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Histopath > Lecture | Neoplasms (part 2) > Flashcards

Lecture | Neoplasms (part 2) Flashcards

1
Q

Cancer grading is subjective and semi-quantitative. T/F

A

True

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2
Q

Is based on the degree of anaplasia and number of proliferating cells

A

Cancer grading

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3
Q

Is based on the shape and regularity of cells, presence and distinct differentiated features

A

Degree of anaplasia

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4
Q

Is based on evidence of rapid growth, which includes large number of mitoses, presence of atypical mitoses, nuclear pleomorphism, and tumor giant cells.

A

Number of proliferating cells

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5
Q

Tumor marker that can also be used yo quantify how much of these cells are actively proloferating

A

Ki67

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6
Q

Correlation of cytological grade and biological behavior is variable. T/F

A

True

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7
Q

The higher the anaplasia, the poorly differentiated the tumor, and the large number of mitosis correlates with a higher grade. T/F

A

True

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8
Q

Refers to the extent of tumor spread; influence choice of surgical approach or treatment modalities

A

Cancer staging

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9
Q

Criteria used in cancer staging:

A
  • Tumor size,
  • Extent of local growth,
  • Presence of lymph node metastasis,
  • Presence of distant metastasis
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10
Q

The bigger the tumor, the most likely it will be resectable. T/F

A

False,
… will not be resectable

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11
Q

One global scheme to address cancer staging; has a specific staging for particular malignancies in the different organs of the body

A

TNM cancer staging

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12
Q

What is TNM cancer staging?

A

T stands for Tumor - evaluates tumor size and the extent of its growth in relation to the structures that is located.

N stands for Nodal metastasis - pertains to the regional lymph nodes

M stands for Metastasis - refers to the distant metastasis

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13
Q

Most cancers arise from a single transformed cell. T/F

A

True. (Evidence-based)

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14
Q

Malignant change in the target cell is referred to as

A

Transformation

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15
Q

Stage 3 usually involves

A

Nodal metastasis

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16
Q

Stage 4 usually means that there is already

A

Distant metastasis

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17
Q

Transformation is the last step in the natural history of a malignant tumor. T/F

A

False,
It is the initial step

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18
Q

Accompanied by mutations of the DNA/genome of the cell

A

Transformation

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19
Q

Diagnosis should be early when the tumor is still small, when it is still amenable for resection. T/F

A

True

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20
Q

Additional treatment modalities if a tumor is very hard to manage due to late diagnosis.

A

Chemotherapy and radiation

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21
Q

Literally means abnormal growth

A

Dysplasia

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22
Q

Malignant transformation is a single-step process. T/F

A

False,
It is a multistep process

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23
Q

Precursor lesion of cancer

A

Dysplasia

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24
Q

In dysplasia, some features of malignancy are present microscopically. T/F

A

T

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25
Q

Dysplasia may develop into malignancy such as:

A

Uterine cervix and colon polyps

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26
Q

Dysplasia is irreversible like neoplasia. T/F

A

False,
It is still reversible unlike neoplasia

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27
Q

What is needed to remove in dysplasia so that the cells will go back to a normal state?

A

Instigating stimuli

If stimuli is not removed, dysplasia would eventually develop into malignancy

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28
Q

Dysplasia is graded as _, and what are its involvement?

A

Low grade - involves the lower portion of the epithelium

High grade - involves the entire layer of the epithelium

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29
Q

Dysplasia may not develop into malignancy. T/F

A

True.
It may not develop into malignancy if there is an early diagnosis and early treatment. If diagnosis and/or treatment is late, it may develop into malignancy.

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30
Q

When abnormality of the cells involves the entire thickness (or almost the entire layer of the epithelium), it will now become ____.

A

High grade dysplasia

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31
Q

If cell abnormality incorporates all the layers of the epithelium (or full thickness of the epithelium) and there’s no invasion of the basement membrane, it will now be called

A

Carcinoma in situ

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32
Q

Once basement membrane is breached, it will now become

A

Invasive carcinoma

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33
Q

The problem with a transformed cell is that it will not be under the tight regulation of the cells because once the tumor is malignant, it becomes a cancer cell and it will now have an ___

A

Autonomous growth

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34
Q

What lengthens as tumor grows?

A

Doubling time of tumor cells

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35
Q

Tumor cells actually needs ________for the cell to become space occupying lesion

A

10 more doublings ([1kg] lethal burden)

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36
Q

30 doublings (?) = ?

A

30 doublings (10^9 cells) = 1g

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37
Q

Fraction of tumor cells in replicative pool

A
  • May be only 20% even in rapidly growing tumors
  • Tumor stem cells
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38
Q

Rate / cellular processes at which tumor cells
are shed or lost

A
  • Apoptosis (when cells signal the arrest/suicide of these tumor cells)
  • Maturation (cancer cells are unable to grow further)
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39
Q

The rate of the tumor growth may be loss or it will stabilize, otherwise the tumor cells will cease to grow. T/F

A

False,
… tumor cells will continue to grow until it becomes very very big

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40
Q

The bigger the tumor, the chances of invasion and metastasis will be increased. T/F

A

True

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41
Q

Transformed cell will divide forming this genetically abnormal cells; these are ?

A

Clone cells

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42
Q

In sun exposure, what causes injury to the DNA of the cell?

A

Ultraviolet radiation (basis for skin cancer)

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43
Q

___ tend to be prone to develop skin cancer compared to ___

A

Caucasians ; blacks / heavily pigmented people

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44
Q

Blacks have low incidence of melanoma, so do normally pigmented areas like ___ on white people

A

Areola

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45
Q

Geographic and environmental factors that may promote tumor growth

A
  • Sun exposure
  • Smoking and alcohol abuse
  • Body mass
  • Environmental vs. Racial factors
  • Viral exposure
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46
Q

Overweight = __% increase in cancer

A

50%

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47
Q

For females, there’s an increased risk of ____, while for males, there’s an increased risk of ___

A

Breast cancer; prostate cancer

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48
Q

What plays a role in breast carcinoma

A

Testosterone and estrogen

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49
Q

What plays a role for the growth of prostatic carcinoma

A

Testosterone

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50
Q

There are also viruses that are ___, example pf this viruses include ___ which causes a cancer of uterine cervix

A

Oncogenic; Human Papillomavirus (HPV)

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51
Q

Hepatitis B virus (HBV) causes ?

________ causes burkitt’s lymphoma and nasopharyngeal carcinoma

Human Herpesvirus-8 causes ?

A

Liver cancer

Epstein-Barr virus (EBV)

Kaposi’s sarcoma

52
Q

Diet high in nitrates can be converted to ___ which is a risk factor for ? cancer

A

Nitrosamines ; colon cancer

53
Q

Japanese immigrants now in japan has a diet that is heavily composed of _____. Thus most of the cancers associated with the japanese are ____, followed by liver, colon, and prostate

A

Fish; stomach

54
Q

Americans has a diet heavily composed of ____. Thus, Japanese immigrants that now live in USA will show a decrease in ____ and an increase in ___.

A

Meat; decrease in stomach cancer; increase in colon cancer

55
Q

Most cancers occur in the elderly aging ___, however there are also childhood malignancies like ____ and ___

A

> (and equal to) 55 years ; leukemias & CNS neoplasms ; and bone tumors

56
Q

There’s a familial transmission of these genetic abnormalities

A

Genetic predisposition

57
Q

What explains the differences in the genetic constituencies among closely related individuals?
Ex: 2 brothers who smoke heavily, one developed cancer later on but the other one did not. What explains this phenomenon?

A

Genetic polymorphism

  • since they’re brothers, they have difference in their genes that will encode certain enzymes. These enzymes may convert a potential carcinogen to a non-carcinogenic substance. Thus, the other brother may have this gene (which encodes the enzyme) while the one brother that developed cancer may lack this gene.
58
Q

Hydrocarbons from smoke can be converted to ___ which can cause lung cancer

A

Epoxides

59
Q

Early age at onset; two or more primary relatives with the cancer; multiple or bilateral tumors

A

Familial cancer syndromes

60
Q

Nonhereditary predisposing conditions

A
  • Chronic inflammation (causes the growth of malignancies)
  • Precancerous conditions
61
Q

Precancerous conditions in nonhereditary predisposing conditions

A
  • Chronic ulcerative conditions / Crohn’s disease (causes colonic cacinoma)
  • Atrophic gastritis of pernicious anemia
  • Leukoplakia of mucous embranes
62
Q

Hepatitis B can cause liver cirrhosis which can be a harbinger for

A

Hepatocellular carcinoma

63
Q

Tumor cells do not necessarily proliferate at a faster rate than their normal counterparts. T/F

A

True

64
Q

Major determinant of tumor growth is ?

A

More cells produced than die in a given time

65
Q

Time taken for number of cells in mass to double

A

Doubling time

66
Q

Detectable size for mass to be palpable?

A

30 doubling time

  • 1.0 cm^3 (1.0 g) = 10^8 to 10^9 cells = doubles 30x
67
Q

Tumor is palpable around ?
When is it not palpable?

A

2cm = palpable
<2cm = not palpable

68
Q

___ can be employed to detect mass lesion

A

Imaging studies like CT scan, X-ray, MRI

69
Q

Sprouting of new capillaries from pre-existing blood vessels; requirement for continued growth of cancers

A

Tumor angiogenesis

70
Q

Absence of blood vessels indicate

A

Tumors grows no larger than 1-2 mm in diameter

71
Q

Tumor will not grow unless they are fed by new blood vessels because these tumors needs nutrients. T/F

A

True

72
Q

Tumors will secrete _____ particularly _____ which enhances the formation of small blood vessels.

A

Growth factors ; Angiogenic factors

73
Q

Small blood vessels will nourish the growing tumor. T/F

A

True

74
Q

Angiogenic factors (7)

A
  1. FGF (Fibroblasts Growth Factor)
  2. TNF-a (Tumor Necrosis Factor alpha)
  3. EGF (Epidermal Growth Factor)
  4. VEGF (Vascular Endothelial Growth Factor)
  5. TGF (Transforming Growth Factor)
  6. PDGF (Platelet-derived Growth Factor)
  7. Angiogenin
75
Q

Cell proliferation is balanced by apoptosis in the absence of tumor angiogenesis; or may be due to cell cycle arrest

A

Tumor dormancy

76
Q

Unregulated growth of cancer cells results from sequential acquisition of somatic mutations in genes that control and differentiation or that maintains the integrity of the genome. T/F

A

True

77
Q

Hereditary predisposition

A

Concept of cancer gene

78
Q

In cancer gene, there is a presence of chromosomal abnormalities in neoplastic cells. T/F

A

True

79
Q

In cancer gene, there is a correlation of _ and _

A

Impaired DNA repair and occurrence of cancer

80
Q

In the concept of cancer gene, there is a close association between _ and _

A

Carcinogenesis and mutagenesis

81
Q

Most common mechanism of mutagenesis relates to

A

Spontaneous errors in DNA replication and repair

82
Q

Genes involved in the pathogenesis of cancer:

A
  • Oncogenes
    -Tumor surpressor genes
  • Mutator genes
83
Q

These are positive effectors of neoplastic phenotype

A

Oncogenes

84
Q

Genes wherein there is loss of function will permit unregulated cell growth

A

Tumor suppressor genes

85
Q

The inactivation of this genes will allow further mutations

A

Mutator genes

86
Q

Alteration in structure of protooncogene results in

A

Abnormal gene product

  • change in nucleic acids sequence by point mutation, deletion, chromosomal translocation which leads to the synthesis of mutant protein that functions abnormally
87
Q

Increase in expression of protooncogenes causes

A

Overproduction of normal gene product

  • increased transcription occurs insertional, mutagenesis, chromosomal translocation, and gene amplification
88
Q

Example of activation by mutation wherein there is a point mutation in codon __ resulting in substitution of _

A

C-RAS in bladder cancer : point mutation in codon 12 = valine to glycine

  • because of the point mutation, C-RAS is activated resulting in urinary bladder cancer
89
Q

Example of Activation by Chromosomal Translocation wherein it is found in 95% of Chronic Myelogenous Leukemia.

A

Philadelphia chromosome

90
Q

In Philadelphia chromosome, ____ on chromosome 9 translocated to chromosome 22 where it is placed in juxtaposition to a site known as ___, wherein an aberrant protein with very high kinase activity is coded

A

C-ABL Protooncogene; Breakpoint Cluster Region (BCR)

91
Q

This BCR will ultimately code for an enzyme with a very high kinase activity which will now result or manifested as

A

Granulocytic hyperplasia (increase in the number of WBCs), a manifestation of Chronic Myelogenous Leukemia

92
Q

Increase number of gene copies

A

Activation by gene amplification

93
Q

____ found in neuroblastoma (a common childhood tumor) or _____ is found in the breast and ovarian cancer.

A

N-myc protooncogene ; erb protooncogene

94
Q

Mechanisms of actions of oncogenes (6)

A
  1. Extracellular growth factors
    • synthesis of PDGF-like factors by neoplastic cells
  2. Cell surface receptors
    • generation of mitogenic signals that override normal control of signaling pathways
  3. Intracellular signal trandpsduction pathways
    • activation of growth factor receptors
  4. DNA-binding nuclear proteins (transcription factors)
    • C-myc activation render cells competent to receive signals for mitosis
  5. Cell cycle proteins (cycling and cyclin-dependent protein kinases)
  6. Inhibitors of apoptosis (bcl-2)
95
Q

Loss of heterozygosity by deletion or somatic mutation predispose to tumor development

A

Tumor suppressor genes

96
Q

What happened if the tumor suppressor gene will be subject to mutation?

A

It becomes defective

97
Q

Deletion or mutation of tumor suppressor genes enables the damaged DNA to progress through the cell cycle. T/F

A

True

98
Q

Most common genetic change in human cancer (deleted or mutated in 80% of cases of colon cancer, frequently in breast cancer, small sell carcinoma of lung, hepatocellular carcinoma, astrocytoma)

Also give its location

A

P53 gene
Location: small arm of chromosome 17

  • protein product of this gene is present in all normal tissues
99
Q

In P53 gene, mutations allow cells with damage DNA to progress through the cycle. T/F

A

True

100
Q

Other tumor suppressor genes:

  • _______ - implicated in familial adenomatous polyposis coli and colorectal cancers
  • ______ - hereditary Wilm’s tumor
  • ______ - neurofibromatosis type 1
  • ______ - 90% of pancreatic cancers
  • ______ - breast and some ovarian cancers
A
  • APC gene
  • WT-1 gene
  • NF-1 gene
  • DPC-4 gene

-BRCA-1 and BRCA-2 genes

101
Q

_____ are called _____ which exercise surveillance over the integrity of genetic information by participating in cellular response to DNA damage

A

Mutator genes ; caretaker genes

102
Q

Loss of these gene functions renders the DNA susceptible to the progressive accumulations of mutation; when these affect protooncogenes or tumor suppressor genes, cancer will result

A

Mutator genes

103
Q

It is estimated that ____ are responsible for 15% of all human cancers

A

Viral infections

104
Q

The strongest association of viruses and human cancer includes:

A
  • HTLV-1 virus = T-cell leukemia and Lymphoma
  • HPV = squamous cell carcinoma of the cervix
  • HBV = hepatocellular carcinoma
  • EBV = Burkitt’s lymphoma and Nasopharyngeal carcinoma
  • HHV-8 = Kaposi’s sarcoma
105
Q

Hepatitis B virus > chronic hepatitis > ________ > _______

A

Liver cirrhosis > liver cancer

106
Q

______ are proven by epidemiological studies and animal studies

A

Chemical carcinogen as mutagens

107
Q

An agent that can permanently alter the genetic constitution of a cell

A

Mutagen

108
Q

About 90% of known carcinogens are mutagenic, and all mutagens are carcinogenic. T/F

A

False,
Most (not all) mutagens are carcinogenic

109
Q

Many compounds known to be potent carcinogens are relatively _____ in terms of chemical reactivity; most require _______ before they can react with cell constituents

A

Inert ; metabolic activation

110
Q

Is a short-term laboratory test done on _______ wherein you will expose this bacteria to these particular chemicals and look for mutations in the genetic material of the bacteria.

It is a test for potential mutagenic capacity of these chemicals

A

AMES test ; Salmonella typhimurium

111
Q

4 stages of chemical carcinogenesis

A
  1. Initiation - mutations in a single cell
  2. Promotion - characterized by clonal expansion of the initiated cell
  3. Progression - growth becomes autonomous; cancer is independent of the carcinogen or promoter; instability of the genome with the end result of further clonal expansion
  4. Cancer - result when cells acquire the capacity to invade and metastasize
112
Q

Are inherently reactive to bind covalently to cellular macromolecules. E.g., ______

A

Direct acting carcinogens ; benzyl chloride

113
Q

________ through enzymatic reactions effected by cellular systems

  • ex: __________ to epoxides (cigarette smoke -> lung cancer)
  • aromatic amines and azo dyes converted to _____ (aniline dyes -> _____)
A

Conversion to a more reactive compound

  • polycyclic aromatic hydrocarbons
  • hydroxyl derivatives ; bladder cancer
114
Q

Bronchogenic carcinoma is a relatively common phenomenon because of

A

Increased smoking cigarettes

115
Q

Cancers attributed to sun exposure, due to ____, namely:

A
  1. Basal cell carcinoma
  2. Squamous cell carcinoma
  3. Melanoma
116
Q

______ are not prone to skin cancer but _____ show increased cases of skin cancer

A

Blacks / heavily pigmented people with more melanin content ; Caucasians

117
Q

Carcinogenic effects of UV radiation occurs at wavelength of

A

290nm to 320nm

118
Q

Effects of uv radiation in cells include

A

Enzyme inactivation, inhibition of cell division, mutagenesis, cell death, and cancer

119
Q

Most important biochemical effect of UV radiation is the _______________ which distorts the backbone of the DNA helix (unless repaired, this genomic injury is mutagenic and carcinogenic)

A

Formation of pyramidine dimers on DNA

120
Q

Material widely used in construction, insulation, and manufacturing

A

Asbestos

121
Q

Characteristic tumor associates with asbestos is

A

Malignant mesothelioma of the pleura and peritoneal cavities

122
Q

These small fibers can cause changes in the cells lining the lung cavity

A
  • ‘Serpentine’ - chrysotile
  • ‘Amphiboles’ - crocidolite and amosite
123
Q

In the ____, asbestos has been banned as a construction material but there is a long latent period of about _____ between exposure and appearance of tumor

A

1970s ; 20years

124
Q

Most common cause of death associated with malignancy

A

Lung cancer

Followed by prostate / breast, colon, stomach, liver, and leukemia

125
Q

What are usually detected late in the clinical course

A

Lungs, prostate, and colon

126
Q

Cause of cancer in males and females:

A

M: Lungs, prostate, and then colon
F: Lungs, breast, and then colon

Histopath (3 decks)

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