Cancer Flashcards

(45 cards)

1
Q

Neoplasia

A

New growth - may be benign or malignant

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2
Q

Regulated growth & cellular differention

A

What distinguishes benign from malignant

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3
Q

Benign Tumor

A

Well differentiated, localized, and demarcated

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4
Q

Malignant Tumor

A

Less well differentiated, grow rapidly, invade neighboring tissues, spread to other body sites

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5
Q

Proliferation

A

the ability of a cell to divide and requires growth signal (eg growth factors)

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6
Q

Immortalized

A

Cancer cells ignore normal growth restraints and have a high proliferative capacity

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7
Q

Differentiation

A

The degree of specialization of a given cell. Become more specialized as they mature.

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8
Q

Terminally differentiated

A

Cells that no longer divide

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9
Q

Cancer cells

A

Less well differentiated or less mature than normal cells

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10
Q

Carcinoembryonic Antigen (CEA)

A

molecules normally only expressed in immature or less differentiated cells - normally produced before birth only

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11
Q

Inverse relationship

A

Between differentiation and the ability of a cell to proliferate

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12
Q

Cell Cycle

A

cell growth and division; many cancer cells show changes in the cell cycle and are autonomous (independent of normal growth controls)

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13
Q

3 causes of growth & maturity abnormalities

A

1) the ability to produce telomerase
2) Changes in pRB that governs the cell cycle rate
3) Changes in p53 that slows the cell cycle to allow for repair of DNA mutations before cell division

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14
Q

Events of the cell cycle

A

Mitosis, followed by cytokinesis, and interphase

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15
Q

Telomeres

A

Repeated sequences not used to make cell proteins

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16
Q

Immortalized

A

Cancer cells can replace telomeres by activating telomerase, thus can divide indefinitely

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17
Q

pRB

A
  • Acts as a break to the cell as this protein governs cell cycle commitment
  • Activity is governed by phosphorylation and disruption leads to increased cell proliferation, seen in cancer
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18
Q

p53

A

A cell protein that has a number of anti-cancer functions centered around DNA repair including:

  • activation of DNA repair proteins
  • Arrest of the cell cycle to allow DNA repair proteins to fix mutations
  • Initiation of apoptosis if DNA damage cannot be reversed
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19
Q

Most cancers

A

Acquired, not inherited

20
Q

Conversion of a normal cell into a cancer cell

A

Requires multiple mutations. Mutations may be point mutations or chromosomal rearrangements

21
Q

Conversion of a normal cell into a cancer cell

A

Requires multiple mutations. Mutations may be point mutations or chromosomal rearrangements

22
Q

Tumor Suppression genes

A

Normally restrain cell growth = “loss of function” eg, pRB, p53, APC, DCC
Mutate BOTH copies

23
Q

Oncogenes

A

Normally promote growth as protooncogenes within cells. eg growth factors, receptors
Mutate ONE copy
Virus

24
Q

DNA repair genes

A

Normally correct damage or mutations in the cellular DNA. Failure to fix these mutations increases the likelihood that cancer will arise

25
Carcinogenesis
The process of tumor formation and a series of mutations is required for cancer
26
Clonal Tumor Cells
Derived from a single progenitor cell and tumor cell markers identify cancer and reflect this clonality
27
Retionoblastoma
A rare childhood cancer of the eye that involves mutation in both alleles of the tumor suppressor gene (pRB)
28
Loss of pRB function
Unregulated growth or cancer
29
Hereditary Nonpolyposis Colon Cancer (HNPCC)
Colon cancer due to mutations in DNA repair genes -The decrease in DNA repair leads to an increase in genome instability called mutator phenotype - increases the likelihood that an individual will develop cancer
30
Familial Adenomatous Polyposis (FAP)
Type of colon cancer | -Changes in both oncogenes and tumor suppressor genes are typically required to develop
31
Transformation
Multiple mutations are required for cancer to occur and often result in changes to growth and adherence that contribute to invasion, angiogenesis, and metastasis
32
Altered biochemical properties
Promote growth - secretes growth factors/hormones and promote spread -Secretes protease
33
Chromosomal Changes
- Aneuploid - loss of diploid state - Translocations and other rearrangements - Metastasis
34
Aberrant Adherence Properties
-Loss of contact inhibition -Anchorage independence Cancer cells invade and spread
35
Initiation-Promotion theory
- Initiation (DNA mutation, irreversible) must occur first - Promotion (stimulate cell proliferation, reversible in early stages) must follow initiation for tumors to form - Progression obtains malignant phenotype including invasiveness, metastasis, autonomous growth and genomic instability
36
To be Malignant
- Invasion of neighboring tissues - Angiogenesis - formation of new blood vessels - Metastasis - spread to new sites
37
Clinical Manifestations of cancer
Distinct diseases with similar underlying cellular changes and common manifestations: - Pain - Cachexia - severe form of malnutrition, associated with anorexia, tumor necrosis factor (TNF) - Declining hematopoiesis - Anemia often observed, tumors in bone or bone marrow suppression can contribute
38
Cancer screening & diagnosis
Cancer cells express TUMOR MARKERS and include: -Prostate-specific antigen (PSA) -CA-125 -Carcinoembroyonic antigen (CEA) Markers are not diagnostic but changes in levels are often consistent with changes in tumor growth or responsiveness to treatment
39
Approaches to cancer treatment
- Surgery - Chemo - Radiation
40
TNM
Staging Tumor - how many Nodes - nodes involved Metastasis - has it spread
41
Papanicolaou Test (PAP)
A cytologic method used to detect cancer cells
42
Cell differentiation
Process whereby proliferating cells are transformed into different and more specialized cell types
43
DNA synthesis
Takes place in the S phase of the cell cycle
44
Invasion
The direct extension and penetration by cancer cells to neighboring tissues
45
Hematogenic spread
Metastasis that occurs by way of the blood vessels