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Pathology 1 > Chapter 5 > Flashcards

Chapter 5 Flashcards

1
Q

What is the most common type of cancer in males

A

Prostate 33%

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2
Q

What is the most common type of cancer in females

A

Breast Cancer 31%

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3
Q

What cancer is most likely to cause death in both males and females

A

Lung and Bronchus cancer

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4
Q

What is the difference between Remission and Cure

A 
Cure = No more cancerous cells
Remission = Canacer has subsided but unknown if all the cancerous cells are gone
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5
Q

What is Neoplasia

A

New Growth AKA tumor

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6
Q

What are the features of a Neoplasia

A 
Autonomous growth
Independent of growth inhibition
Evasion of cell death
Limitless replication
angiogenesis
Adnormal metabolis
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7
Q

What causes Neoplasia to arrise

A

Dysfunction of cellular growth regulation

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8
Q

What are non-modifiable risks for cancer

A

Age
genetics

“things you cant control”

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9
Q

What are modifiable risks of cancer

A 
Anything that can be controlled
Obesity
Excessive alcohol+animal fat
Irradiation
infections
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10
Q

What are the two parts of a Tumor

A

Parenchyma

Stroma

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11
Q

What is the Parenchyma of a Tumor

A 
Transformed cells (neoplastic)
Clonal
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12
Q

What is the Stroma of a Tumor

A

Non-neoplastic portion

Supportive structure of tumor

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13
Q

What part of the Tumor determines biological nature/agressivness

A

Parenchyma

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14
Q

What are the two main types of Tumors

A

Benign

Malignant

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15
Q

What is the nomenclature for a benign tumor

A

Cell type + oma

Fibroma, Chondroma

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16
Q

what is an exception to the nomenclature for a benign tumor

A

Melanocytic nevus

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17
Q

What are the features of a benign tumor

A

Localized
Relatively innocent

Can possibly: Vascular compression, hormone production

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18
Q

what is a benign tumor of glandular tissue

A

Adenoma

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19
Q

What is a benign tumor of capillary endothelia

A

Hemangioma

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20
Q

What is a bening tumor of adipose tissue

A

Lipoma

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21
Q

What is a benign smooth muscle tumor

A

Leiomyoma

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22
Q

What is a malignant tumor also known as

A

Cancer

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23
Q

What is metastasize

A

Spead/invade other tissues

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24
Q

How are cancers named

A

Cell type + Sarcoma or Carcinoma

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25
Q

What will classify a cancer as a sarcoma

A

Derived from mesodermal tissue

bone, Muscle, vasculature

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26
Q

What will classify a cancer as carcinomas

A

Derived from epithelial tissue

organs

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27
Q

What will classify a cancer as a teratoma

A

Contains multiple germ cell layers

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28
Q

What classification of cancer develops at any age?

A

Sarcoma

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29
Q

WHat classification of cancer develops during mid-late adulthood

A

Carcinomas

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30
Q

What is the most common type of tumor classification

A

Carcinomas (90%)

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31
Q

What is Fibroadenoma

A

Benign tumor of the female brest

Mixed tumor

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32
Q

What is a Hamartoma

A

Benign tumor tissue is native to individual site

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33
Q

What is a polyp

A

a mass that projects from the mucosal surface

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34
Q

What are the levels of Carcinoma progression

A

Dysplasia
Carcinoma in situ
Invasive Carcinoma

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35
Q

What is Dysplasia in reference to carcinoma

A

Disorderly proliferation

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36
Q

What is carcinoma in situ

A

Earyl Neoplasia
Localized
no penetration of basement membrane

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37
Q

What is invasive carcinoma

A

Local destruction
Penetration into basement membrane
likely to metastasize

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38
Q

What are the 4 characteristics of a cancer

A

Differentiation & anaplasia
Rate of growth
local invasiveness
metastasis

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39
Q

What is the differentiation difference between a normal cell and benign tumor

A

Normal: Completely differentiated, slow mitosis

Benign: Somewhat well-differentiated, decrease function

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40
Q

What is anaplasia

A

Loss of differentiation

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41
Q

What is associated with anaplasia

A

Severe loss of function
Pleomorphism
Increase of growth speed

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42
Q

What is pleomorphism

A

Various cell sizes/shapes
Less regulation
increase growth
potentialy malignant

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43
Q

How do benign tumors grow

A

Slow/controlled

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44
Q

How to malignant tumors grow

A

Fast/uncontrolled

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45
Q

How are growth speed and differentiation related

A

There is an inverse correlation

differentiation decrease, speed increase

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46
Q

What type of tumor is likely to be encapsulated

A

Bening

Lack of capsule doesn’t mean malignancy

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47
Q

What is a highly reliable tumor characteristic

A

whether it is localized of invading other tissues

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48
Q

What is metastasis

A

secondary implantation into remote tissue

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49
Q

What is the most reliable indicator of malignancy

A

Metastasis

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50
Q

Metastasis is most common among what type of tumors

A

Aggressive

high anaplasia
large size

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51
Q

What part of the tumor influences metastasis

A

The parenchyma

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52
Q

What are the three types of Dissemination

A

Seeding within body cavities
Lymphatic spread
Hematogenous spread

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53
Q

What does Seeding within body cavities pertaining to dissemination

A

Invasion of natural body cavities

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54
Q

What is lymphatic spread pertaining to dissemination

A

Most common mode of carcinoma metastasis

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55
Q

What determines lymphatic spread of a cancer

A

Site and tumor parenchyma

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56
Q

What is Hematogenous spread when pertaining to dissemination

A

Spread through blood

Most common mode of sarcoma metastasis

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57
Q

What is the most common way for a carcinoma to spread

A

Lymphatic spread

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58
Q

What is the most common way for a sarcoma to spread

A

Hematogenous spread

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59
Q

What is Epidemiology

A

Study of heath/disease in population

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60
Q

What is the purpose of Epidemiology

A

to discover risk factors for a disease

Sex, ethnicity, geography, lifestyle

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61
Q

What is the ultimate cause of cancer

A

Genetic alterations

mutations, epigenetics

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62
Q

What age group has the most cancer related morality

A

55-75 years

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63
Q

When do most childhood cancers form

A

Under 15 years old (10%)

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64
Q

What are the most common children cancers

A 
Leukemia
Lymphomas
Retinoblastomas
Neuroblastoma
Osteosarcoma
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65
Q

What are the three categories of hereditary cancer

A

Autosomal dominant
Autosomal recessive
Familial cancer of uncertain inheritance

66
Q

What is autosomal dominant cancer caused by

A

A single inherited mutant allele

67
Q

What is autosomal recessive cancer caused by

A

2 altered alleles due to genomic instability

Ex. Xeroderma pigmentosa

68
Q

What is Xeroderma pigmentosa

A

Sensitivity to UV

Highly susceptible to melanoma

69
Q

What is Familial cancer

A

Cancer that has some familial association
2 or more close relatives
early onset
bilateral

70
Q

What are some types of familial cancer

A 
Colon
Breast
Prostate
Brain
Ovarian
71
Q

what is preneoplastic lesions

A

“pre-cancer”

Increase cancer risk but most do not develop

72
Q

What can cause preneoplastic lesions

A

Acquired lesions
Chronic tissue injury
Inflammation
dysplasia, metaplasia

73
Q

What cancers are associated with these preneoplastic leions

1) GI adenoma
2) Leukoplakia
3) Actinic Keratosis

A

1) Colorectal cancer
2) squamous cell carcinoma
3) Skin Cnacer

74
Q

What is Carcinogenesis

A

Creation of cancer

75
Q

What type of cell damage promotes carcinogenesis

A

Nonlethal genetic damage i.e. mutations, epigenetic changes

76
Q

What are the two ways we can acquire nonlethal genetic damage

A

Acquired: Environmental

Inherited (genetic)

77
Q

What is acquired carcinogenesis limited to

A

Somatic cells

78
Q

What cells are at risk of carcinogenesis for inherited risk

A

All cells

Germline alteration

79
Q

What are the regulatory genes that prevent cancer. and are the number one target for genetic damage

A

Proto-oncogenes
Tumor suppressor genes
Apoptosis genes
DNA repair genes

80
Q

Genetic alterations to regulatory genes is also known as

A

Carcinogenesis

81
Q

What do proto-oncogenes regulate

A

Cell growth

82
Q

What is an oncogene

A

Mutated proto-oncogene

83
Q

What do oncogenes do

A

Cause anaplasia

84
Q

What type of mutation causes oncogenes

A

Dominant (1 allele)

Gain of function

85
Q

What type of mutation changes tumor suppressor genes

A

Recessive (2 alleles)

Loss of function

86
Q

What is karyotype

A

Number and appearance of Chromosomes in the nucles

87
Q

What can damage to karyotype cause

A

Activation of oncogenes

Inactivation of tumor suppressor genes

88
Q

What are small changes to karyotype

A

Deletion

Insertion

89
Q

What are large changes to karyotype

A

Abnormal karyotype

Aneuploidy = abnormal number of chromosomes

90
Q

What are MircoRNAs

A

Non-coding RNA m/c

91
Q

What do mircoRNAs do

A

inhibit gene expression

92
Q

if there is an increased expression of MicroRNAs what regulatory gene is affected

A

Tumor supressor genes

93
Q

If there is a decreased expression of MircoRNAs what regulatory genes is affected

A

Oncogenes

94
Q

What are epigenetic modifications

A

Heritable changes in gene expression

95
Q

What do epigenetic modifications do

A

Silence genes

96
Q

How to epigenetic modification silence genes

A

DNA methylation

Histone modification

97
Q

are epigenetic changes reversible

A

Yes

98
Q

What type of genetic modification does no mutate a gene

A

Epigenetic changes

99
Q

Will one isolated mutation cause cancer

A

No, multiple genes must be impacted

100
Q

What happens to tumors over time

A

They become more aggressive (tumor progression)

Less responsive to therapy

101
Q

What are the Hallmarks of Cancer

A 
Evasion of immune system
Genomic instability
Tumor-promoting inflammation
Change in energy metabolism
Angiogenesis
Self suffifency in growth signals
102
Q

How are cancer cells self sufficient in growth signals

A

Produce own growth factors
Stimulate growth factors from stroma
Alter GF receptors
Can stimulate its own receptors

103
Q

What changes occur to cancer cells response to GF

A

they overexpress receptors

Hyperresponsive to GFs

104
Q

What GF receptor are often over expressed in cancer cells

A

HER2

105
Q

What is signal transduction

A

Passing of a signal from receptor to the nucleus

106
Q

What signal transduction genes are commonly mutated in Tumors, and in leukemias

A

RAS: 30% all tumors
ABL: mutated in leukemias

107
Q

What happens when the nucleus is over-stimulated due to mutated transduction/GF receptors

A

Decreased cellular regulation = More mutations

108
Q

What happens when there is an overstimulation of growth-promoting genes

A

Stimulating cell cycle

Suppression of regulatory genes

109
Q

Alterations to what gene “remove brakes and slam gas”

A

MYC gene

110
Q

What does the MYC gene control

A

CDK activation

Aerobic glycolysis

111
Q

What is the restriction point in the cell cycle

A

G1-S phase transition

112
Q

What do CDKs do at G1-S transition

A

Organize entry

113
Q

What do CDKIs do at G1-S transition

A

Inhibit entry

114
Q

What part of the cell cycle do all cancers need to disable

A

G1-S checkpont

115
Q

What types of proteins to Tumor suppressor genes code for

A

Inhibitory growth proteins

116
Q

What happens when Tumor suppressor genes become non-functional

A

Increased Proliferation

117
Q

What is the Two-hit hypothesis

A

Both alleles must be inactivated in the Tumor suppressor genes to change the phenotype

118
Q

What protein does the Rb gene code for

A

Rb protein

119
Q

What was the first Tumor suppressor gene discovered

A

Rb gene

120
Q

What check point does the Rb protein govern

A

G1-S phase

121
Q

What viral infection can inhibit Rb protein

A

HPV

122
Q

What protein maintains DNA integrity and is known as the guardian of the genome

A

p53

123
Q

When a cell has DNA damage what protein will send it into Quiescence or Senescence

A

p53

124
Q

What gene codes for the p53 protein

A

TP53

125
Q

What is the difference between Quiescence and Senescence

A

Quiescence: Reversible cell cycle arrest (minor damage)

Senescence: permanent cell cycle arrest (major Damage)

126
Q

What cell cycle phase does p53 check for DNA damage and remove cells with damaged DNA

A

G1 phase

127
Q

What viral infections alter both alleles of TP53 (cause Somatic mutations)

A

HPV
EBV
Hep B

128
Q

What is the inherited disease that has TP53 damage

A

Li-Fraumeni Syndrome

129
Q

What protein do both Apoptosis pathways use. Known as the Executioner, common target for cancer cells to destroy to avoid apoptosis

A

Caspse-3

130
Q

What is the Hayflick limit

A

Maximum amount of times a cell can divide (normally 60-70 divisions)

131
Q

What is the reason why cell can only divide so many times

A

Telomeres shorten, TSG recognize the shortening = senescence

132
Q

What protein is rarely active in normal cells but very active in cancer cells. Causes cancer cells to have limitless replicative potential

A

Telomerase (repairs+maintains telomeres)

133
Q

How large can a cancer cell get until it needs sustained angiogenesis

A

1-2mm in diameter

134
Q

What are the major steps in invacion-metastasis cascade

A

1) invasion of ECM
2) Vascular Spread
3) Micrometastases grow+invade

135
Q

What are the steps cancer cells have to take in order to interact with the ECM

A

Lossening of tumor cell
Breakdown of ECM
changes in ECM attachment
Migration

136
Q

Where is the primary tumor located

A

The site of metastasis

137
Q

What are the three types of DNA repair discussed in class

A

Mismatch Repair
Nucleotide excision repair
Homologous recombination repair

138
Q

What is mismatch repair

A

Single base errors are corrected

139
Q

15% of this type of cancer is caused by errors in mismatch DNA repair

A

Sporadic colorectal Cancers

i.e. Herediraty nonpolyposis colorectal cancer

140
Q

What type of repair is done when a segment of DNA is damaged and removed. normally damaged by UV light

A

Nucleotide excision repair

141
Q

What type of disease is associated with defective Nucleotide excision repair

A

Xeroderma pigmentosum

142
Q

What is homologous recombination

A

DNA is exchanged between two homologous chromosomes

Can be used to repair DNA

143
Q

What two genes are responsible for 50% of familial breast cancer. Due to problems with recombination

A

BRCA1 + BRCA2

144
Q

Can chronic inflammation increase cancer risk

A

Yes

145
Q

What are the classes of carcinogenic agents

A

Chemical
Radiant energy
Mircobial

146
Q

What type of carcinogens require no metabolic conversion

A

Direct-Acting

147
Q

What type of carcinogens require metabolic conversion

A

Indirect-acting

148
Q

What are some indirect-acting carcinogens

A

Tabacco smoke
Fossil fuel exhaust
aflatoxin B1

149
Q

What gene is the target for aflatoxin B1

A

TP53

150
Q

Other than mutating a specific gene, what other way can a chemical carcinogen affect gene expression.

A

Mutate the promoter sequence of a gene

151
Q

How can irradiation damage cells

A

Mutagenic effects

Carcinogenesis

152
Q

What is acute radiation syndrome

A

Radiation sickness caused but irradiation carcinogenesis

153
Q

What does UV light cause the formation of

A

Pyrimidine dimers

154
Q

What are the three types of skin cancer caused by UV light

A

Basal cell carcinoma
Squamous cell carcinoma
Melanoma

155
Q

What type of skin cancer is most common

A

Basal cell carcinoma

156
Q

Why type of skin cancer is caused by intense UV exposure

A

Melanoma

157
Q

What is the most common metastatic cancer in the US

A

Skin cancer

158
Q

What classification of viruses cause cancer

A

Oncogenic RNA viruses

159
Q

What was the oncogenic RNA virus that was discussed in class

A

Human T cell lymphotropic virus-1 (HTLV-1)

160
Q

how is HTLV-1 transmitted

A

Sex
blood
breast feeding

161
Q

What are the 4 oncogenic DNA viruses discussed in class

A

HPV
EBV
Hep B and C
Kaposi sarcoma herpesvirus

Pathology 1 (6 decks)

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