Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HMS301 Blood & Neoplasia > Molecular Basis for Cancer > Flashcards

Molecular Basis for Cancer Flashcards

1
Q

4 Basic types of tissues

A

1) Connective tissue
2) Epithelial tissue
3) Muscle tissue
4) Nervous tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Epithelial tissue

A
  • form the covering of all body surfaces, line body cavities & hollow organs.
  • major tissue in glands
  • cells are tightly packed together with very little intercellular matrix.
  • functions = protection, secretion, absorption, excretion, filtration, diffusion & sensory reception.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Shapes of epithelial cells… (may be arranged in single or multiple layers = simple or stratified)

A
  • squamous
  • cuboidal
  • columnar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Simple cuboidal epithelium

A

found in glandular tissue & in the kidney tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Simple columnar epithelium

A

lines the stomach & intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pseudostratified columnar epithelium

A

lines portions of the respiratory tract & some of the tubes of the male reproductive tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Transitional epithelium can be…

A

distended or stretched

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Glandular epithelium is specialized to…

A

produce & secrete substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Connective tissue

A
  • characterized by an abundance of intercellular matrix with relatively few cells.
  • able to reproduce but not as rapidly as epithelial cells.
  • most connective tissues have a good supply but some don’t.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cell types found in connective tissue (3 most common)

A
  • fibroblast
  • macrophage
  • mast cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Types of connective tissue

A
  • loose connective tissue
  • adipose tissue
  • dense fibrous connective tissue
  • elastic connective tissue
  • cartilage
  • osseous tissue (bone)
  • blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Muscle tissue

A
  • composed of cells that have the special ability = shorten or contract in order to produce movement of the body parts.
  • highly cellular & is well supplied with blood.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Contractile proteins in muscle tissue

A

Actin & Myosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Categories of muscle tissue

A
  • skeletal muscle tissue
  • smooth muscle tissue
  • cardiac muscle tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Skeletal muscle fibers

A

are cylindrical, multinucleated, striated & under voluntary control.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Smooth muscle cells

A
  • involuntary
  • are spindle shaped, lack striations & have a single, centrally located nucleus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cardiac muscle tissue

A
  • involuntary
  • branching fibers, 1 nucleus per cell, striations & intercalated disks.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Nervous tissue

A
  • cells communicate with each other by a way of electrical nerve impulses.
  • neurons = 3 parts:
    1. Dendrites = extensions of the cytoplasm that carry impulses to the cell body.
    2. Cell body
    3. Axon = main part
17
Q

Molecular Basis of Cancer = Role of Genetic & Epigenetic Alterations

A

1) Nonlethal genetic damage lies at the heart of carcinogenesis.

2) Tumor is formed by the clonal expansion of a single precursor cells that has incurred genetic damage (tumors are clonal)

3) Principal targets of cancer causing mutations = 4 classes of genes

4) Carcinogenesis results from the accumulation of complementary mutations in a stepwise fashion over time

18
Q

Nonlethal genetic damage lies at the heart of carcinogenesis

A
  • Initial damage or mutation may be caused by:
    a) Environmental exposures = any acquired mutation caused by exogenous agents (viruses, environmental chemicals) or endogenous products of cellular metabolism having the potential to damage DNA (reactive oxygen species) or alter gene expression.

b) Inherited in the germline

c) Spontaneous & random

19
Q

Tumor is formed by the clonal expansion of a single precursor cell that has incurred/sustained genetic damage (i.e., tumors are clonal)

A
  • alterations in DNA are heritable (being passed to daughter cells) = therefore all cells within an individual tumor share the same set of mutations that were present at the moment of transformation.
  • such tumor-specific mutations are
    most often identified by:
    = DNA sequencing (e.g., point mutations)
    = Chromosomal analyses (e.g., chromosomal translocations)
20
Q

What are the 4 classes of genes that are the principal targets of cancer causing mutations?

A

1) Growth promoting proto-oncogenes
2) Growth-inhibiting tumor suppressor genes
3) Genes that regulate apoptosis
4) Genes that are responsible for DNA repair

21
Q

Mutations that activate proto-oncogenes (regulate cell growth & proliferation)

A
  • cause an increase in 1 or more normal functions of the encoded gene product that promote tumorigenesis or an oncogenic appearance
  • cause a “gain-of-function” = they can transform cells despite the presence of a normal copy of the same gene = oncogenes are dominant over their normal counterparts.
22
Q

Mutations that affect tumor suppressor genes

A
  • cause a “loss-of-function”
  • in most instances both alleles must be damaged before transformation can occur = as a result, mutated tumor suppressor genes usually behave in a recessive fashion = however, there are exceptions - sometimes loss of only a single tumor suppressor gene allele (a state termed haploinsufficiency) reduces the quantity of the encoded
    protein enough to release the brakes on cell proliferation & survival.
23
Q

Haplosuffiency

A

loss of only a single tumor suppressor gene allele

24
Q

Such a finding indicates that _____ doses of the gene are essential for normal function.

A

2

25
Q

Genes that regulate apoptosis

A
  • may acquire abnormalities that result in less cell death & therefore enhanced survival.
  • abnormalities = gain-of-function mutations in genes whose products suppress apoptosis & loss-of-function mutations in genes whose products promote cell death.
26
Q

Genes that are responsible for DNA repair

A

Loss-of-function mutations affecting DNA repair genes contribute to carcinogenesis indirectly by impairing the ability of the cell to recognize & repair nonlethal genetic damage in other genes = as a result, affected cells acquire mutations at an accelerated rate = mutator phenotype that is marked by genomic instability.

27
Q

Mutator phenotype

A
  • affected cells are acquire mutations at an accelerated rate
  • marked by genomic instability
28
Q

Carcinogenesis results from the accumulation of complementary mutations in a stepwise fashion over time

A
  • Malignant neoplasms have cancer hallmarks (several phenotypic attributes):
    a) excessive growth
    b) local invasiveness
    c) ability to form distant metastases
29
Q

Carcinogenesis results from the accumulation of complementary mutations in a stepwise fashion over time

A

A) Driver mutations

B) Loss-of-function mutations & Passenger mutations

C) Cell intrinsic mutations = mutations that contribute to tumorigenesis by interfering with host immune responses or altering interactions with the stroma, or by other mechanisms

30
Q

Driver mutations

A
  • these are mutations that contribute to the acquisition (development) of cancer hallmarks.
  • initiating mutation = 1st driver mutation that starts a cell on the path to malignancy.
  • development of a cancer requires that the initiated cell acquire a number of additional driver mutations (each of which also contributes to the development of the cancer) = time this develops is unknown but appears to be lengthy.
  • the persistence of initiated cells during this long preclinical prodrome is consistent with the idea that cancers arise from cancer stem cells (cells with stem cell-like properties & have a capacity for self-renewal & long-term persistence).
31
Q

Passenger mutations

A
  • these are mutations that have no phenotypic consequence
  • more common than driver mutations.
32
Q

Loss-of-function mutations in genes that maintain genomic integrity

A
  • these mutations increase the likelihood of acquiring driver mutations & increase the frequency of passenger mutations.
  • as a result, by the time a cell acquires all of the driver mutations that are needed for malignant behavior, it may bear hundreds or even thousands of passenger mutations.
33
Q

Cell-intrinsic manner mutations

A
  • mutations in many other genes that contribute to tumorigenesis by interfering with host immune response or altering interactions with the stroma, or by other mechanisms.
34
Q

Direct Acting Carcinogens

A
  • don’t require metabolic conversion to become carcinogenic.
  • these agents have cured, controlled, or delayed the recurrence of certain types of cancer (e.g., leukemia, lymphoma, or breast carcinoma), only to evoke a second form of cancer, usually acute myeloid leukemia.
  • examples = alkylating agents, acylating agents.
35
Q

Indirect Acting Carcinogens

A
  • require metabolic conversion to become active carcinogens = carcinogenic products are called ultimate carcinogens.
  • examples = chemical carcinogens:
  • benzo alpha pyrene = tobacco in cigarettes
  • polycyclic hydrocarbons = smoked meats & fish
  • aromatic amines & azo dyes = aniline dye & rubber industries
36
Q

Radiation Carcinogenesis

A
  • radiant energy, in the form of the UV rays of sunlight or as ionizing electromagnetic & particulate radiation is mutagenic & carcinogenic.
37
Q

Why is ionizing radiation worrying even though it’s contribution to the total human burden of cancer is probably small?

A

because those cancers that do occur may arise decades later & long periods of observation are necessary to ascertain their full effect.

38
Q

What is the problem with exposure to UV rays derived from the sun, particularly in fair-skinned individuals?

A

It’s associated with an increased incidence of:
- squamous cell carcinoma
- basal cell carcinoma
- melanoma of the skin

39
Q

Degree of risk of developing cancer when exposed to UV rays is dependent on?

A
  • type of UV rays (UVA, UVB, UBC)
  • intensity of exposure
  • skin pigmentation (quantity of light-absorbing melanin in the skin)
40
Q

Why is Ultraviolet B (UVB) light carcinogenic?

A

because of its ability to cause pyrimidine dimers to form in DNA.

41
Q

Ionizing Radiation - who are at risk or affected?

A
  • individuals pioneering the use of x-rays developed skin cancers.
  • miners
  • survivors of the atomic bombs (on Hiroshima & Nagasaki)
42
Q

Microbial Carcinogenesis
- common theme in the pathogenesis

A

Common theme = infection triggers cell proliferation, which is initially polyclonal but with time becomes monoclonal by acquisition of driver mutations in rapidly dividing cells.

HMS301 Blood & Neoplasia (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions