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TCM Exam 3 > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Types of tumors

A

Benign tumor – does not usually kill (name usually ends in “-oma”)
Malignant tumor – has the potential to kill (naming varies)

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2
Q

2 components of tumors

A

All tumors, benign and malignant, have two basic components
(1) Parenchyma, made up of transformed or neoplastic cells
Clonal = entire parenchyma of neoplasm arises from one genetically altered cell
(2) Stroma, host-derived, non-neoplastic supporting tissue
Scirrhous desmoplastic reaction – rock hard stroma

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3
Q

Cancer

A

a malignant neoplasm

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4
Q

Carcinoma

A

epithelial malignant neoplasm

Exception: Carcinoma in situ lacks the potential to cause metastasis

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5
Q

Melanoma

A

a melanocytic malignant neoplasm

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6
Q

Blastoma

A

tumor composed of very immature undifferentiated cells (usually malignant) resembling fetal blastemal tissue in anlage (e.g. nephroblastoma)

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7
Q

development of a cancer

A 
normal cell.  
Initiating mutation (carcinogen induced)

Initiated precursor with stem cell-like properties

mutation affecting genomic integrity–>

Precursor with mutator phenotyp

additional driver mutations –>

Founding cancer cell

additional mutations, emergence of subclones –> genetically heterogeneous cancer

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8
Q

Benign vs Malignant (epithelial origin)

A

stratified squamous: Squamous cell papilloma vs. Squamous cell carcinoma
Basal cells- malignant is a basal cell carcinoma

Epithelial lining of glands or ducts: Adenoma / papillloma vs Adenocarcinoma

Liver cells: hepatic adenoma vs. hepatocellular carcinoma = hepatoma

Urinary tract epithelium: malignant is transitional cell carcinoma

Placental epithelium: hydatiform mole vs choriocarcinoma

testicular epithelium (germ cells) : malignant is seminoma

Tumors of melanocytes: melanocytic nevus vs. malignant melanoma

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9
Q

tumors, benign vs. malignant, of mesenchymal origin

A

Fibroma vs. Fibrosarcoma
Lipoma vs Liposarcoma
Chondroma vs. Chondrosarcoma
Osteoma vs. Osteogenic sarcoma

blood vessels: Hemangioma vs angiosarcoma

lymph vessels: lymphangioma vs. lymphangiosarcoma

mesothelium: benign fibrous tumr vs. mesothelioma

brain coverings: meningioma vs. invasive meningioma

Hematopoietic cells- malignant is leukemia

lymphoid tissue- malignant is leukemia & lymphoma

Muscle (smooth): Leiomyoma vs Leiomyosarcoma

muscle (striated): rhabdomyoma vs Rhabdomyosarcoma

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10
Q

gross appearance of polyps

A

tubular adenomy vs villous (finger-like) adenoma, e.g.

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11
Q

leiomyoma

A

is the same as the old term “uterine fibroid”

it is benign but has nothing to do with fibrous tissue

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12
Q

what is the key that tells you it is carcinoma/ malignant?

A

it’s invading

tissue loses organization

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13
Q

pleomophic adenoma

A

benign mixed tumor of salivary origin. From one germ cell layer.

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14
Q

Wilms tumor

A

nephroblastoma

derived from renal anlage

malignant

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15
Q

more than one neoplastic cell type

A

teratogenous = derived from more than one germ cell layer

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16
Q

Benign teratogenous tumor

A

mature cystic teratoma (dermoid cyst)

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17
Q

malignant teratogenous tumor

A

immature teratoma, teratocarcinoma

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18
Q

teratoma

A

A tumor arising from Totipotential Germ Cells which have the capacity to differentiate along the three germ layers:
Endoderm (ex.-gut and lung epithelium)
Ectoderm (ex.-skin, parathyroid glands epithelium)
Mesoderm (ex-fat, renal epithelial tubules)

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19
Q

Mature teratoma

A

(benign)
All tissues are mature
Dermoid cyst – mature cystic teratoma of ovary
Monodermal teratoma - contains a single tissue type (struma ovarii)

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20
Q

Immature teratoma

A

(malignant)
Elements of immature tissue (immature cartilage, immature neural tissue)
Regarded as malignant
Can be only one immature element

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21
Q

Malignant teratoma

A

Malignancy (carcinoma, sarcoma, etc.) arising within mature teratoma

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22
Q

Ectoderm deriatives

A

Epidermis & hair, skin, nails, etc.

Brain and nervous system, neuroendocrine cells, melanocytes

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23
Q

Mesoderm derivatives

A

notochord

somites–> muscle, outer covering of internal organs, excretory system, gonads

mesenchyme –> dermis, circulatory system, bones and cartilage

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24
Q

endoderm derivatives

A

embryonic gut –> inner lining of digestive tract, glands including liver and pancreas, inner lining of respiratory tract

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25
Q

Teratoma sites

A

Ovary and Testis

Midline of the body: pineal body, base of skull, mediastinum (anterior), retroperitoneal, sacroccocygeal

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26
Q

Immature Teratoma

A

Immature mesenchyme, neural and/or blastemal elements

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27
Q

Malignant Teratoma

A

Carcinoma, sarcoma and/or germ cell malignancy in teratoma

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28
Q

Hamartoma

A

A benign non-neoplastic tumor-like malformation resulting from faulty development in an organ and composed of abnormally arranged tissue elements normally present in that organ
e.g. pulmonary hamartoma

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29
Q

Choristoma

A

Congenital heterotopic (ectopic) rest of cells (tissue)
Not a neoplasm
Normal tissue in an abnormal location

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30
Q

Cowden Syndrome

A

Part of the PTEN hamartoma tumor syndrome (PTHS)

Autosomal dominant genetic disorder 
Multiple hamartomas (usually skin and thyroid)

Additional growths in many parts of the body

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31
Q

Hyperplasia

A

increase in number of cells/proliferation cells.
May result in the gross enlargement of an organ
+/- cytologic atypia

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32
Q

Metaplasia

A

the potentially reversible replacement of one differentiated cell type with another cell type

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33
Q

Dysplasia

A

Abnormal development or growth of tissues, organs, or cells

expansion of immature cells is often indicative of an early neoplastic process

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34
Q

What does eosinophilic esophagitis look like?

A

can show furrows (rings) in the mucosa

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35
Q

types of squamous epithelial dysplasia and where they occur

A

low grade/ mild

high grade/ moderate

high grade/ severe/ CIS

This can occur in any normal or metaplastic squamous epithelium at any body site
e.g. cervix, anus, oral cavity, skin, bronchus, etc.

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36
Q

characteristics of malignant neoplasia

A

Decreased differentiation and anaplasia
Higher rate of growth
Local invasion
Metastatic potential

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37
Q

Comparisons between Benign and Malignant Tumors: differentiation/ anaplasia

A

benign is well differentiated

malignant- some lack differentiation

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38
Q

Comparisons between Benign and Malignant Tumors: rate of growth

A

benign: usually progressive and slow;

mitotic figures rare and normal

malignant: slow to rapid; mitotic figures may be numerous and abnormal

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39
Q

Comparisons between Benign and Malignant Tumors: local invasion

A

benign: usually do not invate
malignant: locally invasive, infiltrating

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40
Q

Comparisons between Benign and Malignant Tumors: metastasis

A

benign: absent
malignant: frequent

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41
Q

an important exception to the comparison between benign and malignant tumors

A

Some malignant neoplasms are relatively bland looking resembling benign tissues

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42
Q

How do we determine when there is a malignancy (cancer)?

A

When the lesion has the potential to metastasize and cause death”

i.e. When the characteristics of the lesion are similar to those of other lesions previously noted to have metastasized and caused death!

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43
Q

Differentiation

A

Differentiation - how closely the tumor cells resemble the corresponding normal parenchymal cells

Well-differentiated – closely resembles normal
Moderately-differentiated – sort of resembles normal
Poorly-differentiated – does not resemble normal
Undifferentiated - The tissue of origin cannot be determined based on the histopathologic appearance of the neoplasm

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44
Q

Anaplasia

A

– lack of differentiation

Implies “dedifferentiation”, or loss of the structural and functional differentiation of normal cells
Cells appear more bizarre
Almost always indicative of malignancy

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45
Q

Anaplastic cells show

A

Pleomorphism - marked variation in size and shape of the cells and/or nuclei.

Abnormal nuclear morphology -hyperchromatic, large nuclei, bizarre nuclear shapes, prominent nucleoli

Increased mitotic activity, and atypical mitoses

Loss of polarity - cellular orientation is markedly disturbed from normal

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46
Q

Benign vs. Malignant tumors: cell size, mitotic rate, symmetry, margins, necrosis

A

Benign: sized 2-5x normal, normal or up to 2-3x increase mitotic rate, symmetric, circumscribed margins, necrosis is uncommon

Malignant: 2-100x normal cell size, 2-20x increase in mitotic rate with atypical mitoses, asymmetric, indistinct margins, necrosis is common

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47
Q

Features of Malignancy

A

Hyperchromaticity
Marked increase in DNA content per nucleus (more intense staining by Hematoxylin (H of H&E)

Desmoplasia
Increased fibrous tissue surrounding invading parenchymal cells

Angiogenesis
Increased blood vessels
Ischemic tumor necrosis occurs with insufficient angiogenesis
Neo-angiogenesis
Vessels sprout from existing capillaries
Vasculogenesis
Endothelial cells are recruited from the bone marrow

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48
Q

carcinomas and capusles/ invasion

A

Carcinomas have no capsules or invasion of parenchyma through the tumor capsule

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49
Q

Grading Neoplasms

A

Histologic grade - essentially differentiation (anaplasia)

Nuclear grade – essentially pleomorphism (bizarreness)

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50
Q

Alterations in Malignant Transformation

A

Self-sufficiency in growth signals

Oncogene activation with oncoprotein production (gain of function)

Insensitivity to growth-inhibitory signals

Evasion of apoptosis

  • p53 and other tumor suppressor gene inactivation (loss of function)
    Activation of anti-apoptotic genes (gain of function)
    Inactivation of apoptotic genes (loss of function)

Limitless replicative potential

Sustained angiogenesis

Ability to invade and metastasize

Defects in DNA repair
- May fail to repair DNA damage (loss of function)

Alterations in cell metabolism (e.g. Warburg effect)

Ability to evade host immune response

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51
Q

EGF-receptor family

ERBB1 (EGFR) and ERRB2(HER)

A

Adenocarcinoma of lung

Breast carcinoma

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52
Q

receptor for neurotrophic factors: RET

A

Multiple endocrine neoplasia 2A and B

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53
Q

KIT

A

GI stromal tumors

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54
Q

ALK

A

Adenocarcinoma of the lung

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55
Q

KRAS

A

Colon, lung, and pancreatic tumors

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56
Q

NRAS

A

Melanomas, hematologic malignancies

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57
Q

GNAS

A

Pituitary adenoma, other endocrine tumors

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58
Q

ABL

A

Chronic myeloid leukemia

Acute lymphoblastic leukemia

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59
Q

BRAF

A

Melanomas

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60
Q

JAK2`

A

Myeloproliferative disorders

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61
Q

C-MYC

A

Burkitt lymphoma

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62
Q

N-MYC

A

Neuroblastoma

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63
Q

L-MYC

A

Small-cell carcinoma of the lung

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64
Q

CCND1 (Cyclin D)

A

Mantle cell lymphoma

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65
Q

PAX Genes acting as proto-oncogenes

A

PAX 3 and PAX 7- embryonal rhabdomyosarcoma

PAX 5- b-cell leukemias/ lymphomas

PAX 8 - renal, thyroid and ovarian carcinomas

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66
Q

Chronic myelogenous leukemia genes

A

(9;22)(q34;q11)/BCR-ABL

Affected genes:
ABL 9q34
BCR 22q11

67
Q

Burkitt lymphoma genes

A

translocation: (8;14)(q24;q32)

Affected gnese: c-MYC 8q24
IGH 14q32

68
Q

Ewing arcoma genes

A

translocation: (11;22)(q24;q12)

affectd genes: FL1 11q24
EWSR1 22q12

69
Q

Mutations: CDK4; D cyclins

A

Form a complex that phosphorylates RB, allowing the cell to progress through the G1 restriction point

70
Q

Mutations: INK4/ARF family (CDKN2A-C)

A

(cell cycle inhibitor)

p16/INK4a binds to cyclin D-CDK4 and promotes the inhibitory effects of RB

p14/ARF increases p53 levels by inhibiting MDM2 activity

71
Q

Mutations: RB

A

Tumor suppressive “pocket” protein that binds E2F transcription factors in its hypophosphorylated state, preventing G1/S transition; also interacts with several transcription factors that regulate differentiation

72
Q

Mutations: p53

A

Tumor suppressor altered in the majority of cancers; causes cell cycle arrest and apoptosis. p53 is required for the G1/S checkpoint and is a main component of the G2/M checkpoint.

73
Q

NF1 gene

A

Neurofibromatosis type 1

74
Q

NF2

A

Neurofibromatosis type 2

75
Q

PTCH

A

Gorlin syndrome (familial)

basal cell carcinoma (sporadic cancer)

76
Q

PTEN

A

Cowden syndrome

77
Q

RB

A

Retinoblastoma; osteosarcoma

78
Q

VHL

A

Von Hippel Lindau syndrome

sporadic cancer: renal cell carcinoma

79
Q

E-cadherin

A

protein

Gastric carcinoma, lobular breast carcinoma

80
Q

TP53 gene

A

protein: p53

Li-Fraumeni syndrome (diverse cancers)

81
Q

BRCA1, BRCA2

A

Familial breast and ovarian carcinoma

82
Q

WT1

A

Wilms tumor

83
Q

MEN1

A

Multiple endocrin neoplasia-1

sporadic cancers: pituitary, parathyroid, and pancreatic endocrine tumors

84
Q

Rate of growth

A

Rate of tumor growth - determined by three main factors
Doubling time of tumor cells
Fraction of tumor cells in the replicative pool
Rate at which cells are shed/die

85
Q

doubling of neoplastic cells and clinical detection

A

30 doublings –> 1 gm. 10 to the 9th cells, which is the smallest clinically detectable mass.

86
Q

Mechanisms by which tumors evade the immune system

A

T cell recognition of tumor antigen leading to T cell activation

Lack of T cell recognition of tumor

Lack of T cell recognition of tumor

Inhibition of T cell activation

87
Q

Warburg Effect

A

metabolic alterations

Also known as aerobic glycolysis

Tumor cells shift their glucose metabolism away from the oxygen hungry mitochondria to aerobic glycolysis leading to lactose (fermentation)

Mode of glycolysis allows visualization of tumors via positron emission tomography (PET)

88
Q

Differences Between Oxidative Phosphorylation, Anaerobic Glycolysis, and Aerobic Glycolysis

A

Oxidative phosphorylation-
Produce CO2 and 36 mol ATP/1 mol glucose

Anaerobic glycolysis-
Produce lactate and 2 mol ATP/1 mol glucose

Aerobic glycolysis -
Warburg observed that cancer cells tend to convert most glucose to lactate regardless of whether oxygen is present (aerobic glycolysis/fermentation via the glycolytic pathway)

95% of glucose used to produce metabolic intermediates used in synthesis of cellular components & 4 mol ATP/1 mol glucose

89
Q

what unequivocally marks a tumor as malignant?

A

Metastasis unequivocally marks a tumor as malignant because “benign tumors do not metastasize”
However benign conditions can “spread”

Local invasion is a less reliable indicator of malignancy

90
Q

local invasion by malignant tumors

A

Infiltrate, invade, destroy adjacent tissue
Metastasize to other parts of body
Not (or incompletely) encapsulated

91
Q

Metastasis

A

Tumor implants discontinuous with the primary tumor

Patterns of metastasis:
- Direct seeding of body cavities or surfaces

Lymphatic spread
- Transport through the lymphatics to lymph nodes
Sentinel Lymph Nodes

Hematogenous spread

  • Portal blood supply drains to the liver
  • Caval blood travels to the lung
  • Hepatic, renal, and adrenocortical cancer propagate in veins
92
Q

Mechanisms of metastasis development within a primary tumor.

A

A, Metastasis is caused by rare variant clones that develop in the primary tumor.

B, Metastasis is caused by the gene expression pattern of most cells of the primary tumor, referred to as a metastatic signature.

C, A combination of A and B, in which metastatic variants appear in a tumor with a metastatic gene signature.

D, Metastasis development is greatly influenced by the tumor stroma

93
Q

The metastatic cascade

A

Changes (“loosening up”) of tumor cell-cell interactions
Degradation of ECM
Attachment to ECM components
Migration (locomotion ) of tumor cells
Clumping in vessels
Adhesion to the endothelium
Egress through the vascular basement membrane

94
Q

Batson (Paravertebral) Veins /Plexus

A

Venous connections that extend from pelvis to the skull along the vertebral column
Important in dissemination of some metastatic cancers throughout the spine
Classic for prostatic cancer, but similar for renal, breast, rectal and bladder cancers

95
Q

Sentinal lymph nodes

A

Inject vital dye and/or radioactive tracer into tumor or biopsy cavity and follow flow to lymphatics to the sentinel node(s)
Originally developed for skin melanomas
Now used for lots of cancers, especially breast cancer

96
Q

Cancer Cachexia

A

Marasmus-like protein-energy malnutrition

97
Q

Paraneoplastic Syndromes

A

Symptom complexes that cannot readily be explained by
Local or distant spread of the tumor or
By the elaboration of hormones indigenous to the tissue from which the tumor arose

Symptoms from
Products produced by the tumor cells (e.g. hormones) or
Immune reaction of the body to the tumor cells (e.g. myasthenia gravis with neoplasms of the thymus)

Occurs in ~10% of persons with malignant disease

98
Q

cancer related to cushing syndrome

A

small cell carcinoma of the lung

ACTH is the causal mechanism

99
Q

cancer related to syndrome of inappropriate antidiuretic hormone secretion (SIADH)

A

small cell carcinoma of lung

causal mechanism: Antidiuretic hormone

100
Q

cancer related to hypercalcemia

A

squamous cell carcinoma of lung

causal mechanism: parathyroid hormone-related protein (PTHRP), TGF-alpha, TNF, IL-1

101
Q

cancer related to polycythemia

A

gastric carcinoma
renal carcinoma

causal mechanism: erythropoietin

102
Q

causal mechanism of carcinoid syndrome

A

causal mechanism: serotonin, bradykinin

103
Q

Carcinoid syndrome

A

Heart:

  • pulmonic and tricuspid valve thickening and stenosis
  • endocardial fibrosis

Liver: hepatomegaly

GI: diarrhea, cramps, nausea, vomiting

Skin: cutaneous flushes, apparent cyanosis

Respiratory: cough, wheezing, dyspnea

Retroperitoneal and pelvic fibrosis

104
Q

Paraneoplastic syndrome: myasthenia

A

from tymic neoplasms

105
Q

Paraneoplastic syndrome: acanthosis nigricans

A

from Gastric carcinoma
Lung carcinoma
Uterine carcinoma

causal mechanism: immunological; secretion of epidermal growth factor

106
Q

paraneoplastic syndrome: dermatomyositis

A

bronchogenic or from breast carcinoma

causal mechanism: immunological

107
Q

paraneoplastic syndrome: venous thrombosis (Trousseau phenomenon)

A

from pancreatic carcinoma

causal mechanism: tumor products (mucins that activate clotting)

108
Q

paraneoplastic syndrome: disseminated intravascular coagulation

A

from acute promyelocytic leukemia and prostatic carcinoma

causal mechanism: tumor products that activate clotting

109
Q

paraneoplastic syndrome: nonbacterial thrombotic endocarditis

A

from advanced cancers

causal mechanism: hypercoagulability

110
Q

Incidence

A

probability of being diagnosed with a disease during a given period of time
Number of new cases of a disease divided by the number of persons at risk
Usually expressed as new cases/year per 100,000 population

111
Q

Morbidity

A

= illness

Indicated by prevalence

112
Q

Prevalence

A

the total number of cases of disease existing in a population
Total number of cases of a disease existing divided by the total population
Usually expressed as total cases per 100,000 persons

113
Q

mortality

A

= death

114
Q

mortality rate

A

number of deaths divided by the total population

Indicated by deaths per year per 100,000 people

115
Q

cancer and age

A

Carcinomas tend to occur in the later years of life (>55 years)
Main cause of death ♀40 to 79 and ♂ 60 to 79
~10% of all deaths in children ˂ 15
Common childhood cancers are significantly different from adults
Acute leukemia and primitive neoplasms of the central nervous system are responsible for approximately 60% of childhood cancer deaths
The common neoplasms of infancy and childhood are “small round blue cell tumors”
Neuroblastoma
Wilms tumor (nephroblastoma)
Retinoblastoma
Acute leukemias/lymphomas

116
Q

cancer and chimney sweeps

A

In 1775 London surgeon Sir Percival Pott attributed scrotal skin cancer in chimney sweeps to chronic exposure to soot

note: NOT testicular cancer

117
Q

The change in incidence of various cancers with migration from Japan to the United States

A

provides evidence that the occurrence of cancers is related to components of the environment that differ in the two countries.

118
Q

alkylating carcinogens include

A

anticancer drugs. Cause many cancers, especially leukemias

119
Q

Procarcinogens that require metabolic activation

A

polycyclic and heterocyclic aromatic hydrocarbons
aromatic amines, amides, azo dyes
natural plant and microbial products:
** Aflotoxin B1 (Liver cancer via p53 inactivation)
** Betel nuts (oral cancer)

120
Q

Occupational cancers from arsenic and arsenic compounds

A

skin carcinoma, (lung)

121
Q

occupational cancers from asbestos

A

Lung, esophageal, gastric, and colon carcinoma; mesothelioma

from construction, brake linings, floor tiles

122
Q

occupational cancers from benzene

A

acute myeloid leukemia

123
Q

occupational cancers can also come from…

A

beryllium and beryllium compounds
cadmium and cadmium compounds
chromium compounds
nickel compounds

124
Q

cancer related to radon and its decay products

A

lung carcinoma

from decay of minerals containing uranium, hazard in quarries and underground mines

125
Q

cancer from vinyl chloride

A

hepatic angiosarcoma

from monomer for vinyl polymers (PVC industry)
note– it’s not from PVC itself

126
Q

Radiation carcinogenesis

A

Ultraviolet Rays–>
Nonmelanoma (squamous cell/ basal cell) skin cancers (total cumulative exposure)

Melanomas (sunbathing)

Ionizing radiation (Electromagnetic or particulate)

127
Q

Oncogenic RNA viruses

A

HTLV-1–> adult T-cell leukemia/ llymphoma

HCV–> hepatocellular carcinoma

128
Q

Oncgenic DNA viruses

A

HBV–> hepatocellular carcinoma
HPV –> carcinomas of cervix, anus, penis & oropharynx (types 16 & 18); papillomas
HHV-8–> Kaposi sarcoma & primary effusion lymphoma
EBV–> Burkitt lymphoma, Hodgkin lymphoma& nasophryngeal carcinoma

129
Q

oncogenic fungi

A

aspergillus- aflotoxin B1–> hepatocellular carcinoma (p53 mutation)

130
Q

oncogenic parasites

A

schistosoma haematobium–> bladder cancer

131
Q

oncogenic bacteria

A

H. pylori–> extranodal marginal zone (MALT) lymphoma and gastric adenocarcinoma

132
Q

Genetic Predisposition To Cancer

A

Large # of cancer types have combined environmental influences and hereditary predispositions
2 hit theory
Hit 1 in first mutated gene (abnormal) is inherited
Hit 2 in second mutated gene (originally normal) is acquired

Genes associated with hereditary cancers are generally also involved in the much more common sporadic forms of the same tumor

133
Q

Defective DNA Repair- autosomal recessive

A

xeroderma pigmentosa
ataxia telangiectasia
bloom syndrome
fanconi anemia

134
Q

Xeroderma pigmentosa

A

Nucleotide excision repair abnormality associated with extreme sensitivity to ultraviolet (UV) rays affects the eyes and skin (cancers), may also have CNS problems (increased pyrimidine dimers)

135
Q

Ataxia telangiectasia

A

ATM gene defect (involved in DNA repair) associated with progressive difficulty with coordinating movements, weakened immune system, leukemias and lymphomas

136
Q

Bloom syndrome

A

Helicase abnormality associated with short stature, sun-sensitive skin changes, an increased risk of cancer, and other health problems

137
Q

Fanconi anemia

A

FA process defects associated with aplastic anemia, hypopigmentation, café-au-lait spots, skeletal problems, defects of the genitourinary tract; gastrointestinal tract; heart; eye and ears with hearing loss and acute myeloid leukemia

138
Q

Hereditary nonpolyposis colorectal cancer (HNPCC) = Lynch syndrome

A

autosomal DOMINANT

DNA mismatch repair abnormality leading to microsatellite instability associated with colorectal, endometrial, gastric, ovarian, ureteral, CNS, small bowel, hepatobiliary tract and skin cancers

139
Q

inherited cancer syndromes

A

Usually a point mutation in a single allele of a tumor supressor gene
The second event incite tumorigenesis involve a second mutation in the other remaining previously normal allele

140
Q

nonhereditary predisposing conditions

A

chronic inflammation

Precancerous conditions: repair leads to cellular dysplasia

  • leukoplakia (oral cavity, vulva, penis)
  • adenomatous polyps
  • solar keratosis
141
Q

asbestosis –>

A

meothelioma, lung carcinoma

142
Q

inflammatory bowel disease –>

A

colorectal carcinoma

143
Q

lichen sclerosus et atrophicus –>

A

vulvar squamous cell carcinoma

144
Q

chronic pancreatitis –>

A

pancreatic carcinoma

can be related to alcoholism

145
Q

chronic or recurrent bronchitis –>

A

lung carcinoma,

agents: asbestos, smoking

146
Q

reflux eophagitis, barrett esophagus –>

A

esophageal carcinoma

agent: gastric acids

147
Q

Sjogren syndrome, hashimoto thyroiditis, H. pylori gastritis –>

A

MALT lymphoma

148
Q

agent associated with cholangiocarcinoma

A

liver flukes (Opisthorchis viverrini)

149
Q

gastritis/ ulcers –>

A

gastric adenocarcinoma, MALT

agent: h. pylori

150
Q

hepatitis –>

A

hepatocellular carcinoma

agent: hep B and/ or C virus

151
Q

osteomyelitis –>

A

carcinoma in drainingn sinuses

152
Q

agent involved in cervical carcinoma

A

HPV

153
Q

agent involved in bladder carcinoma

A

schistosoma haematobium

154
Q

grading and staging of tumors

A

Grading of a cancer is based on the degree of differentiation of the tumor cells and, in some cancers, the number of mitoses or architectural features

Staging of cancers is based on the size of the primary lesion, its extent of spread to regional lymph nodes, and the presence or absence of blood-borne metastases
The major staging system currently in use is the American Joint Committee on Cancer Staging.
T for primary tumor
N for regional lymph node involvement
M for metastases

155
Q

most important prognostic indicator

A

stage

156
Q

skin lethality

A

melanoma more likely to be lethal

basal cell carcinoma less likely to be lethal

157
Q

thyroid lethality

A

undifferentiated carcinoma of the thyroid more likely to be lethal

papillary carcinoma of the thyroid less likely to be lethal

158
Q

breast lethality

A

infiltrating ductal carcinoma of the bresat more likely to be lethal

tubular carcinoma of the breast less likely to be lethal

159
Q

leukemia lethality

A

acute leukemia more likely to be lethal

chronic lymphocytic leukemia less likely to be lethal

160
Q

bladder cancer lethality

A

grade III papillary transitional cell carcinoma of the bladder more likely to be lethal

grade 1 less likely

161
Q

lung lethality

A

small cell carcinoma of the lung more likely to be lethal

carcinoid tumor of the lung less likely to be lethal

162
Q

fibrosarcoma lethality

A

retroperitoneal fibrosarcoma more likely to be lethal

subcutaneous fibrosarcoma less likely to be lethal

163
Q

clinical endometrial cancer staging

A 
stage 2- the cancer has grown into the cervix
stage 3a- spread to ovary
3b- has spread into the vagina
3c- spread into the lymph nodes
stage 4a- in bladder or bowel
4b- in other organs
164
Q

cytology sampling

A

Exfoliative-the microscopic examination of desquamated cells for diagnostic purposes. The cells are obtained from lesions, sputum, secretions, urine, and other material by aspiration, scraping, a smear, or washings of the tissue

Aspiration biopsy cytology (ABC)-the microscopic study of cells obtained from superficial or internal lesions by suction through a fine needle.

TCM Exam 3 (10 decks)

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