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ANAT 212 > Lecture 21 > Flashcards

Lecture 21 Flashcards

1
Q

describe history of cancer

A

Oldest described cancer ~3000 BC in ancient Egyptian textbook on trauma surgery and indicates there is no treatment
Cancers found in fossilized bone tumors and
mummified humans.

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2
Q

what did hippocrates think of cancer

A

460-370BC
used term carcinos and carcinoma to describe it
cancer projections look like a crab - open up patients and see tumors with vasculature and looks like crab - projections spreading out

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3
Q

what did galen think of cancer

A

130-200AD
used word oncos - greek for swelling to describe it
(oncology)

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4
Q

describe humoral theory

A

Hippocrates believed that excessive black bile (one of the 4 humors) caused cancer. Believed through the Middle Ages (~1300 years).
black bile, yellow bile, blood and phlegm

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5
Q

describe infectious disease theory

A

some believed in 17th and 18th centuries that cancer was infectious
would isolate patients with cancer from others

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6
Q

describe modern day theory

A

viruses, chemical carcinogens, and radiation
tabacco, smoking, UV light, exposure

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7
Q

describe cancer and tumorigenesis

A

dna damaging event
normal cells stop dividing but cancer cells do not stop (immortalized)
have additional traits that allow them to grow and spread

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8
Q

name the hallmarks of cancer

A

sustaining proliferative signalling
evading growth suppressors
enabling replicative immortality
activating invasion and metastasis
genome instability and mutation
resisting cell death

inducing angiogenesis
deregulating cellular genetics
tumor promoting inflammation
avoid immune destruction

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9
Q

describe sustaining poliferative signaling

A

does not respond way normal cells do to extracellular signaling
like growth factors - if high amounts = divide more, if low = dormant
cancer cells have constituitive signalling = permanently on signalling that keeps them going

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10
Q

describe enabling replicative immortality

A

dont stop dividing
do it forever

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11
Q

describe activating invasion and metastasis

A

ability to activate metastasis
if primary tumor removed immediately = good
dying is from primary tumor moving from original spot and sets up somewhere else - via lymphatic system = kills patients
becomes dangerous and hard to treat

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12
Q

describe genome instability and mutation

A

divide indefinetly

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13
Q

what is cellular transformation

A

every transformed cell is immortalized but not every immortalized cell is transformed - cell must be transformed in order to form tumor

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14
Q

describe peyton rous and sarcoma

A

Cancer thought at beginning of 20th century to be infectious
In 1909, Rous studied sarcoma in a chicken (avian)
Could transmit tumor
fragment through
implantation - surgically

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15
Q

what did peyton rous do - experiment

A

Filtered tumor homogenate was infectious and led to new tumors
Carcinogenic agent was a virus, now called Rous sarcoma virus (RSV)
remove sarcoma and break into small chunks of tissue, grind up with sand, collect filtrate, only small particles left, inject into chicken = now infected with sarcoma
small quantities of a cell free filtrate have sufficed to transmit susceptible chickens, since filtering = makes particles smaller than cells

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16
Q

what is foci

A

cells that grow on top of each other - transformed

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17
Q

name the 7 characteristics of cellular transformation

A
  1. Immortalization (ability to proliferate indefinitely)
  2. Altered morphology (round shape)
  3. Loss of contact inhibition (ability to grow over one another)
  4. Anchorage-independent growth (growing without attachment to solid substrate)
  5. Reduced requirement for growth factors
  6. Increased transport of glucose
  7. Tumorgenicity
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18
Q

describe loss of contact inhibition

A

allows cells to grow on top of each other - since transformed

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19
Q

describe anchorage independent growth

A

can grow in soft agar like jello

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20
Q

describe pet scan

A

2-Deoxy-2-(18F)fluoro-d-glucose positron- emission tomography (FGD-PET) makes it possible to visualize tumors in the body that have concentrated large amounts of glucose

radiolabelled version of glucose - tumors love glucose, will start to give off positrons and is picked up by scanner

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21
Q

describe the general scientific mood in the 1970s regarding what causes cancer

A

Some believed tumor viruses are causative agents of all human cancers - now we know its not trues
Others believed instead that cellular genes may
often be responsible for cancer.

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22
Q

name a few exs of viruses implicated in human cancer causation

A

epstein barr = burkitt lymphoma
HCV = hepatocyte carcinoma
HPV = cervical carcinoma

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23
Q

what is rsv

A

retrovirus
use encoded enzyme (reverse transcriptase - single rna coding strand) to reverse transcribe rna genomes into cdna = can integrate into cellular host genome

24
Q

what does a retrovirus virion need to have

A

gag= core proteins
pol = codes for rt and integrase
env= envelope protein

25
Q

describe rsv and src

A

rsv has additional gene compared to other avian retroviruses
= SRC (sarcoma) based on its role in triggering formation of sarcomas
if taken out = no sarcoma, nom transformation

26
Q

what cells is src found in

A

src dna sequence in both rsv infected and uninfected cells
used dna hybridized probe to sequence viral genome
something similar to src sequence found in genome = normal genome of host cells
picked up in many species of birds

27
Q

describe model for capture of src by ALV

A

ALV pro-viral DNA (red) integrates by chance next to c-src and then gets transcribed and packaged into new viral particle (RSV)

randomly positions into host genome
accidental integration next to c-src = kept cellular src sequence
high levels of src in viral infection = lead to cellular transformation events

28
Q

what is c-src

A

cellular src gene= proto oncogene

29
Q

what is v-src

A

viral src gene = oncogene

30
Q

name a few connections between retrovirus-associated oncogenes and oncogenes present in non-virally induced human tumors

A

rous sarcoma - chicken - src (first one found), non receptor tk, colon carcinoma
abelson leukemia - mouse - abl - non receptor tk, cml

31
Q

what does src proteins function as

A

tyrosine kinase

32
Q

what is a kinase

A

an enzyme that removes high-energy phosphate
group from ATP and transfers it to a suitable protein
substrate
to a downstream protein on tyrosine aas
signalling cascades - also from inside to outside of cells
Determined first for Src using anti-Src antibody inside experiment
It’s a tyrosine kinase (phosphorylates specific Tyrosine amino acids in substrates).

33
Q

can src autophosphorylate

A

yuh

34
Q

describe action of protein kinases and signalling

A

Kinases generally phosphorylate and thereby modify the functional state of substrate proteins
activates binding partner and goes off and does stuff
= proliferation, angiognesis, apoptosis, protein synthesis - many effects on cells
many, phosphorylation can activate or inactive them

35
Q

give ex of Akt/PKB signalling

A

Akt/PKB kinase influences multiple biological processes by phosphorylating a number of downstream substrates

36
Q

are all oncogenes kinases

A

many but NOT ALL oncogenes are kinases

37
Q

describe signalling of protein kinases

A

external signal –> nucleus gene transcription
bind and activated = phosphorylation –> many paths and effects = affect cytoplasmic pathways or gene expression

38
Q

what is an oncogene

A

A gene that increases the selective growth advantage of the cell in which it resides
will outgrow

39
Q

what is a proto oncogene

A

cellular src in our genes
A normal gene that can become an oncogene as a result of mutations or increased expression (changes in expression)

40
Q

what is a tumor supressor

A

A gene that when inactivated or lost leads to an increase in the selective growth advantage of the cell in which it resides
road blocks, like brakes, stop oncogenes

41
Q

describe normal cell cycle

A

proto onco = gas and tsg = brakes are equal

42
Q

describe mutations leading to cancer

A

proto onco –> onco = too much gas
tsgs inactivated = no brake
usually both in combination - mutations add up

43
Q

describe early experiments towards identifying nonviral oncogenes

A

Researchers speculated that carcinogens function as mutagens that in turn induce cancer by turning proto-oncogenes (like the ones identified by retrovirologists)
into oncogenes
To test this, they introduced DNA of cancer cells into normal recipient cells by a process called transfection= take some of dna and coat with calcium phosphate and enters cell - identify non viral oncogenes

44
Q

describe early transfection experiments towards identifying nonviral oncogenes - gen

A

take pieces of dna and transfect using calcium phosphate to normal mouse fibroblasts –> like monolayer with foci forming, inject transformed cells into mouse host = forms tumor
incorporated small fragments - did not need virus to form tumour - could get through carcinogens

45
Q

describe early transfection experiments towards identifying nonviral oncogenes - specific

A

Used NIH 3T3 cells, immortalized fibroblasts that are great at taking up DNA
Treated mouse cell line with 3-methylchloranthrene (3-MC), a potent carcinogen that is a component of coal tars - mutagenic = causes changes in dna

46
Q

describe turning proto oncogene into oncogene

A

dna rep not perfect = changes increases as age
dna damaging events - studies must be age normalized

47
Q

describe amplification

A

A genetic alteration producing a large number of copies of a small segment of the genome
through mistakes - multiple copies of genes in genome
higher levels of expression protoonco–>onco

48
Q

describe indel

A

insertion or deletion of a few nucleotides
causes pieces to be integrated or lost

49
Q

describe translocation

A

A specific type of rearrangement where regions of two nonhomologous chromosomes are joined (e.g. Philadelphia chromosome)
fusion between pieces of dna = lead to new proteins and stuff

50
Q

describe point mutation

A

single-nucleotide substitutions (e.g. A to G)
missense = aa change bc another nt, cause stop codons, some benign, codes for diff aa then

51
Q

do all mutations drive cancer

A

NAHHHH

52
Q

describe driver mutations

A

a mutation that directly or
indirectly confers a selective growth advantage
to a cell
proto onco –> onco
pathogenic

53
Q

describe passenger mutations

A

a mutation that does not
confer a selective growth advantage (“along for
the ride”)

54
Q

what is selective growth advantage

A

the difference between birth and death rate in a cell population
Allows cancer cells to outgrow the surrounding ‘normal’ cells

55
Q

describe how tumor mutation burdens vary

A

vary across cancers
aml and breast = low mutations
some = driver and some = passenger
melanoma = v high mutation rate, not all driver, most are passenger

56
Q

what are sarcomas

A

Cancers arising in bone or in the soft tissues of the body including muscle are called sarcomas

ANAT 212 (34 decks)

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