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Block 1 Week 4 > Cancer Genetics 1 > Flashcards

Cancer Genetics 1 Flashcards

1
Q

What is Cancer?

A
  • the uncontrolled growth and spread of abnormal cells

- has wide range of diseases, can appear in any tissue

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2
Q

Known causes of cancer?

A
  • external factors (lifestyle; smoking alcohol etc)

- internal factors (inherited genetic mutations, hormones, immune conditions)

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3
Q

What are the 4 main cancer types?

A

1) lymphoma
2) carcinoma
3) sarcoma
4) leukemias

All cancers start benign then move into cancerous phase

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4
Q

lymphoma

A

Lymphatic system cancers (excess in lymph nodes, Thymus, and/or Spleen)

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5
Q

carcinoma

A
  • cancer of epithelia
  • benign precursors= adenomas
  • include Breast, Lung, Pancreas
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6
Q

what are sarcomas? 3 common types?

A
  • connective tissue tumors
    1) Muscle : Myosarcomas
    2) Fibroblast: Fibrosarcomas
    3) Cartilage: Chondroma (benign), or Chondrosarcoma (malignant).
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7
Q

Leukemias

A
  • blood cell tumors

- causes too many blood cells

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8
Q

percentage of new cancer diagnoses that are preventable?

A
  • Almost half (42%)
    ex: smoking, excess body weight, physical inactivity, excess alcohol consumption, poor nutrition, viral infections, skin cancer
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9
Q

How does smoking affect risk of lung cancer? What happens do cancer when someone stops smoking?

A
  • Smokers 25x more likely to develop lung cancer than nonsmokers
  • reduce smoking & reduce mortality of most common cancers (lung, colorectal, breast, and prostate)
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10
Q

Cancer and hereditary?

A
  • small proportion of cancers are strongly hereditary
  • combo of inherited predisposiotn & similar lifestyle conditions thought to be responsible for majority of familial cancer
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11
Q

What kinds of cancers make up the most NEW cases?

A

1) Breast 266K
2) Lung 234K
3) Prostate 164K

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12
Q

What kinds of cancers make up the the top DEATHS?

A

1) Lung 153K
2) Colon 50K
3) Breast 41K

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13
Q

What is the clinicians staging system (2 steps)

A

1) TNM (tumor, lymph node, metastasis)
- assesses cancer growth by:
1) Extent of primary tumor
2) Absence/ presence of lymph node involvement
3) absence/presence of distant metastases
2) use TNM to determine stage of 0-IV

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14
Q

stage 0? stage 1? stage IV?

A 
0= in situ
1= being early 
IV= being the most advanced (less probability of controlling cancer when here)
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15
Q

Alternative staging systems and why need them?

A
  • in cases like lymphoma, will not see tumors/ metastasis the way you would in tissue, so hard to use same staging protocol
  • or if want descriptive/ statical analysis of tumors/cancers
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16
Q

what is the staging system for descriptive & statistical analysis of tumor registry data?

A

1) cancer cells present only in layers of cells where they developed & have not spread= in situ
2) if cancer cells have penetrated beyond original layer of tissue it is invasive; described as LOCAL, REGIONAL, DISTANT depending on extent of the spread

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17
Q

Edward smith?

A

-fairly accurate writings of breast cancer from Egyptians
seen 3500 years ago on his papyrus
- describes bulging tumors of the breast that has no cure.

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18
Q

Hippocrates & cancer?

A

-in 460BC
-named tumors resembling a crab “Karkinos”
(word “cancer” is derived via Latin),
-suggested Breast Cancer was caused by “Black Bile”…

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19
Q

Paracelsus and cancer?

A
  • suggested (1567 ) that a gas in mined ore (radon) caused a wasting disease in miners
  • first time IDed lifestyle as a risk for cancer
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20
Q

John Hilland cancer?

A

-made the first direct link of cancer to chemical substances -noted that excessive use ofsnuffmay cause nasal cancer

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21
Q

SirPercivall Pott and cancer?

A

wrote a paper on the high incidence of scrotal cancer inchimney sweeps

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22
Q

How does cancer arise?

A
  • an altered balance in homeostasis of apoptosis and cell division
  • normal cell division & apoptosis= homeostasis
  • increased cell division, normal apoptosis= tumor
  • normal cell division, decreased apoptosis= tumor
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23
Q

What happens when apoptosis & cell replication homeostasis is interrupted?

A
  • uncontrolled cellular growth
  • unhealthy cells outcompete healthy cells
  • destroys correct functioning of major organs & tissues
  • by increasing the # of cells but not the space available to them; can change shape, gene expression,cell-cell connections & reduced supply of nutrients
24
Q

generally speaking how do tumors arise?

A
  • arise from normal tissues

- created by cells that have lost ability to assemble & create tissues of normal form/function

25
Q

Three classifications of tumors?

A

-benign or malignant

26
Q

benign mean?

A

-grown locally w/o invading adjacent tissues

27
Q

malignant mean?

A

-invade nearby tissues & spawn metastases

28
Q

How does cancer transform from benign to malignant?

A
  • Malignant transformation is multistep process

- cancer cells need to adopt a lot of abnormal characteristics.

29
Q

What does it mean when say cancer is “multifactorial”?

A

-means is influenced by both genotype and environment

30
Q

what is personalized medicine?

A
  • when ID specifc mutations in certain cancer & address only those changes
  • if can remove/ fix the change then can prevent cancer growth
31
Q

10 hallmarks of cancer?

A

1) Evading apoptosis
2) Self-sufficiency in
Growth signals
3) Insensitivity to anti-growth signals
4) Sustained angiogenesis
5) Tissue invasion & metastasis
6) Limitless replicative potential
7)Genome instability and mutation
8) Tumor-promoting inflammation
9) Deregulating Cellular energetics
10) Avoiding immune destruction

32
Q

What usually causes the disregulation of homeostasis in cancer cells?

A

1) cancer caused by somatic mutations in genes that regulate cell proliferation, programmed cell death, & genome stability
2) a predisposition for cancer can be inherited via germline transmission of mutant genes

33
Q

describe typical cancer progression?

A

-cancer is a sequential, progressive disease, requires a small # of mutations over an extended period of time to become malignant

34
Q

Steps of cancer progression from benign to malignant

A

1) first clonal expansion: an initiating mutation that increases cell proliferation occurs in the first cell
2) this cell replicates and passes it’s mutation to all progeny
3) one of it’s progeny obtain a second mutation…spreads M1 + M2 to all progeny
4) progeny w/ M1+ M2 obtains M3…gives all 3 to progeny now have a cancer cell

35
Q

Is clonal expansion have to contain heterogenous cells?

A
  • NO
  • can have cells that contain 2 or 3 different mutation events
  • the 2, 3, and 4 mutations and subsequent clonal expansion can also happen simultaneously
36
Q

cancer is caused by a combination of what?

A

1) hereditary factors

2) environmental factors

37
Q

what are the hereditary factors that cause cancer?

A

-germline transmission of mutations that predispose people to develop cancer

38
Q

what are the environmental factors that cause cancer?

A
  • exposure to env carcinogens that increase frequency of somatic mutations
  • ex: smoking, diet, lifestyle
39
Q

What are 3 types of highly hereditary cancers?

A

1) prostate
2) colorectal
3) breast cancer
- still hereditary factors account for <50%
- may seem MORE hereditary since families usually share same env as well

40
Q

carcinogens vs mutagens?

A
  • Carcinogens almost always modify DNA
  • Mutagens (mutation causing agents) ALWAYS modify DNA
  • both can lead to cell damage & loss of homeostatic control on apoptosis vs cell replication
41
Q

What is a carcinogenic assay? Positive & negatives?

A
  • treat animals w/ different doses of potential carcinogen
  • wait for tumor to appear
  • take forever, but effective
42
Q

Mutagen assay?

A

-Ames Test (Bruce Ames)
Step 1: Mutant Bacteria lacking histidine was plated on media w/ and w/o histidine. Appeared on media lacking histidine when suspected Mutagen was added
-mutagen altered the DNA, allowed it to replicate even in absence of histidine

43
Q

What happened in Ames test when tested all suspected chemical mutagens A-Z? Why? (suspected cuz showed mutagenic properties in rats)

A
  • only X,Y,Z showed mutagenic activity
  • realzied the rest of the mutagens were being altered by liver metabolism into their mutagenic form. But the chemicals themselves were only CARCINOGENIC
44
Q

Modified Ames test?

A
  • used liver extract to allow metabolic modification of carcinogen from pro-mutagen into mutagen
  • some agents that failed previous Ames test were positive for mutagen promoting characteristics when in presence of liver metabolic enzymes
45
Q

Evading apoptosis

hallmark?

A

-negative effects on apoptosis -cells stop recognizng signals that cause apoptosis so cells don’t die & accumulate

46
Q

Self-sufficiency in growth signals hallmark?

A

-cells don’t require external growth factors from blood for proliferation, can initiate proliferation on own

47
Q

Insensitivity to anti-growth signals hallmark?

A

-loose signal that says to stop replicating so engages in continuous proliferation

48
Q

Sustained angiogenesis hallmark?

A
  • cancer cells recruit blood supply, to satisfy increased resource requirements
  • can instigate growth of vascularization
49
Q

Tissue invasion & metastasis hallmark?

A

-cancer cells able to leave original place and invade another tissue

50
Q

Limitless replicative potential hallmark?

A
  • cells have time clock that says how many times can divide b4 death (based on tissue location & organism)
  • cancer cells ignore signals; can become immortal cells
51
Q

What happens if remove the antigen causes limitless replicative potential?

A
  • the cell will remember what number replication it was on when it began it’s continuous proliferation
  • will return to that # division once antigen removed
52
Q

Genome instability and mutation hallmark?

A

-an enabling characteristic; effects all other hallmarks, can cause them to occur

53
Q

Tumor-promoting Inflammation hallmark?

A
  • outgrowth from uncontrolled cell division is recognized
  • generates friction & lack of resources, which alters normal cell env & leads to inflammation
  • is an enabling characteristic cuz can cause more cell damages and cause other hallmarks to occur
54
Q

Deregulating cellular energetics hallmark?

A
  • too many cells growing in 1 spot, have to split resources (energy, aa etc);
  • causes growing cells to experience abnormal energy levels, leads to more ROS
55
Q

Avoiding immune system destruction hallmark?

A
  • usually when have uncontrolled growth of cells, immune system ID & removes them
  • in cancer; immune system fails
56
Q

How treat cancer if immune system is failing at catching & disposing of cancerous cells?

A

-take out T cells, modfiy receptors in vitro, allows immune system to recognize cancer cells (personalized medicine)

Block 1 Week 4 (7 decks)

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