jak2 Tyr K

ABL NonReceptor TK

RAS

PI3K/BRAF

Amp of MYC

A

EGF – Lung Cancer

HER2 – Breat Cancer

Jak2 – Myeloproliferative Disorder

ABL – Chronic Myelogenous Leukemia and Acute Lymphoblastic Leukemia

RAS – many cancers

PI3K – Many cancers

MYC – Burkitt Lymphoma and Neuroblastoma

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45
Q

What are 4 antiproliferative effects of RB in cancers?

A

LOF mutations in RB

Gene Amp of CDK4/CD

Loss of p16/INK4a (CDK inhibitors)

E7 protein of HPV

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46
Q

What is the steps of p53 action?

A

1) ATM/ATR kinases sense DNA damage
2) they Phosph p53, (MDM2 unbinds it)
3) p53 upregulates CDK inhibitors (p21)
4) cell cycle arrest – repairs damage or apoptosis

(p53 – E6 protein of HPV)

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47
Q

Li-Fraumeni Syndrome have what problem?

A

They inherit one defective copy of TP53 and have a high incidence of cancer

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48
Q

Major Tumor Suppressor Genes

APC

A

Neg Regulator of WNT (degrades B-Catenin)

in Familial Adenomatous Polyposis (AD)

and Colon Carcinomas

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49
Q

Major Tumor Suppressor Genes

E-Cadherin

A

Binds to B-Catenin / growth inhibition of epi cells

Familial Gastric Cancer (AD) – (CDH1)

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50
Q

Major Tumor Suppressor Genes

CDKN2A

A

codes for p16/INK4a –> inhibits Rb

Familial Melanoma (AD)

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51
Q

Major Tumor Suppressor Genes

TGF-B

A

inhibits cell proliferation in normal tissues

in carcinomas

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52
Q

Major Tumor Suppressor Genes

PTEN

A

Codes for a lipid phosphatase (PI3K/AKT)

Cowden Syndrome (AD) – which is Breast and Endometrial Carcinoma

53
Q

Major Tumor Suppressor Genes

NF1

A

Encodes a GTPase –> neg regulates RAS

Neurofibromatosis Type 1 (AD)

54
Q

Major Tumor Suppressor Genes

NF2

A

encodes merlin – cytoskeletal protein

Neurofibromatosis Type 2

55
Q

Major Tumor Suppressor Genes

WTI

A

TF for develpoing genitourinary tissues

WIlms Tumor

56
Q

Major Tumor Suppressor Genes

PTCH1

A

encodes membrane receptor – a neg. regulator of SHH

Gorlin Syndrome (AD) – BCC and Medulablastoma

57
Q

Major Tumor Suppressor Genes

VHL

A

Ubiquitin Ligase – which degrades Hypoxia inducible factor (HIF)

Von Hippel-Lindau Syndrome (AD) – renal cell carcinoma, and pheochromacytoma

58
Q

Selected Proto-Oncogenes (Mode of activation/ associated human tumor)

EGF Recptor Family

A

Mutation/Amplification

Mut – Adenocarcinoma of Lung

Amp – Breast Carcinoma

59
Q

Selected Proto-Oncogenes (Mode of activation/ associated human tumor)

ALK (receptor tyrosine k)

A

Translocation, Point Mutation

Adenocarcinoma of lung, Lymphomas, Neuroblastoma

60
Q

Selected Proto-Oncogenes (Mode of activation/ associated human tumor)

RAS/BRAF

A

Point Mutation/Translocation

Melanomas, Leukemias, Colon Carcinoma

61
Q

Selected Proto-Oncogenes (Mode of activation/ associated human tumor)

ABL (Non-receptor tyrosine kinase)

A

Translocation – Chronic Myelongenous Leukemia

Point Mutation – Acute Lymphonblastic Leukemia

62
Q

Selected Proto-Oncogenes (Mode of activation/ associated human tumor)

MYC

A

(MYC) Translocation – Burkitt Lymphoma

(NMYC) Amplfication – Neuroblastoma

63
Q

Selected Proto-Oncogenes (Mode of activation/ associated human tumor)

ERBB1

ERBB2

A

ERBB1 – encodes EGFR – point mutations in Lung Adenocarcinomas

ERBB2 – encodes HER2 == point mutations in Breast Carcinomas

64
Q

ABL, NOTFCH1, Jak2 are bigger in what type of cancers?

A

Leukemias and Lymphomas

65
Q

What are the Three RAS genes in humans?

where were they discovered?

A

HRAS, KRAS, NRAS

were discovered in transforming retrovirsues

66
Q

What Carcinomas are RAS mutations more frequent?

A

Pancreatic Adenocarcinomas

Cholangiocarcinomas

Colon, Endometrial and Thyroid Cancers

Lung Adenocarcinomas and Myeloid Leukemias

67
Q

Where are mutations in BRAF more frequent?

A

Hairy Cell Leukemias

Melanomas

Benign Nevi

others-

68
Q

Disruption of SHH signaling during embryonic development can lead to?

A

Holoprosencephaly, Cyclopia

69
Q

What is the most common malignant brain tumor in childhood?

A

Medullablastoma

70
Q

What other cancers are associated (higher risk) for patients with Wilms Tumor?

A

Hepatoblastoma

Pancreatoblastoma

Adrenocortical Tumors

Rhabdomyosarcomas

71
Q

MYC is known as . . .

and associated with what tumors?

A

the Major Transcriptional Regulator of Cell Growth

NMYC, and LMYC are paralogs

ASSOCIATED WITH: Burkitt Lymphoma, Neuroblastoma, common carcinomas

Burkitt Lymphoma – (8:14) translocation

72
Q

What is a paralog?

A

a gene that is related to another gene by descent from a single ancestral gene – may have a different DNA seq. and biological fxn

73
Q

Selected Tumor Suppressor Genes: what syndrome/cancer?

Rb

A

Familial Retinoblastoma

74
Q

Selected Tumor Suppressor Genes: what syndrome/cancer?

TP53

A

Li-Fraumeni Syndrome

75
Q

Selected Tumor Suppressor Genes: what syndrome/cancer?

MSH

A

Hereditary Nonpolyposis Colon Carcinoma

76
Q

Selected Tumor Suppressor Genes: what are the associated oncoproteins with each?

APC

NF1

NF2

PTCH

RB

VHL

E-Cadherin

TP53

BRCA1/BRCA2

MSH

WT1

A

APC – Adenomatous polyposis coli protein

NF1 – neurofibromin 1

NF2 – merlin

PTCH – Patched

Rb – Retinoblastoma protein

VHL – Von Hippel Lindau protein

E-Cadherin – E-Cadherin

TP53 – p53 protein

BRCA1-BRCA2 – Breast Cancer 1/Breast Cancer 2

MSH – MSH1

WT1 – WIlms Tumor 1

77
Q

What are the following regarded as?

Tp53

APC

Rb

A

Tp53 – Guardian of the Genome

APC – Gatekeeper of colonic neoplasia

Rb – Governor of the cell cycle

78
Q

What HPV proteins associate with the following?

TP53

RB

A

TP 53 – E6

RB – E7

79
Q

How many hits and on what chromosome does it take to produce retinoblastoma?

A

It takes 2 Hits to the 13q14 chromosome to produce retinoblastoma

(Familial vs Sporadic cases)

80
Q

What are the 4 key regulators of the Cell cycle?

A

P16/INK4a

Cyclin D

CDK4

Rb

81
Q

How does HPV E7 protein cause oncogenesis in humans?

A

E7 binds to hypophosphorylated Rb and detaches it from E2F – allowing E2F to bind and cause cell cycle progression

(E7 has a high affinity for Rb)

82
Q

Tp53 is on what chromosome?

and can inhibit what?

A

17p13.1

angiogenesis

83
Q

Where is the WT1 Gene located?

A

11p13

regulates the mesenchymal to epi transition of kidney developement . . . causes Wilms Tumor

84
Q

How do tumor cells cause evasion?

A

By expressing PD-LI – which binds to PD-1

causes evasion of the immune systrem (one of the hallmarks of cancer)

Monoclonal Abs target this

85
Q

How does CTLA4 play in cancer cells?

A

It can act as an off swithc when bound to CD80/86 on the surface of APC.

It has serious side affects when targeted by drugs – better to target PD-L1**

86
Q

Wat Key enzme is involved in modulation production of inflammtory mediators by immune cells?

A

PDE4 (Phosphodiesterase 4) – degrades cAMP

87
Q

Psoriasis patients have an increased risk of what cancer?

A

Non-Melanoma SKin Cancer

IE: BCC, SCC etc.

88
Q

How is vascularization of tumors controled?

What specific factors regulate it?

A

A Balance of Angiogenic and Anti-Angiogenic factors produced by tumor and stromal cells

P53, – inhibits it

RAS, MYC, MAPL, – upregulate VEGF –> promotes it

89
Q

What is the first metastatic site that tumors can be predicted to go to?

A

Capillary Beds – mainly Liver, Lungs

90
Q

When talking about metastasis, what is organ tropism?

A

Tropism – is because of expression of certain receptors on tumor cells that fit with ligands on certain organs – which is why we see the cancer spread there.

91
Q

What is Dormancy?

A

Is when a tumor cell has “gone quiet”

Like a leopord in the jungle awaiting to attack its prey. . . . .

92
Q

What are Oncofetal Ags?

A

They are proteins that are normally only found during fetal development – but show up in cancers of adults

93
Q

Genomic Instability:

HNPCC syndrome have defects in:

Xeroderma Pigmentosum have defects in:

Bloom Syndrome, Ataxia-Telangiectasia, Fanconi Anemia are hypersensitive to?

BRCA1/BRCA2:

RAG1,RAG2, AID:

A

HNPCC – defects in mismatch repair system

XP – defefcts in nucleotide excision repair system – pyrimidine dimers

BS, AT, FA – hypersensitive to DNA Damaging agents – ionizing radiation

BRCA’s – Breast Cancer

RAG – lymphoid neoplams

94
Q

What are cancer-enabling effects of inflammatory cells and resident stromal cells?

A

Release of factors that promote proliferation

Removal of Growth Suppresors

Enhanced resistance to cell death

Angiogenesis

Invasion and Metastasis

Evading Immune Destruction

95
Q

Note: Anemia, Fatigue, vs Cachexia

A

ANemia – low BC count – low oxygen levels

Fatigue – low energy levels due to anemia and misc

Cachexia – equal loss of protein and fat (due to increased BMR)

96
Q

Oncogenes (Translocations)

Chronic Myelogenous Leukemia

A

(9:22)(q34:q11)

ABL– 9q34

BCR – 22q11

97
Q

Oncogenes (Translocations)

Acute Myeloid Leukemia

A

(8:21)(q22:q22)

(15:17)(q22:q21)

98
Q

Oncogenes (Translocations)

Burkitt Lymphoma

A

(8:14)(q24:q32)

99
Q

Oncogenes (Translocations)

Mantle Cell Lymphoma

A

(11:14)(q13:q32)

100
Q

Oncogenes (Translocations)

Follicular Lymphoma

A

(14:18)(q32:q21)

101
Q

What are the difference between miRNA’s and LncRNA’s?

A

miRNA’s (miR’s) – modulate the translation of specific seq of mRNA

LncRNA’s – (exceed coding mRNAs) they can bind to regions of chromatin, restricting RNA Polymerase access to coding genes within the region

102
Q

Epigenetic Reg Genes – (Fxn and Tumor)

DNMT3A

A

DNA Methylation

Acute Myeloid Leukemia

103
Q

Epigenetic Reg Genes – (Fxn and Tumor)

MLL1

MLL2

A

MLL1 – Histone Methyl – Acute Leukemia in Infants

MLL2 – Histone Methyl – Follicular Lymphoma

104
Q

Epigenetic Reg Genes – (Fxn and Tumor)

CREBBP/EP300

A

Histone Acetlyation

Diffuse Large B Cell Lymphoma

105
Q

Epigenetic Reg Genes – (Fxn and Tumor)

ARID1A

A

Nucleosome/Chromatin Remodeling

Ovarian Clear Cell Carcinoma/Endometrial Carcinoma

106
Q

Epigenetic Reg Genes – (Fxn and Tumor)

SNF5

A

Nucleosome/Chromatin Remodeling

Malignant Rhabdoid Tumor

107
Q

Epigenetic Reg Genes – (Fxn and Tumor)

PBRM1

A

Nucleosome/Chromatin Remodeling

Renal Carcinoma

108
Q

What are the different Chemical Carcinogens?

A

Direct-Acting Carcinogens

Indirect-Acting Carcinogens

Promotion of Chemical Carcinogenesis

(through initiation and promoters)

most require metabolic activation to become ultimate carcinogens

109
Q

Nonmelanoma skin cancers are associated with ____ exposure to UV Radiation?

Where as Melanomas are associated with ____ exposure as occurs with sunbathing

A

Nonmelanoma – total cumulative exposure to UV radiation

Melanomas – associated with intense intermittent exposure

110
Q

UVB light causes what?

A

Formation of Pyrimidine dimers in DNA

– Meyloid Leukemias, Thryoid Cancer (frequently)

– Breast, Lungs, Salivary glands (Interm)

111
Q

What is the main Oncogenic RNA Virus?

A

HTLV-1

112
Q

What are the Oncogenic DNA Viruses?

A

HPV

EBV (& Burkitt Lymphoma)

HBV/HCV

Merkel Cell Polyomavirus

HHV-8

113
Q

Can a neoplasm (benign or malignant) cause death?

A

Yes

114
Q

What are Paraneoplastic Syndromes?

A

they are symptoms that are not explained by the location of the tumor/ or by elaboration of the hormones indigenous to the tissue of location.

115
Q

Paraneoplastic Syndromes

Cushing Syndrome

A

Small Cell Carcinoma of the Lung

Pancreatic Carcinoma

Neural Tumors

116
Q

Paraneoplastic Syndromes

SIADH

A

Small Cell Carcinoma of Lung

Intracranial Neoplasms

117
Q

Paraneoplastic Syndromes

Hypercalcemia

A

Squamous cell carcinoma of lung

Breast and Renal Carcinoma

Adult T- Cell leukemia/lymphoma

118
Q

Paraneoplastic Syndromes

Hypoglycemia

A

Ovarian Carcinoma

Fibrosarcoma

(Mesenchymal sarcomas)

119
Q

Paraneoplastic Syndromes

Myathenia (Nerve and Muscle)

A

Bronchogenic Carcinoma

Thymic Neoplams

120
Q

Paraneoplastic Syndromes

Acanthosis Nigricans

A

Gastric Carcinoma

Lung Carcinoma

Uterine Carcinoma

121
Q

Paraneoplastic Syndromes

Hypertrophic Osteoarthropathy (and clubbing of fingers)

A

Bronchogenic Carcinoma

Thymic Neoplasms

122
Q

What is Migratory Thromboplebitis (Trousseau Syndrome)

DIC (Disseminated Intravascular Coagulation)

A

MT: it can be encoutered due to deep-seated cancers: Pancreatic or Lung Carcinomas

DIC: is associated with APML (Acute Promyelocytic Leukemia) and Prostatic Adenocarcinoma

123
Q

What is Grading vs Staging of a tumor?

A

Grading – is based on the degree of differentiation

Staging – is due to size, LN spread, and malignancy

(We care more about Staging diagnosis)

124
Q

Immunohistochemistry

  • list the different histochemicals
A

Cytokeratin

EMA (EPithelial Membrane Ag)

LCA (CD45) (Leukocyte Common Ag)

Peroxidase

Non-Specific Esterase

GFAP (Glial Fibrillary Acidic Protein)

125
Q

In medicine we have gone from treating the organ to a molecular target - name the targets.

Lung

Breast

Prostate

Colon

Brain

A

Lung – Mutated KIT

Breast – Mutated HER2

Prostate – Mutated EGFR

Colon – Mutated BRAF

Brain – Mutated PI3K

126
Q

What is Chromothripsis?

A

It is a single catastrophic event that leads to MULTIPLE double-stranded breaks in DNA

It is repaired by error prone mechanisms – and can lead to tumors/cancers

127
Q

Note Table 7-12 Selected Tumor Markers

A
128
Q

Carcinoembryonic Ag (CEA) is found in what?

Alpha-Fetal Protein?

A

Carcinomas of the Colon, Pancreas, Stomach, Breast

produced in Hepatocellular Carcinomas, Teratocarcinomas, yolk sac stuff, embryonal cell carcinomas

129
Q

PSA, CEA, AFP lack both specificty and sensitivity required for?

A

Early Detection of cancers – and are good for detection of recurrences.

MOD Exam II - Neoplasia (1 decks)

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