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Pathology > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Neoplasia

A

Process of uncontrolled growth. Accumulation of cells d/t proliferation and/or evasion of apoptosis

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2
Q

Neoplasm / Tumor

A

Abnormal mass of tissue. Growth exceeds and is uncoordinated w/ normal tissue. Persists in same excessive manner after cessation of stimuli which evoked the change.

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3
Q

What are the features of neoplasms?

A

Progressive, purposeless, pathological proliferation of cells. Loss of cell division control. DNA damage at growth control genes “checkpoints” is central. Carcinogens → DNA damage → Neoplasm
Too much proliferation, not enough apoptosis.

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4
Q

Benign Tumor

A

Neoplasm that grows w/o invading adjacent tissue / spreading to distant sites (metastasis). Usually well-circumscribed (w/ a lack of invasion). Generally amenable to local surgery. Well differentiated

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5
Q

Malignant Tumors

A

Neoplasm that invades surrounding tissue. Usually spreads to distant sites (metastasis). Well or poorly differentiated.

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6
Q

Intermediate Tumor

A

Locally invasive tumor. Not benign but w/ no tendency for metastasis. (Locally malignant)

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7
Q

Carcinoma in Situ

A

Dysplasia. Pre-invasive cell proliferation. Cytological features of malignancy. Cell morphology looks abnormal.

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8
Q

A neoplasm is composed of parenchyma and stroma. What are the components / function of the parenchyma?

A

Comprised of clonal neoplastic cells, this determines its biologic behavior. Tumor derives its name based on the parenchymal component. (neoplastic cells / tumor cells) Morphology: large nuclei, disordered arrangement

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9
Q

A neoplasm is composed of parenchyma and stroma. What are the components / function of the stroma?

A

Comprised of CT, blood vessels, macrophages, lymphocytes (tumor infiltrating lymphocytes - TILs). These cells determine the growth and evolution of the tumor. Scant stroma = soft/fleshy tumor.

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10
Q

Desmoplasia / Scirrhous

A

Hyperplasia of activated fibroblasts. Collagen deposition, stains blue color w. trichrome stain.
Abundant collagenous stroma in a tumor/neoplasm. This makes the tumor feel stony hard = (Scirrhous)
Prostate / Breast cancers

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11
Q

Adenoma

A

Epithelial Tissue, Benign, Glandular

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12
Q

Papilloma

A

Epithelial Tissue, Benign, Non-glandular
Benign epithelial tumors from surface lining, based on gross appearance. Tumor of squamous, transitional, ductal epithelium. Finger-like / warty projections from epithelial surfaces - branching pattern.

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13
Q

Carcinoma

A

Epithelial Tissue, Malignant

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14
Q

-oma suffix

A

Mesenchymal Tissue, Benign

Exceptions: granuloma, hematoma, hamartoma, choristoma

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15
Q

-sarcoma suffix

A

Mesenchymal Tissue, Malignant

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16
Q

Cystadenomas

A

Adenomas w/ cavities or cysts

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17
Q

Polyp

A

Club-shaped growth. Benign epithelial tumor/hyperplasia. Projects from mucosal surface into lumen of a hollow viscus. Rarely malignant. Polyp describes the shape/appearance.

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18
Q

Choristoma

A

Tumor-like condition. Normal tissue located in the wrong place. The rest of one tissue is ectopic (in a foreign place).

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19
Q

Hamartoma

A

Tumor-like condition. Non-neoplastic tumor-like lesion w/ DISORGANIZED and HAPHAZARD growth of tissues normally found at a given site. Right tissue in the right place, just disorganized. Example: pulmonary hamartoma = “jumbled” cartilage, bronchial epithelia, CT
Coin Lesion: firm/descrete, often calcified, <2cm

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20
Q

General features of carcinomas / sarcomas (malignant neoplasms)

A

Capsule generally absent, rapid growth, invasion present, atypical mitosis present

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21
Q

General features of benign tumors

A

Capsule generally present, slow growth, invasion absent, no atypical mitosis seen

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22
Q

Lymphoma

A

Cancer derived from lymph nodes or lymphoid tissue. Most are non Hodgkin’s lymphoma. Stomach is most common extranodal site for a primary malignant lymphoma.

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23
Q

Leukemia

A

Cancer derived from bone marrow stem cells. CLL (chronic lymphocytic leukemia) is most common in adults (and in general). ALL is the most common childhood leukemia and cancer.

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24
Q

Teratoma

A

Tumor composed of more than one parenchymal cell type. But Monoclonal - begins w/ only one cell. Derived from more than one germ layer. Tissue of origin: totipotent cells (gonads). Mature teratoma = dermoid cyst. Immature = teratocarcinoma

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25
Q

Peutz-Jeghers Syndrome

A 
Type of Hamartoma
Hereditary Intestinal Polyposis Syndrome
Autosomal dominant genetic disease
Benign hamartomatous polyps in GI tract + hyperpigmented macules (lips & oral mucosa)
[black patches in lips/mouth]
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26
Q

Monoclonality

A

Origin of tumors from a single precursor cell
All neoplasms are monoclonal: both benign and malignant tumors derive from single precursor cell. New subclones arise from the descendants of original cell by multiple mutations.
Non-neoplastic proliferations are polyclonal

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27
Q

Criteria to differentiate benign vs malignant neoplasm

A

Differences based on appearance and behavior
Criteria:
1. Rate of growth
2. Differentiation and anaplasia (no differentiation)
3. Local Invasion
4. Metastasis

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28
Q

% of cells that are in S phase of cell cycle. Distinguish b/t normal tissue, malignant neoplasm, benign neoplasm

A

Normal Tissue: 1%
Benign Neoplasm: 1 - 10%
Malignant Neoplasm: 20 - 80%

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29
Q

Neoplasm Increased Growth Rate: Doubling Time

A

30 doublings = 1g

10 more doublings = 1kg

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30
Q

Neoplasm Increased Growth Rate: Fraction of tumor cells in proliferative pool

A

% of cells in S phase
Submicroscopic phase: higher growth fraction.
Later stages: low growth fraction <20%

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31
Q

Neoplasm Increased Growth Rate: Cell production vs cell loss

A

High growth fraction = grow rapidly

Low growth fraction = grow slowly

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32
Q

PCNA & Ki-67

A

PCNA = proliferating cell nuclear antigen score
Ki-67
Both used as markers for cellular proliferation (mitotic activity)
If low = decreased proliferation
If high = cell will proliferate

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33
Q
  1. Well-differentiated tumor
  2. Moderately differentiated tumor
  3. Poorly differentiated tumor
  4. Anaplastic / Undifferentiated tumor
A
  1. Benign
  2. Benign/malignant
  3. Malignant/benign - poor resemblance to normal tissue
  4. Complete lack of differentiation (structural & functional)Anaplasia is hallmark of high grade malignant tumor
    No resemblance to normal tissue, high met potential
    May only be ID’d by expression of cell markers / cytological findings.
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34
Q

Three factors that help you recognize CELLULAR ATYPIA

A

Seen only in pre-malignant and malignant tumors. Recognized by: 1. cellular pleomorphism 2. nuclear changes: nuclear/nucleolar pleomorphism, dense/irregular outline, hyperchromicity
3. (1:1 N/C ratio) (normal = 1:5)

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35
Q

Pleomorphism

A

Variation in size & shape of cells & nuclei

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36
Q

Hyperchromasia

A

Abundant DNA Extremely dark staining

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37
Q

Nucleus-to-cytoplasm ratio

A

Normally 1:5

Increased ratio 1:1 or 1:2

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38
Q

Cytologic features of anaplasia or poorly differentiated tumors

A

Nuclear & cellular pleomorphism, hyperchromatic nucleus, ↑N/C ratio, prominent nucleoli, abundant & atypical mitoses, bizarre tumor giant cells, loss of tissue architecture/function, more agressive

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39
Q

What are tumor giant cells and what is their significance?

A

Tumor giant cells represent anaplasia. Single huge polymorphic nucleus or > 2 nuclei. Hyper-chromatic and large nuclei.

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40
Q

What is the significance of recognizing anaplasia?

A

Presence of anaplasia implies a poorly differentiated neoplasia. More aggressive tumor w/ poorer prognosis.

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41
Q

Abnormal mitotic figures

A

Cell is proliferating. Key is that they are not the normal shape! Does not mimic any normal figures in prophase, metaphase, telophase. Mitoses alone don’t define malignancy, but the more abnormal the mitoses, the more likely the neoplasm is malignant.

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42
Q

Two important factors in tumor angiogenesis

A

VEGF & FGF

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43
Q

Pro-Angiogenic Factors (Angiogenic Factors)

A

VEGF
bFGF
HIF

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44
Q

Anti-angiogenic factors

A

Thrombospondin-1
Angiostatin
Endostatin
Tumstatin

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45
Q

How big can a tumor get w/o angiogenesis?

A

2mm is max size: limited by the ability of nutrients to diffuse into it. Produces tumor angiogenic factors that stimulate proliferation of blood vessels. Central ischemic necrosis when tumor outgrows its blood supply.

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46
Q

E-cadherin

A

Attaches cells together. In many malignant tumors, E-cadherin is not produced. Reduces cohesiveness of tumor cells.

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47
Q

Laminin / Laminin Receptor

A

Allow cellular attachment to matrix component.

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48
Q

Collagenases / MMPs

A

Tumor cells or fibroblasts/inflammatory cells release collagenases (MMPs) to degrade type IV BM collagen. Tumor cells can induce stroma cells to produce these enzymes that degrade the ECM.

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49
Q

Fibronectin

A

Binding of fibronectin to its receptor helps tumor cell migration. Tumor cell secreted motility factor plays a critical role in migration (locomotion). Tumor cells secrete molecules to promote invasion.

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50
Q

CD44

A

Expression of CD44 on tumor cells seems to favor metastasis

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51
Q

What are the three routes of metastasis?

A

Seeding of body cavities
Lymphatic Spread - most common in carcinoma > adenoma
Hematogenous Spread - most common in sarcomas

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52
Q

No lymphatic spread in which three carcinomas?

A

Follicular carcinoma: local invasion
Renal cell carcinoma: renal vein
Hepatocellular carcinoma: hematogenous spread

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53
Q

Hematogenous Spread

A

Typical of sarcomas, and carcinomas in late stage. Arteries are more difficult for tumor to penetrate. Cells follow venous flow to other organs. Liver and lungs frequently involved. Can cause tumor emboli.

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54
Q

Metastases characteristics

A

Multiple mass lesions w/ central areas of umbilication (ischemia and infarction).

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55
Q

Sentinel Lymph Node

A

1st node in a regional lymphatic system that receives lymph flow from primary tumor. Detected by radio labeled tracers or blue dyes. Used for detecting spread of melanomas, breast cancers, colon cancers, others

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56
Q

Most common site and symptom for bone metastasis

A

Vertebral column: batson paravertebral venous plexus connects vena cava and vertebral bodies. Pain is most common Sx of bone mets. Best relieved by local radiation therapy. 2 types: osteoblastic and osteolytic metastasis.

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57
Q

Factors Indicating Osteoblastic Metastasis

A

Radio-dense loci on x-ray. ↑serum alk phosphatase: indicates reactive bone formation. Example: prostate cancer is the most common type that has mets to bone. Example: prostate cancer.

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58
Q

Factors indicating Osteolytic Metastasis

A

Lucencies (dark spots) in bone on x-ray. Path. fractures. Tumors produce factors that activate osteoclasts:
PG E2, Osteoclast activating factor, IL-1
Potential for hypercalcemia. Example: multiple myeloma

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59
Q

Most common met site for stomach adenocarcinoma

A

Virchow’s left supraclavicular node

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60
Q

Most common met site for breast cancer

A

Lung, bone

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61
Q

Most common met site for colorectal cancer

A

Liver

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62
Q

Most common met site for renal adenocarcinoma

A

Lung

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63
Q

Most common met site for lung cancer

A

Adrenal / Liver

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64
Q

Most common met site for melanoma

A

Liver / Lung

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65
Q

Most common met site for prostate

A

Bone

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66
Q

Most common met site for testicular cancer

A

Para-aortic nodes

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67
Q

What is BrdU used for?

A

BrdU is a thymidine analong. Thymidine is a nucleotide used in DNA synthesis. Uptake in S phase. High nucleotide uptake implies that a large number of tumor cells are in the S phase, which will proceed to mitoses and undergo proliferation. High uptake suggests high grade tumor and poor prognosis.

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68
Q

What is mitotic index used for?

A

Used to grade tumors. Higher mitotic index = higher grade of tumor = poorer prognosis.

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69
Q

Four Grades of Neoplasia

A

I: Well differentiated
II: Moderately differentiated
III: Poorly differentiated
IV: Nearly anaplastic

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70
Q

TNM Staging system of neoplasia

A

T = size of primary tumor
T0 = In situ T1-4 = 4 is largest (increasing size)
N = nodal involvement
N0 = no nodes N1-3: extent of nodal involvement
M= distant mets
M0 = No mets M1-2: extent of mets

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71
Q

Dukes staging system

A

Used for colorectal cancers

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72
Q

Ann Arbor staging system

A

Used for Hodgkin and non Hodgkin lymphomas

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73
Q

Top cancer deaths in males

A

Lung & bronchus 30%
Prostate 9%
Colon & rectum 9%

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74
Q

Top cancer deaths in females

A

Lung & bronchus 26%
Breast 15%
Colon & rectum 9%

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75
Q

Top cancer incidence in males

A

Prostate 25%
Lung & bronchus 15%
Colorectal cancers 10%

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76
Q

Top cancer incidence in females

A

Breast 27%
Lung & bronchus 14%
Colorectal cancers 10%

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77
Q

The death rate from _________ cancer is higher in Japan as compared to the US

A

Stomach Cancer

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78
Q

_________ cancer is more common in Zew Zealand than in Iceland

A

Skin cancers. Persons w/ fair skin, light hari, blue/green eyes are more at risk for skin cancers.

79
Q

Arsenic is associated w/ what types of cancer?

A

Lung, skin, hemangiosarcoma

80
Q

Asbestos is associated w/ what types of cancer?

A

Lung, mesothelioma, GIT (esophagus, stomach, large intestine)

81
Q

Nickel is associated w/ what types of cancer?

A

Nose, lung

82
Q

Radon is associated w/ what types of cancer?

A

Lung. Radon and smoking are synergistic for developing lung cancer.

83
Q

Vinyl chloride is associated w/ what types of cancer?

A

Angiosarcoma of liver

84
Q

Pts working in industries involving aniline dyes typically develop _________ cancer.

A

Bladder cancer

85
Q

Pts exposed to asbestos typically develop this type of cancer

A

Mesothelioma

86
Q

Pts who smoke typically develop this type of cancer

A

Carcinoma of oropharynx and lung

87
Q

Most common cancer types in young adults

A

Leukemia, lymphoma, CNS, soft tissue

88
Q

Most common cancer types in infancy and childhood

A

Neuro/Retino/Nephro - Blastomas
Acute leukemia
Rhabdomyosarcoma

89
Q

Dysplasia

A

Disordered growth. Loss in uniformity in individual cells. Loss in their architectural orientation. Pleomorphism and mitoses are more prominent than in normal tissue. May be a precursor to cancer but does not invariably progress to cancer.

90
Q

Distinguish b/t CIN1/2/3, Carconima in Situ, and Invasive carcinoma of the cervix.

A

CIN1 = 1/3 immature cells (mild) (low grade)
CIN2 = b/t 1/3 and 2/3 immature cells (moderate)
CIN3 = over 2/3 (CIN3 and worse are all “severe”)
Carcinoma in situ: full thickness is immature cells
Invasive Carcinoma: breach basement membrane

91
Q

Carcinoma in Situ (CIS)

A

Full-thickness dysplasia extending from BM to surface of epithelium. Applicable only to epithelial neoplasms.

92
Q

Invasion

A

Growth into surrounding tissue by direct expansion

93
Q

Oral leuko-plakia can turn into what type of cancer through what process?

A

Oral Leuko-plakia to squamous cell carcinoma thru dysplasia.

94
Q

Barrett esophagus (metaplasia) can turn into what type of cancer?

A

Barrett esophagus (metaplasia) to AdeoCA of esophagus via dysplasia.

95
Q

Metaplasia

A

Normal cell type is replaced by another cell type

96
Q

Chronic atrophic gastritis of pernicious anemia can evolve into what cancer type?

A

Gastric adenocarcinoma thru dysplasia

97
Q

Chronic ulcerative colitis can evolve into what cancer type?

A

Adenocarcinoma of colon thru dysplasia

98
Q

Hep B or C infection can evolve into what cancer type?

A

Hepato-cellular carcinoma thru process of macro-nodular cirrhosis

99
Q

Simple/Complex hyperplasia of endometrium → atypical hyperplasia (intra-epithelial neoplasia - EIN) → Endometrial adeno-carcinoma

A

This didn’t make a good flashcard. Tiny Russian man.

100
Q

Solar keratosis of skin can become what type of cancer?

A

Skin cancer - usually squamous cell carcinoma

101
Q

What are the 7 essential alterations for MALIGNANT transformation?

A
  1. Self-sufficiency in growth signals
  2. Insensitivity to growth-inhibitory signals
  3. Evasion of apoptosis
  4. Limitless replicative potential
  5. Sustained angiogenesis
  6. Ability to invade & metastasize
  7. Defects in DNA repair
102
Q

What are the 4 classes of normal regulatory genes?

A

Growth promoting proto-oncogenes
Growth inhibiting tumor suppressor genes
Genes regulating apoptosis
Genes regulating DNA repair

103
Q

New class of regulatory molecules that directly effect regulation of cell growth

A

MicroRNAs (miRNAs)

104
Q

Tumor Suppressor Genes

A

Suppress cell cycle. Require loss of both alleles to stimulate cancer growth. Protein kinases stimulated which produce cyclins which help the cell progress into the cell cycle: G1 to S phase.

105
Q

Proto-oncogene

A

Responsible for regulation of growth & differentiation. Once activated, becomes an oncogene. Activated by mutation, chromosomal translocation, amplification.

106
Q

What are the mechanisms involved in the activation of a proto-oncogene to an oncogene?

A

DNA damage caused by chemical carcinogens, radiation, infectious agents, point mutation, translocation, amplification.

107
Q

What are the two main ways that an oncogene causes unregulated cell proliferation?

A

A normal protein is overproduced

A mutant protein is produced and has an aberrant function

108
Q

ERBB2 (HER-2 / NEU)

[EGF-receptor family]

A

Amplification of this growth factor receptor gene leads to BREAST CANCER and OVARIAN CANCER

109
Q

RET

[Receptor for neurotrophic factors]

A

Point mutation in this growth factor receptor gene leads to MEN 2A & 2B and familial medullary thyroid carcinomas

110
Q

KRAS

[GTP-binding]

A

Point mutation in the gene coding for this protein that is involved in signal transduction leads to PANCREAS, COLON, LUNG cancer

111
Q

ABL

[non-receptor tyrosine kinase]

A

Translocation in the gene coding for this protein involved in signal transduction leads to Chronic Myeloid Leukemia and Acute Lymphoblastic Leukemia

112
Q

BRAF

[RAS signal transduction]

A

Point mutation in the gene coding for this protein involved in signal transduction leads to MELANOMAS

113
Q

β-Catenin

[WNT signal transduction]

A

Point mutation or over expression of the gene coding for this protein involved in signal transduction leads to Hepatoblastomas, hepatocellular carcinoma

114
Q

C-MYC

[transcriptional activator]

A

Translocation of the gene coding for this nuclear-regulatory protein causes BURKITT’S LYMPHOMA

115
Q

N-MYC

[transcriptional activator]

A

Amplification of the gene coding for this nuclear-regulatory protein causes NEUROBLASTOMA, SMALL CELL CARCINOMA of lung

116
Q

Cyclin D

A

Translocation of the gene coding for this cell cycle regulator causes MANTLE CELL LYMPHOMA

Amplification of the same gene causes BREAST and ESOPHAGEAL cancers

117
Q

What is the cause and manifestations of MEN 2a & 2b?

A 
Mutation of the RET proto-oncogene
Familial occurrence of a combo of:
medullary thyroid carcinoma
Bilateral pheochromocytoma
Hyperparathyroidism d/t hyperplasia of tumor
118
Q

How does the Philadelphia Chromosome cause __________ cancer?

A

c-abl proto-oncogene on c9 is translocated to c22, right next to bcr (oncogene). bcr-abl hybrid/fusion on c22 codes for protein with ↑tyrosine kinase activity. This stimulates proliferation of granulocytic precurosrs, giving rise to CHRONIC MYELOID LEUKEMIA

119
Q

Imatinib mesylate (Gleevec)

A

Treatment for Chronic Myeloid Leukemia (CML). Inhibits tyrosine kinase activity that is over expressed d/t Philadelphia chromosome.

120
Q

What causes Burkitt’s Lymphoma?

A

Translocation of C-MYC proto-oncogene from c8 to a site adjacent to Ig heavy chain (IgH) on c14. This causes over-expression / amplification of C-MYC which leads to excess transcription signals.

121
Q

What are the three types of Burkitt’s Lymphoma?

A
  1. African = Endemic = jaw mass
  2. Sporadic = abdominal mass
  3. HIV-associated
122
Q

BCL-2 genes

A

Anti-apoptotic genes: Produce gene products that prevent mitochondrial leakage of cytochrome c (signal for apoptosis)

123
Q

What translocation causes B-cell follicular lymphoma?

A

BCL-2 (anti-apoptotic) translocated from chromosome 14 to 18. Overexpression prevents apoptosis of B-cells
This is the most common lymphoma.

124
Q

What amplification causes Neuroblastoma? How do you dx it?

A

Amplification of N-MYC is present in 30-40% of neuroblastomas. Dx: homogenously staining regions (HSR) of chromosome or double minutes on karyotype.
Usually arise in adrenals/kidney of children. Present as abdominal mass.

125
Q

What is the function and associated cancer of the APC Gene?

A

Prevents nuclear transcription.

Familial polyposis coli (FAP) (Adenocarcinoma of colon)

126
Q

What is the function and associated cancer of the BRCA-1 and BRCA-2 genes?

A

Regulate DNA Repair
Breast and Ovarian Cancer
1 is assoc w/ both
2 is more assoc w/ ovarian cancer

127
Q

What is the function and associated cancer of the RB gene?

A

Inhibits G1 to S phase
Retinoblastoma
Osteogenic Sarcoma
Soft tissue sarcoma

128
Q

What is the mechanism through which the WNT Signaling Pathway can cause FAP, non-familial colorectal cancer, sporadic adenomas?

A

APC down-regulates beta-catenin which prevents its accumulation. Inactivation of APC leads to increased levels of beta-catenin which then translocate to the nucleus and promote proliferation of molecules associated w/ cancer. Continuous WNT signaling causes proliferation and cancer.

129
Q

Knudson’s “two-hit” hypothesis for retinoblastoma

A

RB inhibits G1 to S phase (anti-oncogene)
Have to inactivate BOTH alleles to develop retinoblastoma. In familial cases, kid has 1st hit in all somatic cells of body. 2nd hit in retinal cells causes cancer. In sporadic cases both normal Rb alleles must be lost to somatic mutation in one of the retinoblasts.

130
Q

What is the function and associated cancer of the p53 gene

A

Tumor suppressor gene: Inhibits G1 to S phase, repairs DNA, activates BAX (pro-apoptotic)
Lung, Colon, Breast, Li-Fraumeni Syndrome

131
Q

How does p53 arrest cell cycle at G1/S?

A

p53 acts via p21 (cyclin/CDK4 inhibitor) Induces pro-apoptotic genes: BAX (member of BCL-2 family)

132
Q

What is the relationship b/t HPV and p53?

A

HPV E6 & E7 inhibit p53, p21, RB

HPV E6 only inhibits p53, E7 inhibits all of the above

133
Q

What is the function and associated cancer of the VHL gene?

A 
VHL = tumor suppressor gene on chromosome 3p. Part of ubiquitin ligase complex. Regulates nuclear transcription via HIF-1alpha. 
Hereditary renal cell carcinomas (RCC)
Pheochromocytomas
Hemangioblastoas of CNS
Retinal angiomas
Renal cysts
134
Q

What is the Warburg Effect?

A

Aerobic glycolysis: even w/ hi O2, cancer cells take up lots of glucose and convert it to lactose via the glycolytic pathway. This can be detected by PET scans. Most tumors are PET positive, rapidly growing ones are even more PET positive.

135
Q

Telomerase

A

If overexpressed, will provide limitless replicative potential. Normally shortened and loose function after 60-70 doublings which activates p53 ∴ cell cycle arrest/apoptosis by BAX. If telomerase is maintained, prevents p53 activation and has limitless replicative potential.

136
Q

Epigenetics

A

Reversible, heritable changes in gene expression that occur w/o mutation. Involves post-translational modifications of histones and DNA methylation, both of which affect gene expression. DNA methylation reduces expression and histone modifications lead to the compaction of DNA into heterochromatin.

137
Q

MicroRNA (miRNA)

A

family of 19-24 nucleotide noncoding RNAs that regulate messenger RNA function at the posttranscriptional and translational level. Can be used for diagnostic, prognostic therapeutic purposes (current research)

138
Q

What are carcinogenic agents?

A

Cause genetic damage and induce neoplastic change.
Chemicals / Radiation / Viruses or other microbes
Account for 80-90% of cancers

139
Q

What are chemical carcinogens and how do they act?

A

Highly reactive electrophiles that remove electrons from DNA, RNA or proteins ∴ cause cell damage. Direct acting = act w/o modification. Indirectly acting (pro-carcinogens) = require metabolic activation (by liver).

140
Q

What are the steps involved in chemical carcinogenesis?

A

Initiation and promotion. For cancer to develop you need an initiator (DNA damage) followed by a continuous promoter. If not continuous, body has time to repair damage b/t promoter applications.

141
Q

Initiation step of chemical carcinogenesis

A

Produce cell alteration, not sufficient alone for tumor formation, permanent DNA damage, rapid and irreversible

142
Q

Promotion step of chemical carcinogenesis

A

Induces tumors in initiated cells. Non-tumorigenic by themselves. Don’t affect DNA, reversible.

143
Q

Chlorambucil, Busulfan, Melphalan are Direct or Indirect acting chemical carcinogens? Involved in initiation or promotion?

A

Direct. Initiation. Don’t require chemical transformation. React w/ electron rich sites in cell - attach DNA

144
Q

Polycyclin Aromatic Hydrocarbons (from cigarette smoke) is a direct or indirect acting chemical carcinogen? Involved in initiation or promotion?

A

Indirect. Initiation. Requires metabolic conversion in vivio - ultimate carcinogen. Most carcinogens metabolized by cytochrome P-450 dependent monoxygenases.

145
Q

Sources and associated cancers of polycyclic aromatic hydrocarbons

A

Cigarette smoke, smoked meats and fish. Lung and bladder cancers.

146
Q

Aromatic Amines and Azo Dyes

A

Chemical carcinogen. Ultimate carcinogen. Formed by action of cytochrome P-450 oxygenase systems. Effects Liver

147
Q

Beta-naphthylamine

A

Chemical carcinogen. Bladder cancer in heavily exposed workers in aniline dye and rubber industries.

148
Q

Aflatoxin B1

A

Naturally occurring carcinogen. Mycotoxin produced by fungus: Aspergillus flavus in improperly stored corn, rice, peanuts. China & Africa. Potent hepatic carcinogen. Hepatocellular carcinoma. p53 mutations

149
Q

Nitrosamines and Amines

A

Carcinogens. Formed in gut of humans. Gastric carcinoma. Originate in stomach from reaction of nitrostable amines and nitrates used as a preservative. Converted to nitrites by bacteria.

150
Q

Asbestos

A

Bronchogenic carcinomas
MESOTHELIOMAS
Gastro-intestinal cancers

151
Q

Chromium, Nickel

A

Lung Cancer

152
Q

Arsenic

A

Skin Cancer

153
Q

Promoters of chemical carcinogenesis

A

Estrogen: liver tumors
Diethyl-stilbesterol: post-menopausal endometrial cancer, vaginal cancer in offspring exposed in utero.
High dietary fat ∴ increased bile acids: colon cancer

154
Q

How does UV radiation cause cancer? What type of cancers?

A

Skin cancers: basal cell carcinoma, squamous cell carcinoma, melanoma
Forms pyrimidine dimers which damage DNA
Normal DNA repair: NER pathway (nucleotide excision repair). Pts w/ enzyme defects mediating DNA repair are particularly susceptible (xeroderma pigmentosum)

155
Q

How does ionizing radiation cause cancer?

A

Direct effect, Indirect effect via free radicals. Increased risk w/ higher dose, high LET (linear energy transfer) as in particulate radiation (neutrons & alpha-rays) than w/ low LET or EM radiation (x-rays & gamma-rays)
CHROMOSOME BREAKAGE, Translocation, Point Mutation

156
Q

Neoplasms induced by atomic bomb radiation

A

Leukemias (all except CLL)
Thyroid Cancer (papillary type)
Breast/Lung cancers - less common
Skin, bone, gut are least susceptible

157
Q

Neoplasms commonly found in x-ray workers

A

Radiation dermatitis

Skin cancers

158
Q

What is a weird cause of osteosarcoma?

A

Wearing watches w/ dials painted w/ luminous RADIUM

159
Q

How do Hep B & Hep C cause cancer? What is the role of HBx in Hep B?

A

Hep B & C: Chronic liver cell injury (d/t immune system) & regenerative hyperplasia.
Only Hep B produces HBx protein: activates growth promoting genes - Insulin-like GF: binds to p53

160
Q

Associated neoplasms from Epstein-Bar Virus

A

Burkitt Lymphoma
Hodgkin Lymphoma
B-cell Lymphoma in immunosuppressed pts
Nasopharyngeal carcinoma

161
Q

Which subtypes of HPV are associated w/ cancer? How does HPV result in cancer?

A

Cervical Cancer: HPV 16, 18, 31
Viral DNA is integrated into host genome.
E6 blocks p53
E7 blocks Rb
HPV 6 & 7 are low risk: no DNA integration “Warts” Benign squamous papilloma

162
Q

Human T-cell leukemia virus Type 1 (HTLV-1)

A

Transmitted via intercourse, blood & breast feeding.
Tax gene: stimulates transcription of viral mRNA
Activates c-Fos, IL-2, GM-CSF
Inactivates p16INK4a
CD4 tropism∴prefers CD4 cells

163
Q

What cancer is HIV/HHV associated w/

A

Human Herpes Virus 8 (HHV-8) - Kaposi Sarcoma

HIV - Lymphoma

164
Q

How is helicobacter pylori infection associated w/ neoplasia?

A

CagA (cytotoxin associated gene A) - stimulates growth factor pathway.
Gastric lymphoma (MALT lymphomas)
Gastric carcinoma

165
Q

Estrogen is associated w/ what neoplasias?

A

Breast cancer, squamous cell carcinoma of cervix, leiomyoma of uterus.

166
Q

Contraceptive hormones are associated w/ what neoplasias?

A

Breast cancer, benign/malignant liver tumors

167
Q

Anabolic steroids are associated w/ what neoplasias?

A

Benign/malignant liver tumors

168
Q

Cancer cachexia

A

Loss of body fat, wasting and profound weakness

Caused by: loss of appetite, metabolic changes, TNF!

169
Q

What are para-neoplastic syndromes?

A

Distant effects of a tumor unrelated to primary tumor or metastasis. May represent earliest manifestation of a cancer. Occur in 10-15% of cancer pts. Tumor produces a hormone that circulates in body - enters blood, has effect in other area of body.

170
Q

para-neoplastic syndrome of lung cancer

A

Can secrete ACTH causing Cushing syndrome, diabetes, wt loss, hypertension

171
Q

para-neoplastic syndromes of small cell carcinoma of lung

A

SIADH / Hyponatremia

172
Q

Acnathosis Nigricans

A

Black, verrucoid appearing lesion of the skin (usually axilla) Associated w/ stomach carcinoma. (also leser-trelat sign)

173
Q

Leser-Trelat Sign

A 
Associated w/ stomach carcinoma: multiple outcroppings of pigmented seborrheic keratosis
Visceral malignancy (also acnathosis nigricans)
174
Q

Sx and Dx of Carcinoid Syndrome

A

Associated w/ carcinoid tumors (neuroendocrine tumors_
Appendix or small intestine:Tumor releases serotonin
Sx: flushing, diarrhea, bronchospasm, tachycardia: attacks provoked by palpation of abdominal mets or by alcohol ingestion. Dx: urinary excretion of 5-hydroxy-indoleacetic acid (5-HIAA), a metabolite of serotonin

175
Q

Mechanism of hypercalcemia as a para-neoplastic syndrome

A

Release of PTH related peptide (bone mets not necessary) SQUAMOUS CELL CANCER OF LUNG
Low serum PTH
Osteolytic bony mets (release of osteolytic factors PGE2, IL-1)
Breast cancer can cause both osteolytic effects and bone formation

176
Q

Hormone and assoc. cancer of hypocalcemia para-neoplastic syndrome

A

Calcitonin

Medullary cancer of thyroid

177
Q

Hormone and assoc. cancer of gynecomastia para-neoplastic syndrome

A

Hormone: beta-HCG

Chorio cancer of testis

178
Q

Hormone and assoc. cancer of Eaton-Lambert Syndrome (para-neoplastic syndrome)

A

Myasthenia gravis-like syndrome

Small cell cancer of lung

179
Q

When should you use IHC (imunohistochemical)techniques to Dx a tumor?

A

When cell of origin is unknown. Used for undifferentiated tumors.

180
Q

How would you know that a tumor is epithelial in origin?

A

If the tumor is positive for cytokeratin, keratin, or epithelial membrane antigen (EMA), it indicates an epithelial origin.

181
Q

How would you know that a tumor is mesenchymal in origin?

A

Vimentin, Desmin: muscle-specific actin (origin-muscle)

182
Q

What are three markers for neuronal tumors?

A

NSE = neuron-specific enolase
Chromogranin
Synaptophysin
Also, neuroendocrine tumors like small cell carcinoma of the lung and carcinoids stain w/ NSE

183
Q 
IHC Markers indicate what tumor type?
Thyroglobulin
CD10 (CALLA)
Placental alkaline phosphatase
vWF, CD31
A

Thyroid Cancer
Acute Lymphoblastic leukemia
Seminoma
Vascular Neoplasms

184
Q

What is a tumor marker?

A

Substance found in the blood, urine, or body tissues that can be elevated in cancer, among other tissue types

185
Q

Tumor marker: CEA - Carcino-embryonic antigen - indicates what type of cancer?

A

Colon, Pancreas, Stomach, Breast Cancer

Digestive + Breast Cancer

186
Q

Tumor marker: PSA - prostate-specific antigen - indicates what type of cancer?

A

Prostate Cancer

187
Q

Tumor marker: beta-human chorionic gonadotropin

(beta-HCG) indicates what type of cancer?

A

Trophoblastic tumors (chorio-carcinoma)

188
Q

Tumor marker: CA-125

A

Indicates ovarian carcinoma

189
Q

Tumor marker: alpha-fetoprotein (alpha-AFP)

A

Indicates hepato-cellular carcinomas

Germ cell tumors of testes or ovary

190
Q

Tumor marker: NSE***

A

Small cell carcinoma of lung***

191
Q

Tumor marker: Calcitonin

A

Medullary thyroid carcinoma

192
Q

Tumor marker: CA 19-9

A

Colon cancer

Pancreatic cancer

193
Q

Tumor marker: CA 15-3

A

Breast cancer

Pathology (6 decks)

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