Neoplasia Lecture Flashcards

1
Q

Neoplasms

A

New growths

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2
Q

Benign tumors

A

Does not invade or metastasize (ex: Lipoma) most of these tumors end in -Oma

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3
Q

Malignancies

A

Invade metastasize

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4
Q

Harmartomas

A

Overgrowths. Build up of epithelial tissue and collagen in lung

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5
Q

Tissue of origin: Epithelium

A

Carcinoma

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6
Q

Tissue of Origin: Messenchymal Tissue

A

Sarcom

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7
Q

Tissue of Origin: Blood

A

Leukemia

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8
Q

Tissue of Origin: Lymphoid Tissue

A

Lymphoma

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9
Q

What is the Stroma?

A

It is the connective tissue for cancer and is not malignant

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10
Q

What is the origin of blastoma?

A

Blast cells

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11
Q

What is mesenchyme tissue?

A

Derivative of the mesoderm that produces connective tissue, fat, musculoskeletal tissue and blood/fat tissue. Sarcomas and leukemias/lymphomas are mesenchymal tumors.

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12
Q

What is the origin of glioma?

A

Glial cells

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13
Q

What is the origin of lymphoma?

A

Lymphoid cells

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14
Q

What is the origin of melanoma?

A

Melanocytes

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15
Q

What is the origin of mesothelioma?

A

Mesothelioma (lining of abdominal, pleural, and pericardial cavities)

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16
Q

What is the origin of seminoma?

A

Germ Cells (testicular)

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17
Q

What is the origin of teratoma (sometimes benign)?

A

germ cells (multiple germ layers: ectoderm, endoderm, mesoderm)

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18
Q

What is the origin of choristoma?

A

(tissue that is out of place (heterotopic); e.g., pancreas in stomach)

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19
Q

Surgical pathology

A

Diagnosis of disease by gross examination, histomorphology, immunohistochemistry, and other methods

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20
Q

Cytopathology

A

Diagnosis of disease by microscopic analysis of cells and cellular aggregates

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21
Q

Autopsy pathology

A

Diagnosis of disease in deceased patients by gross examination,
histomorphology, immunohistochemistry, and other
methods

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22
Q

Define Gross pathology

A

Findings from unmagnified (naked eye) examination of specimens (colon: tan, 2 cm polyp)

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23
Q

Define histopathology

A

Findings from the microscopic examination of stained tissues (esophagus, distal, biopsy: adenocarcinoma)

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24
Q

Cytopathology

A

Findings from the microscopic examination of
individual cells or groups of cells (e.g., Pap smear showing
cervical carcinoma)

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25
Q

Molecular pathology

A

findings from the examination of the DNA
and/or RNA of specimens (e.g., ductal carcinoma of breast
showing HER2 amplification)

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26
Q

Key microscopic features of malignancy

A

Nuclear irregularities (atypical):
- Irregular contours (jagged, notched)
- Increased size (nucleus to cytoplasm ratio)
- Large and or multiple nucleoli
- “open” chromatin or hyper chromatic (dark from too much chromatin)
Overall patter:
-Invasion into surrounding tissues
-irregular 3-D structures

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27
Q

What does Grade mean?

A

Degree of differentiation of the tumor
- Low grade: well - differentaiated (looks like tissue of origin)
- High grade: poorly differentiated (looks less like tissue of origin) to undifferentiated (anaplastic)

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28
Q

What does Stage mean?

A

Anatomical extent of the tumor
- designation: “T__ N__ M__” where T = tumor size/extent,
N = nodal status, and M = metastasis

29
Q

Tissue name based on origin: fat

A

Benign: lipoma
Malignant: liposarcoma

30
Q

Tissue name based on origin: smooth muscle

A

Benign: leiomyoma
Malignant: leiomyosarcoma

31
Q

Tissue name based on origin: glandular epithelium

A

Benign: adenoma
Malignant: adenocarcinoma

32
Q

Three main ways cancer can metastasize

A

Hematogenous
Lymphatic
transcoelomic
(pericardial, peritoneal,
and pleural cavities)

33
Q

Sporadic cancers

A

Are somatic cells that have mutations due to exposure to chemicals/radiation

34
Q

Familial Cancer

A

Are from germ line cells that are exposed to chemicals/radiation

35
Q

Define Exome

A

The entire coding sequence of the genome

36
Q

What is transcoelomic metastasis?

A

When cancer travels through peritoneal fluid

37
Q

Which mutation is a tumor suppressor

A

TP53

38
Q

What is clonal evolution?

A

Accumulating mutations turn normal cells to cancerous cells

39
Q

What is driver mutation?

A

Leads to malignancy

40
Q

What is passenger mutations?

A

No effect on carcinogenesis

41
Q

Too much BCL2 does what?

A

allows tumor cells to avoid apoptosis. Ex follicular lymphoma

42
Q

Hallmark I

A

cancer cells avoid apoptosis

43
Q

Hallmark 2

A

cancer cells use growth signaling pathways

44
Q

Hallmark 3

A

cancer cells escape control of growth

45
Q

What is the RB protein?

A

prevents cancer cells from going through G1 to S phase

46
Q

What is retinoblastoma?

A

A rare intraocular tumor caused mutation of RB

47
Q

Two hit model shows what?

A

That cancer cells needs to knock out both copies of a tumor suppressor gene to get a malignancy

48
Q

Hallmark 4

A

Tumors grow their own blood supply

49
Q

What is the angiogenic switch?

A

A therapeutic target

50
Q

Hallmark 5

A

Cancer cells divide without end

51
Q

What is the action of p53?

A

Shuts down the cell division when telomeres are too short to protect itself from becoming a cancer cell

52
Q

What happens when there is little to no telomerase activity?

A

Shortening telomeres -> senescence

53
Q

What happens when there is high telomerase activity?

A

Shortening telomeres - > telomeres restored - > immortalization

54
Q

Hallmark 6

A

Cancer cells invade and spread

55
Q

Action of E-cadherin loss and matrix metalloproteinases

A

Allows invasion

56
Q

Define heterotypic signaling

A

communication between tumor cells and normal cells

57
Q

Warburg effect

A

Cancer cells (even when there’s O2 present) only use glycolysis

58
Q

Why do cancer cells use warburg effect?

A

it helps make the macromolecules that they need to grow

59
Q

What happens with TGF Beta?

A

The cancer cells turn it off so they cannot be detected by immune cells

60
Q

Loss of APC can lead to?

A

Familial adenomatous polyposis FAP, very high risk. Tx prophylactic colectomy

61
Q

KRAS mutations

A

Most frequent; predict decreased responsiveness to monoclonal AB therapy against epidermal growth factor receptor (EGFR)

62
Q

Melanoma Characteristics

A

Irregular border, multiple colors, nodularity. About half of melanomas have BRAF mutations.

63
Q

Action of kinase inhibitors

A

Inhibit BRAF

64
Q

What virus causes primary effusion lymphoma and Kaposi Sarcoma?

A

Human herpes virus 8 (HHV-8)

65
Q

What virus causes Burkitt lymphoma?

A

Epstein-Barr virus (EBV)

66
Q

What virus causes Cervical Carcinoma?

A

HPV

67
Q

What virus causes hepatocellular carcinoma?

A

Hepatitis B virus, Hep C virus

68
Q

How does HPV cause cervical cancer?

A

Protein E6 binds to p53 and protein EL7 binds to RB which causes proliferation