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MHD Exam 1 > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

neoplasia

A
  • disorder of cell growth
  • triggered by series of acquired mutations of single cell and its clones
  • monoclonal, autonomous, irreversible
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2
Q

cancer

A

-generic term for malignant neoplasm

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3
Q

parenchyma

A
  • neoplastic cells
  • largely determines biological behavior
  • source for the name of the neoplasm
  • neuroectodermal, epithelial or mesenchymal in origin
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4
Q

stroma

A
  • CT, blood vessels, and immune system cells

- support growth and spread of neoplasm

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5
Q

classification of tumor

A
  • based on cell of origin
  • most tumors originate from one cell (monoclonal) and of one parenchyma cell type
  • some rare tumors contain cells from more than one germ layer (teratomas)
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6
Q

mesenchyme cells

A
  • fibrous tissue
  • chondroid (cartilage)
  • osteoid (bone)
  • blood vessels
  • smooth muscle
  • skeletal muscle
  • lymphoid tissue
  • hematopoeitic cells
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7
Q

fibrous tissue tumors

A

benign- fibroma

malignant- fibrosarcoma

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8
Q

chondroid tumors

A

benign- chondroma

malignant-chondrosarcoma

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9
Q

osteoid tumors

A

benign- osteoma

malignant- osteosarcoma

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10
Q

blood vessels tumors

A

benign- hemangioma

malignant- angiosarcoma

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11
Q

smooth muscle tumors

A

benign - leiomyoma

malignant- leimyosarcoma

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12
Q

skeletal muscle tumor

A

benign - rhabdomyoma

malignant- rhabdomyosarcoma

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13
Q

lymphoid tissue tumor

A

lymphoma

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14
Q

hematopoietic cells tumor

A

leukemia

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15
Q

stratified squamous cells tumor

A

benign- squamous papilloma

malignant- squamous cell carcinoma

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16
Q

epithelial lining of glands of ducts tumor

A

benign- adenoma

malignant- adenomacarcinoma

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17
Q

mixed tumors derived from 1 germ cell layer

A
  • single neoplastic clone capable of divergent differentiation (more than 1 neoplastic cell type)
  • ex. salivary gland and gonads
  • totipotential germ cells differentiate into any cell type found in the human body
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18
Q

salivary gland mixed tumor

A
  • pleomorphic adenoma = benign
  • derived from one germ cell layer
  • has a clone capable of epithelial and myoepithelial differentiation
  • neoplastic epithelial cells scattered in neoplastic myxoid stroma
  • malignant mixed tumor of the salivary gland = malignant
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19
Q

gonadal mixed tumor

A
  • mature teratoma = benign
  • immature teratoma and teratocarcinoma =malignant
  • arises from totipotential germ cells
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20
Q

benign tumor characteristics

A
  • well-differentiated (resemble normal tissue counterpart) to dysplastic
  • grows slowly
  • most stay ecapsulated and stay localized
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21
Q

characteristics of malignant neoplasms

A
  • well differentiated to very de-differentiated (anaplastic)
  • pleomorphic (variations in nuclear size and shape)
  • abnormal nuclear morphology (high N/C rate, hyperchromatic, and prominent nucleoli)
  • mitoses
  • rate of growth is variable and unpredictable, and it usually varies with degree of differentiation
  • they infiltrated and destroy locally
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22
Q

dysplasia

A
  • disordered growth
  • considered benign but is pre-cancerous
  • principally found in epithelium
  • mutations leading to cytological and architectural changes of epithelial cells
  • pleomorphism, hyyperchromatic nuclei, high N/C ratio, mitotic figures above basal layer, disorderly maturation, disordely architecture
  • DOES NOT PENETRATE BASEMENT MB
  • mild to moderate dysplasia may be reversible, especially if the inciting causes are removed but it can be a precursor to a malignant transformation
  • often occurs in metaplastic epithelium
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23
Q

metastasis pathways of dissemination

A
  • seeding within natural body cavities (ex. ovarian carcinomas seed peritoneal cavity)
  • lymphatic spread- more typical of carcinomas and will usually deposit into the closest lymph node
  • hematogenous spread- more typical of sarcomas
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24
Q

cancer variables

A
  • geography
  • environment
  • age
  • race
  • acquired predisposing conditions
  • genetic predisposition
  • genetic + inherited factors
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25
Q

geography differences and cancer

A

different exposures to environ carcinogens and different access to preventitive care

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26
Q

environ and cancer

A
  • tobacco- lung, upper airway, bladder, pancreas, kidney, and esophagus
  • alcohol- oral cavity, pharynx, larynx, esophagus, and liver (secondary to cirrhosis)
  • obesity- esophagus, pancreas, colon/rectum, breast, endometrium, kidney, thyroid, and bladder
  • occupational exposure (polycyclic hydrocarbons in coal etc = lung, aromatic amines in dye and rubber = bladder, and asbestos in construction = mesothelioma, lung cancer)
  • sunlight, radiation, and sexual exposures
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27
Q

proposed mechanisms of obesity and cancer link

A
  • elevated insulin levels
  • increased estrogens
  • decreased adiponectin
  • proinflammatory state
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28
Q

age and cancer

A
  • most cancers in >55
  • carcinomas most common
  • incr mutations and decr immune competence
  • in kids = >10% of deaths and mainly leukemia and CNS neoplasms
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29
Q

heredity and cancer

A
  • autosomal dominant cancer syndromes (familial adenomatous polyps of colon, familial retinoblastoma)
  • autosomal recessive syndromes of defective DNA repair (xeroderma pigmentosum)
  • familial cancers of uncertain inheritance
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30
Q

acquired predisposing conditions to cancer

A
  • chronic inflammation- activated immune cells produce reactive oxygen species that leads to metaplasia
  • precursor lesions - barret esophagus, squamous metaplasia of bronchus, and endometrial hyperplasia
  • immunodeficieny states- especially T-cell deficiences
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31
Q

T/F

cancer arises from the clonal expansion of a single progenitor cell that has incurred damage

A

Tru

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32
Q

four classes of target regulatory genes which have mutations in cancer

A
  • growth promoting proto-oncogenes
  • growth inhibiting tumor suppressor genes
  • genes that regulate apoptosis
  • genes involved in DNA repair
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33
Q

proto-oncogenes

A

normal cellular genes whose products promote cell proliferation

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34
Q

oncogenes

A
  • mutant or overexpressed versions of normal proto-oncogenes
  • function autonomously
  • encode transcription factors, growth regulating proteins, cell survival proteins
  • lost dependence on normal growth promoting signals
  • potent carcinogenic factors
  • dominant- mutation of a single allele can lead to cellular transformation
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35
Q

ABL

A
  • oncogene
  • gene product =tyrosine kinase (signal transduction)
  • chronic myelogenous leukemia (CML)
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36
Q

C-MYC

A
  • oncogene
  • gene product- transcription factor (nuclear regulatory protein)
  • burkitt lymphoma
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37
Q

ERB-2

A
  • Tyrosine Kinase gene product
  • breast, ovarian, gastric carcinoma
  • oncogene
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38
Q

RAS

A
  • oncogene
  • gene product = GTPase
  • colon, pancreatic carcinoma
  • most commonly mutated proto-oncogene in human tumors
  • member of a family of small G proteins that bind GTP and GDP (inactive = bound to GDP and active = bound to GTP)
  • active RAS stimulates downstream regulators of proliferation so that the cell is forced into a continuously proliferating state
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39
Q

L-MYC

A
  • oncogene
  • gene product- transcription factor
  • lung cancer
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40
Q

RET

A
  • oncogene
  • gene product = tyrosine kinase
  • multiple endocrine neoplasia
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41
Q

C-KIT

A
  • oncogene
  • gene product= cytokine (growth factor) receptor
  • GI stromal tumor
42
Q

Active RAS signal transduction pathway

A
  • RAS —- PI3K —- AKT —– mTOR —–activation of transcription with D-cyclins —- MYC protein
  • RAS —- RAF —- MAPK —- activation of transcription with D-cyclins —- MYC protein
43
Q

tumor suppressor genes

A
  • normally prevent uncontrolled growth
  • mutation or loss leads to transformed cell
  • usually both normal alleles must be damaged
44
Q

RB

A
  • tumor suppressor gene
  • Rb gene product blocks G1–S phase of cell cycle
  • retinoblastoma and osteosarcoma
  • “governor of the cell cycle”
  • retinoblastoma gene (RB) = first tumor suppressor gene discovered and the basis for Knudson’s two-hit hypothesis
  • active RB shuts off E2F which blocks its transcription which would normally activate transcription
  • mutated RB is hyperp-lated and inactive so E2F is free to activate transcription
45
Q

p53

A
  • tumor suppressor gene
  • p53 gene product blocks G1–S phase of cell cycle
  • most human cancers and Li-Fraumeni syndrome
  • “Guardian of the Genome”
  • most commonly mutated gene in cancers
  • in the face of stress, it activates temporary cell cycle arrest (quiescence), induces permanent cell cycle arrest (senescence), and triggers programmed cell death (apoptosis)
  • activates p21 (CDK inhibitor) for G1 arrest and GADD45 for DNA repair. If the repair fails, it activates BAX to apoptose the cell
46
Q

-BRCA1

A
  • tumor suppressor gene
  • gene product: DNA repair protein
  • breast and ovarian cancer
47
Q

BRCA2

A
  • tumor suppressor gene
  • gene product: DNA repair protein
  • Breast cancer
48
Q

retinoblastoma

A
  • intra-ocular neoplasms of children
  • median age at presentation =2 yr
  • poor vision, strabismus, whiteish hue to pupil
  • neuronal origin
  • occurs when kids are born heterozygous for the RB gene and then get a mutation to become KO early in life. When it occurs in adulthood it is caused by multiple mutations
49
Q

Li-Fraumeni syndrome

A
  • patients inherit one defective copy of p53 in the germline
  • one additional hit = 25x greater risk of developing cancer by age 5 (sarcomas, breast cancer, leukemia, brain tumors, adrenal cortex carcinomas, and multiple primary tumors)
50
Q

anti-apoptotic gene examples

A

BCL-2 and BCL-XL

51
Q

pro-apoptotic gene examples

A

BAX and BAK
-antagonize BCL and activate Bax/Bak channels in mitochondria to cause leakage of cytochrome c and other proteins to activate caspases which cause apoptosis

52
Q

Fas

A

-death receptor

53
Q

caspases 8-9

A

-initiates other caspase executioners

54
Q

extrinsic death receptor pathway

A

1) FasL activates the Fas death receptor
2) the Fas receptor activates the procaspase-8 death induced signaling complex to caspase 8
3) caspase 9 activates BID which activates BAX/BAK at the mitochondria
4) stress, radiation, and chemicals induce DNA damage which causes p53 to respond and activate BAX/BAK as well
5) BAX/BAK cause cytochrome c and APAF-1 to leak out and activate Caspase-9
6) If IAP is present, it will inhibit Caspase 9
7) Caspase 9 activates caspase 3 which causes apoptosis

55
Q

What happens if BCL-2 is activated by translocation?

A
  • perpetuation of anti-apoptosis

- follicular B-cell lyphoma

56
Q

What 4 things are needed for neoplasm development?

A
  • loss of growth restraints (and evade apoptosis)
  • development of limitless replicative potential
  • sustained angiogenesis
  • malignant neoplasms develop the ability to evade and metastasize
57
Q

telomeres

A

-short, repeat sequences of DNA
-with each somatic cell duplication, small section isn’t duplicated and telomeres shorten
-DNA ends appear broken
cell cycle arrest

58
Q

telomerase

A

stabilizes telomere length

59
Q

What happens if p53 is KO and telomerase is active?

A

cancer

  • loss of p53 activates salvage and non-homologous end joining pathway causing DNA damage
  • telomerase allows the cell to live forever
60
Q

sustained angiogenesis

A
  • vascularization of neoplasm is necessary for growth
  • get nutrients and oxygen
  • new endothelial cells secrete growth factors like PDGF and insulin-like growth factor
61
Q

angiogenesis inducer

A
  • VEGF
  • hypoxia inducible factor (HIF-1alpha) transcription factor
  • Von Hippel Lindau (VHL) suppressor
62
Q

inhibitor of angiogenesis

A

thrombospondin 1 (TSP-1)

63
Q

homing of cancer

A

certain cancers move to certain organs for unknown reasons
-ex lung cancer often goes to the adrenals. We have a large amount of skeletal muscle in the body but we rarely see cancer there

64
Q

Metastatic Cascade

A

1) Clonal expansion, growth, diversification, and angiogenesis
2) metastatic subclone
3) adhesion to and invasion of the basemement mb
4) passage through the ECM
5) intravasation
6) interaction with host lymphoid cells
7) tumor cell embolus
8) adhesion to basement mb at a new location
9) extravasation
10) metastatic deposit
11) angiogenesis
12) growth

65
Q

sequence of events in the invasion of epithelial basement mbs by tumor cells

A

1) E-cadherins mediate adhesion of epithelial cells to each other, and this function is lost in some cancers which facilitates detachment from primary tumor
2) degradation of basement mb and interstitial CT
3) attachment of cells to ECM proteins
4) migration of tumor cells through degraded basement mb and zones of matrix proteolysis

66
Q

carcinogenic agents

A
  • inflict genetic damage

- chemicals, radiant energy, and microbial agents

67
Q

direct acting chemical carcinogens

A
  • require no metabolic conversion
  • ex cancer chemos (alkylating agents)
  • years down the line, these patients can develop cancer unrelated to the original cancer due to chemo causing mutations
68
Q

indirect acting carcinogens

A
  • require metabolic conversion to become ultimate carcinogens
  • polycyclic hydrocarbons (tobacco, animal fats)
  • aromatic amines (dye and rubber)
  • the susceptibility to cancer possibly depends on the allelic form of the enzyme inherited
69
Q

chemical carcinogens

A
  • react with nucleic acids (RNA, DNA) and/or proteins
  • carcinogenicity may be augmented by agents called promoters
  • some chemical carcinogens may act in concert with viruses or radiation to induce neoplasias
70
Q

promoters

A
  • compounds which are nontumorigenic which facilitate the induction of cell proliferation
  • initiation-promotion sequence
  • there has to be some other cancer promoting mutations present but then the promoter facilitates the development of cancer
71
Q

vinyl chloride

A
  • liver

- angiosarcoma

72
Q

nitrosamine (smoked foods)

A
  • stomach

- gastric

73
Q

asbestos

A
  • lung

- mesotheliom, bronchogenic carcinoma

74
Q

arsenic

A
  • skin

- squamous cell carcinoma

75
Q

naphthalene dyes

A
  • bladder

- urothelial carcinoma

76
Q

aflatoxin B

A
  • liver

- hepatocellular carcinoma

77
Q

sources of radiation carcinogenesis

A
  • sunlight (UV)
  • x-rays
  • nuclear fusion/ionizing radiation
  • fission by-products
  • radionucleotides
78
Q

mechanism of action for ionizing radiation

A
  • chromosome breakage, translocations, point mutations
  • leads to genetic damage and carcinogenesis
  • associated cancer = papillary carcinoma of the thyroid
79
Q

UV light

A
  • damages DNA by forming pyrimidine dimers
  • normally repaired by nucleotide excision repair pathway
  • associated cancers = skin squamous cell, basal cell, and melanoma
80
Q

radiation carcinogenesis

A
  • long latent period
  • radiation initiation is irreversible
  • continued exposure is additive
81
Q

xeroderma pigmentosum

A
  • autosomal recessive syndrome of defective DNA repair
  • defect in nucleotide excision repair pathway
  • markedly increased predisposition to skin cancerr
82
Q

microbial oncogenesis - RNA

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

- T cell leukemia/lymphoma

83
Q

Microbial oncogenesis - DNA

A
  • human papillloma virus- benign warts, cervical cancer
  • epstein barr virus - burkitt lymphoma, nasopharyngeal carcinoma
  • hepatitis B and C virus - hepatocellular carcinoma, chronic inflammatory cells can cause injury to cells that can jumpstart carcinogenesis
84
Q

microbial oncogenesis

bacteria

A

-helicobacter pylori - gastric adenocarcinoma, MALT lymphoma

85
Q

HTLV-1

A
  • infects many T cells and initially causes polyclonal proliferation by autocrine and paracrine pathways triggered by the TAX gene.
  • Simultaneously, TAX neutralizes growth inhibitory signals by affecting TP53 and CDKN2A/p16 genes
  • ultimately, a monoclonal T cell leukemia/lymphoma results when one proliferating T cell suffers additional mutations
86
Q

what Ags are overexpressed in melanomas

A

tyrosinase, gp100, and MART

87
Q

antitumor effector mechanisms

A
  • cytotoxic T lymphocytes
  • NK cells
  • macrophages
  • humoral mechanism: no in-vivo evidence but monoclonal Abs can be therapeutically effective
88
Q

Immunosuppressed patients are at ____ risk for cancer development (and examples)

A
  • increased

- congenital immune deficiences, transplant recipients, AIDs

89
Q

How can cancers evade the immune system

A
  • eliminate strongly immunogenic subclones
  • fail to express HLA class I, escape CTL attack
  • suppress host immune response (secrete TGF- beta, express FasL, and/or activate regulatory T cells)
  • produce thicker coat of glycocalyx molecules blocking access to immune cells
90
Q

effects of tumor on host

A
  • can compress adjacent structures
  • can ulcerate through surfaces
  • can produce hormones
91
Q

cancer cachexia

A
  • loss of body fat, lean body mass
  • weakness, anorexia, anemia
  • cytokine mediated- TNF, proteolysis inducing factor
  • no satisfying treatment if neoplasm can’t be removed
92
Q

paraneoplastic syndrome

A
  • symptom complexes that can’t be readily explained by local or distant spread
  • hormone elaboration not indigenous to tumor parenchyma
93
Q

cancer grading

A
  • based on cytologic differentiation of the tumor cells, an attempt is made to estimate the aggressiveness of the tumor
    1) degree of cellular differentiation
    2) degree of cellular pleomorphism
    3) degree of loss of normal architecture
    4) mitotic index
94
Q

cancer staging

A
  • size of primary tumor (T1.T2, T3, OR T4)
  • extent of spread to lymph nodes = (N0, N1, N2, OR N3)
  • presence or absence of metastasis = (M0, or M1)
  • called the TNM System
  • American Joint Committe (AJC) system uses 0 to IV staging system
95
Q

______ is of greater clinical value. (Either grading or staging)

A

staging

96
Q

which cancers have grading shown particular relevance

A

prostate cancer and chondrosarcoma

97
Q

how do you diagnose cancer? What evidence do you use to make the diagnosis?

A
  • clinical data like HPI, social hx, family hx, ROS, PE
  • radiologic studies contribute significantly
  • tissue sampling
98
Q

tissue sampling in cancer

A
  • should be adequate and representative of lesion

- large excision, small biopsy, fine-needle aspiration, and cytology smears (pap)

99
Q

Scientific methods useful in cancer diagnosis

A
  • histologic and cytologic examination
  • immunohistochemistry
  • biochem studies
  • ultrastructural studies (electron microscopy)
  • molecular bio studes
100
Q

Alpha-fetoprotein (AFP)

A

-tumor marker for liver carcinomas, tumor of yolk sac remnants, and gonadal tumors

101
Q

carcinoembyonic antigen (CEA)

A

-tumor marker for colon, pancreas, lung, stomach, and breast

102
Q

tumor markers are generally more valuable for detecting ______ of disease

A

recurrence (rather than primary diagnosis)

MHD Exam 1 (6 decks)

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