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MCB 10 > Lecture 15 > Flashcards

Lecture 15 Flashcards

1
Q

Characteristics of cancer cells

A
  • divide continually and quicker than normal cells
  • contain heritable mutations
  • transplantable
  • dedifferentiated
  • have a different appearance
  • cell surface has different types and/or number of antigen
  • lack contact inhibition
  • induce angiogenesis
  • invasive
  • metastasize
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2
Q

dedifferentiated (characteristic of cancer cell)

A

lose their specialized identity

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3
Q

angiogenesis

A

formation of local blood vessels

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4
Q

invasive (characteristic of cancer cell)

A

squeeze into any space available

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5
Q

metastasize (characteristic of cancer cell)

A

move to new location in body

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6
Q

origins of cancer cell (4)

A
  • activation of stem cells that produce cancer cells
  • dedifferentiation - lose their specialized identity
  • increase in proportion of a tissue that consists of stem cells or progenitor cells
  • faulty tissue repair
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7
Q

cancer by loss of specialization

A

specialized cells lose some of their distinguishing features as mutations occur when they divide
-result: dedifferentiation

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8
Q

what can cause cancer?

A
  • loss of specialization
  • shifting balance of cell types in a tissue
  • uncontrolled tissue repair
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9
Q

acute vs chronic injury

A

acute: resting epithelium –> injury and activation of tissue –> repair (–> injury and activation of tissue)
chronic: persistent activation of stem cells –> cancer

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10
Q

proto-oncogenes

A

normal versions of genes that promote cell division

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11
Q

What happens when expression is at the wrong time or in the wrong cell type?

A

it leads to cell division and cancer

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12
Q

oncogenes

A

proto-oncogenes in their mutated form

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13
Q

how many copies of an oncogenic mutation is sufficient to promote cell division?

A

one copy

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14
Q

oncogenes: overexpression of a normal function

A

overexpression of the proto-oncogene is caused by moving a proto-oncogene next to a highly transcribed gene

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15
Q

when is an oncogene activated?

A

when a proto-oncogene moves next to another gene. the gene pair is transcribed together

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16
Q

fusion protein

A

the double gene product

-it activates or lifts control of cell division

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17
Q

Chronic Myelogenous Leukemia (CML)

A

-Most patients have a translocated Philadelphia chromosome (tip of 9 on 22)
-Abl (chromosome 9) and bcr (chromosome 22) genes produce a fusion protein
-BCR-ABL oncoprotein is a tyrosine kinase that excessively stimulates cell division
-Understanding cellular changes allowed development of new drug, Gleevec, for
treatment

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18
Q

Her-2/neu

A

-Product of an oncogene
Excessive levels in approximately 25% of breast cancer patients
-Too many receptors
-Too many signals to divide
-Monoclonal antibody drug, Herceptin, binds to receptors, blocking signal to divide

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19
Q

tumor suppressor genes

A
  • Cancer can be caused by loss of genes that inhibit cell division
  • Tumor suppressor genes normally stop a cell from dividing
  • Mutations of both copies of a tumor suppressor gene is usually required to allow cell division
  • Genes can also be lost by deletion or silenced by promoter hypermethylation
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20
Q

Retinoblastoma (RB)

A

-The RB gene is on chromosome 13
-The RB protein binds transcription factors so that they cannot activate genes that carry
out mitosis. Normally halts the cell cycle at G1
-Study of RB was the origin of the “two-hit” hypothesis of cancer causation

21
Q

two-hit hypothesis

A

-Two mutations or deletions are required. One in each copy of the RB gene
-For sporadic cases (non-inherited). Retinoblastoma is a result of two somatic
mutations
-For familial cases (inherited), individuals harbor one germline mutant allele for the RB gene in each of their cells. This is followed by a somatic mutation in the normal allele

22
Q

p53

A

-The p53 gene is the “guardian of the genome”
-Determines if a cell has repaired DNA damage
-If damage cannot be repaired, p53 can induce apoptosis
-More than 50% of human cancers involve an abnormal p53 gene
-Rare inherited mutations in the p53 gene cause a disease called Li-Fraumeni syndrome
- Family members have many different types of
cancer at early ages

23
Q

What are the two main forms of breast cancer?

A
  1. Familial form: A germline mutation is inherited and then a somatic mutation occurs in a breast cell
  2. Sporadic form: Two somatic mutations affect the same cell

Mutations in many genes can cause cancer

24
Q

BRCA

A

-The two major breast-cancer susceptibility genes are BRCA1 and BRCA2
- Encode proteins that join two others to form a complex that allows repair of double-stranded DNA breaks
-Mutations in these genes have different incidences in different populations
-Inheriting BRCA mutations increases the risk
of other types of cancer

25
Q

Other genes

A

genes whos protein products affect those of BRCA1, BRCA2, and p53 can cause breast cancer

26
Q

gatekeeper genes

A

directly control mitosis and apoptosis

27
Q

caretaker genes

A

control mutation rates and may have an overall effect, when mutant, in destabilizing the genome

28
Q

How can people lower the chance of developing cancer?

A
  • avoiding high-risk environmental factors, such as smoking and excess sun exposure
  • taking “chemopreventative” nutrients such as folic acid and vitamin D
  • cruciferous vegetables
29
Q

method to study cancer - population study

A

compares incidence of a type of cancer among different groups of people

30
Q

method to study cancer - case control

A

identify differences between patients with a type of cancer and healthy individuals matched for mutiple characteristics

31
Q

method to study cancer - prospective studies

A

two or more groups of individuals follow a specific regimen (e.g. , det or activity plan) and are checked regularly for cancer

32
Q

Cancer treatment

A 
New types of cancer drugs:
- Stimulate cells to regain specialized
characteristics
- Inhibit telomerase
- Induce apoptosis
- Inhibit angiogenesis
Genomics information is increasingly used
- Enables physicians to better matchpatient to treatment
33
Q

cytogenetics

A

a subdisipline within genetics. deals with chromosome variations.

  • excess genetic material has a milder effects on health than a deficit
  • still, most large-scale chromosomal abnormalities present in all cells disrupt or halt prenatal development
34
Q

what are the essential parts of a chromosome?

A

telomeres
origins of replication sites
centromere

35
Q

portrait of a chromosome - heterochromatin

A

darkly staining

-consists mostly of repetitive DNA

36
Q

portrait of a chromosome - euchromatin

A

lighter straining

-contains most protein-encoding genes

37
Q

portrait of a chromosome - telomeres

A

chromosome tips composed of many repeats of TTAGGG

-shorten with each cell division

38
Q

centromeres

A

the largest constriction of the chromosome and where spindle fibers attach

  • the bases that form the centromere are repeats of a 171-base DNA sequence
  • replicated at the end of S-phase; facilitated by centromere protein
  • CENP-A is passed to next generation - an example of an epigenetic change
39
Q

subletelomeres

A

the chromosome region between the centromere and telomeres

  • consists of 8,000 to 300,000 bases
  • near the telomere, the repeats are similar to the telomere sequence
  • contains at least 500 protein-encoding genes
  • about 50% are multigene families that include pseudogenes
40
Q

how many chromosome types do humans have?

A
  • autosomes are numbed 1-22 by size
  • sex chromosomes are X and Y

karyotype - a chromosome chart

41
Q

centromere positions

A

At tip – Telocentric
Close to end – Acrocentric
Off-center – Submetacentric
At midpoint – Metacentric

42
Q

how are karyotypes useful

A

1) can confirm a clinical diagnosis
2) can reveal effects of environmental toxins
3) can clarify evolutionary relationships

43
Q

how to visualize chromosomes

A

chromosomes are extracted then stained with a combination of dyes and DNA probes

44
Q

how is tissue obtained from a person?

A 
Tissue is obtained from person
- Fetal tissue:
Amniocentesis
Chorionic villi sampling
Fetal cell sorting
Chromosome microarray analysis
- Adult tissue:
White blood cells
Skinlike cells from cheek swab
45
Q

Amniocentesis

A

how fetal (15-16 months) tissue is obtained

  • detects about 1,000 of the more than 5,000 known chromosomal and biochemical problems
  • fetal cells suspended in the fluid around the fetus are sampled
  • ultrasound is used to follow needle’s movement
46
Q

chrionic villi sampling

A

-Performed during 10-12th week of pregnancy - cels of the chorion are sampled
-Provides earlier results than
amniocentesis
-However, it does not detect metabolic problems
- And has greater risk of spontaneous
abortion

47
Q

fetal cell sorting

A

-Fetal cells are distinguished from maternal cells by a fluorescence-activated cell sorter
- Identifies cell-surface markers
-A new technique detects fetal
mRNA and DNA in the bloodstream of the mother

48
Q

FISH (fluorescene in situ hybridization)

A

DNA probes labed with fluorescing bind complementary DNA

-fluorescent dots correspond to copies of chromosome 21

MCB 10 (11 decks)

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