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z:Cell 300 > Lecture 23: Cancer > Flashcards

Lecture 23: Cancer Flashcards

1
Q

The incident of cancer now is _____

A

increasing

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2
Q

carcinomas arise from _____ and comprise ______

A

-epithelial cells of specific origin (ex. gut or skin)
-90% of human cancers

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3
Q

Sarcomas arise from _____

A

connective tissue

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4
Q

leukemias/lymphomas arise from _____

A

immune cells

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5
Q

Sarcomas and leukemias/lymphomas: arise from cells of _____

A

mesodermal origin including muscle, bone, blood vessels, fibroblasts, and circulating cells of the blood and lymph

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6
Q

Tumors are further characterized by ______

A

the tissue of origin (e.g. lung carcinoma or colon carcinoma)

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7
Q

Oncogene (def.)

A

gene capable of inducing cell transformation (cause cancer)

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8
Q

Benign Tumor is defined by _______

A

-abnormal cell proliferation confined to its normal
location
-Cannot invade surrounding tissues or spread to other organs. (e.g. wart)

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9
Q

Malignant Tumor is defined by _______

A

-abnormal cell proliferation that is both invasive and metastatic
-can invade and destroy adjacent normal tissue
as well as spreading to distant sites through the circulatory system

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10
Q

________ synonymous with cancer

A

Malignant Tumor

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11
Q

normal cell division + normal apoptosis = _____

A

homeostasis

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12
Q

increased cell division + normal apoptosis = _____

A

tumor

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13
Q

normal cell division + decreased apoptosis = _____

A

tumor

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14
Q

Benign tumors ______ whereas malignant tumors
______ and move _______

A

-remain at their site of origin
-destroy integrity of structure
-to distal sites (metastasis)

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15
Q

differences between benign tumor and malignant tumor

A

-malignant tumor metastasizes (spread from original location)
-benign tumor doesn’t affect normal tissue function
-malignant tumor affect normal tissue function

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16
Q

malignant tumor is result of ______

A

-accumulating mutations in genome

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17
Q

cancer typically happens later in life because ______

A

you need to accumulate mutations to the genome

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18
Q

Normal cells vs cancer cells: Density dependent growth inhibition/contact inhibition

A

-normal cells: yes
-cancer cells: no

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19
Q

Normal cells vs cancer cells: Growth factor requirement

A

-normal cells: High
-cancer cells: Low (bypass the check & balance)

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20
Q

Normal cells vs cancer cells: Anchorage dependence

A

-normal cells: Yes
-cancer cells: No

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21
Q

Normal cells vs cancer cells: Proliferative life span

A

-normal cells: Finite
-cancer cells: Infinite

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22
Q

Normal cells vs cancer cells: Adhesiveness

A

-normal cells: High
-cancer cells: Low

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23
Q

Normal cells vs cancer cells: Morphology

A

-normal cells: Flat
-cancer cells: Rounded

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24
Q

in normal cells, high density ____ but this doesn’t occur in cancer cells

A

inhibits growth

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25
Q

increase growth = quality of ______

A

division is compromised

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26
Q

Tumor cells have a _____ morphology from normal cells

A

different

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27
Q

Tumor cells often have _____ ratio (a characteristic of rapidly growing cells) because cell division is ______ and normal function ______

A

-high nucleus to cytoplasm
-dependent on nuclear material
-in the cytoplasm is not important

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28
Q

in tumor cells, _____ and ____ is lost

A

-contact inhibition and polarity

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29
Q

Studying cancer cells takes advantage of the fact that ____

A

transformed cells have different morphology & growth characteristics (can easily identify them)

30
Q

Studying oncogenes goal

A

Find gene(s) in tumor cells that when expressed in non-transformed cells—result in loss of contact inhibition

31
Q

Studying oncogenes method

A

1) DNA from human tumor cells -> transfected mouse NIH3T3s cells
2) culture for 2 weeks
3) extract DNA from transformed NIH3T3 cells growing among untransformed cells -> loss of contact inhibition
4) Transform new mouse cells (2nd cycle) for enrichment for oncogene DNA
5) Phage library is made from DNA isolated from secondary transfectants
6) Plate phage on E.coli which kills E-coli and create hole in plate of E-coli
7) Each plaque (hole) has human DNA from the cancer
8) Replica on filter paper + add Alu probe (Alu is unique to human so it’s used to identify human DNA)
9) Identify phage from library that has oncogene (human DNA)

32
Q

mouse NIH3T3s cells are ______ so they _____

A

immortal but not transformed (cancer) so they exhibit contact inhibition

33
Q

Creating phage library method

A

1) Genomic DNA (from transformed mouse cells that contain human tumor DNA)
2) Shear DNA
3) Ligate genomic DNA into phage
4) Recombinant phage has mouse and human DNA

34
Q

In the human genome, _____ are much more prevalent than genes

A

Alu sequences (~300 base pairs)

35
Q

If a human DNA fragment contains a gene, chances are that _____

A

it contains one or more Alu sequences

36
Q

Using the phage library was used to identify _____

A

the human gen that produces a mutant Ras (the first human oncogene identified)

37
Q

point mutation (def.)

A

a single nucleotide change

38
Q

Oncogenic activation of Ras is the result of a ______

A

point mutation that keeps Ras in the GTP bound form (activated form)

39
Q

Ras mutation

A

Gly12 >Val 12 (GGC codon to GTC)

40
Q

Mutated ras oncogenes are found in _____

A

a lot of cancers , especially the deadliest ones

41
Q

Mutated Ras can cause cause because _______

A

it induces the transcription of many genes that contribute to the metastatic phenotype (cell cycle progression, survival, growth, migration)

42
Q

Many cancer cells target proteins in _____

A

Ras signaling pathways (like RTK, Ras, Raf 1, Mek)

43
Q

Drugs ending in “mab” are ______. They target ____

A

monoclonal antibodies
RTK receptors on the cell surface

44
Q

Oncogenes act _______to increase rates of cancer so ____

A

synergistically
mutations in multiple oncogenes = increase rate of cancer

45
Q

_____is a transcription factor that regulates ______. Uncontrolled expression (______) associated with _____

A
  • C-myc
    -cellular proliferation
    -gene amplification or mutations
    -many tumors
46
Q

Cancer is a _____ process in which cells acquire the ______ through a ______

A

-complex multi-step
-full malignant phenotype
- progressive accumulation of alterations

47
Q

Normal cell to malignant tumor steps

A

normal cell –> (initiation/<—–DNA repair ) initiated cell —> (promotion) preneoplastic cell –> (progression) neoplastic cell –> (metastasis) malignant tumor

48
Q

Two basic categories of oncogenic mutations

A

1) Gain of function mutations
2) Loss of function mutations

49
Q

Gain of function mutations (def.)

A

result in conversion of proto-oncogenes to oncogenes

50
Q

Loss of function mutations (def.)

A

mutations in gene that encodes proteins (tumor suppressors) that inhibition proliferation

51
Q

proto-oncogene (def.)

A

the normal cellular gene from which an oncogene originates (gene that is the precursor of a given oncogene); promote cell survival or proliferation

52
Q

tumor suppressors normal function

A

inhabits cell survival or proliferation

53
Q

caretaker genes normal function

A

repair or prevent DNA damage

54
Q

Genetic properties of mutant gene: proto-oncogenes

A

mutations are genetically dominant (only needs one mutant copy of gene)

55
Q

Genetic properties of mutant gene: tumor-suppressor genes

A

mutations are genetically recessive (needs two mutant copies of gene)

56
Q

Genetic properties of mutant gene: caretaker genes

A

mutations are genetically recessive (needs two mutant copies of gene)

57
Q

Scenarios leading to Gain of Function Mutants

A

1) Point mutations or deletions-resulting in gene encoding constitutively active protein (dominant)
ex. RasD, Her2, ErbB mutants

2) Chromosomal translocation-resulting in hybrid gene encoding protein with altered activity (dominant)
ex. Trk oncoprotein

3) Chromosomal translocation-resulting in growth regulatory gene becoming under control of different promoter (dominant)
ex.c-myc/Burkitt’s lymphoma

4)Amplification (abnormal DNA replication)-of proto-oncogene region leading to overproduction of protein
ex. n-myc/neuroblastoma

58
Q

Her2 receptor and EGF receptor are _____

A

RTK (when constitutively active, its leads to uncontrolled signaling for cell proliferation)

59
Q

Point mutations or deletions lead to genes encoding RTKs _______ and

A

-that are constitutively active in the absence of ligand
-uncontrolled signaling leading
to cell proliferation

60
Q

Anti-Her2 (monoclonal) has been developed as ______

A

new treatment for breast cancer

61
Q

Trk receptor mutation that leads to cancer

A

-chromosomal translocation resulting in hybrid gene (tropomyosin + Trk receptor)
-tropomyosin region mediates ligand-independent dimerization and activation of kinase domains in Trk region&raquo_space; uncontrolled signaling

62
Q

The proto-oncogene _____is amplified in certain tumors

A

Myc

63
Q

Scenarios leading to Tumorigenic Loss of Function Mutants

A

Loss or mutations of genes that encode proteins that:
*Promote apoptosis»inability to induce cell death
*Repair DNA»rapid accumulation of mutations in cells
*Function as receptors or signal transducing proteins that are required for pathways that inhibit growth»inability to respond to appropriate signals
*Regulate cell cycle check-points» inability arrest the cell cycle following DNA damage or chromosomal abnormalities

64
Q

Loss of function mutants are usually _____

A

recessive&raquo_space;Both copies of genes have to be lost or mutated in order for tumorigenic phenotype to develop

65
Q

Risk of developing cancer can be mitigated _____

A

through lifestyle and diet

66
Q

Most cancers development is not due to _____

A

family history

67
Q

Immune-braking system (def.)

A

Programmed death-ligand 1 (PD-L1) on cells binds to its receptor (PD-1) on activated T-cells and inhibits their ability kill target cells.

68
Q

PD-L1 in tumor cells is _____

A

highly expressed on many tumor cells»evade anti-tumor immunity

69
Q

Blocking _____ allows T cell to kill tumor cell

A

PD-L1 or PD-1

70
Q

overactive T-cell can be _____

A

cancer like (cause cancer)

71
Q

CAR T-cell therapy (“living drugs”)

A

1) Remove blood from patient to get T-cells
2) Make CAR T cells in lab (insert gene for CAR) –> displays CAR (chimeric antigen receptor)
3) Grow millions of CAR T cells
4) Infuse CAR T cells into patient
5) CAR T cells bind to cancer and kill them

z:Cell 300 (17 decks)

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