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From Flashcardlet > Pathology - Neoplasia: cancer epidemiology & pathogenesis > Flashcards

Pathology - Neoplasia: cancer epidemiology & pathogenesis Flashcards

1
Q

radon: what cancer?

A

lung - due to uranium decay , mines

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2
Q

vinyl chloride: what cancer?

A

angiosarcoma
liver
due to refrigerants (mentioned PVC pipes)

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3
Q

asbestos: what cancer?

A

mesothelioma - from roofing, tiles

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4
Q

Cancer is most frequent at what ages

A

young and old

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5
Q

children: which cancers most common?

A

Leukemia/lymphoma, CNS tumors, sarcoma

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6
Q

Three categories of hereditary cancer

A
  • Inherited cancer syndromes
  • Familial cancers
  • Syndromes of defective DNA repair
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7
Q

Inherited cancer syndromes examples

A

Dominantly inherited
Retinoblastoma
Familial polyposis coli

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8
Q

familial cancers

A

Most common sporadic cancers have familial forms too
Breast, colon, ovary, brain
Occur earlier, are often deadlier

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9
Q

Syndromes of defective DNA repair examples

A

Recessively inherited

Xeroderma pigmentosum

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10
Q

Acquired preneoplastic syndromes

A

1) Persistent regenerative cell replication
2) Hyperplastic and dysplastic proliferations

these pts with these “syndromes” are more likely to get cancer

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11
Q

Persistent regenerative cell replication examples

A

ex: Chronic skin fistula → squamous cell carcinoma
ex: Cirrhosis → Liver cancer

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12
Q

Hyperplastic and dysplastic proliferations examples

A

Atypical endometrial hyperplasia → endometrial cancer (lining of uterus thicker)
Dysplastic bronchial mucosa → lung cancer

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13
Q

Chronic atrophic gastritis →
Chronic ulcerative colitis →
Leukoplakia →

A

stomach cancer
colon cancer
squamous cell carcinoma

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14
Q

what causes cancer “in a nut shell”

A

non-lethal genetic damage

cell acquires damage but cell doesn’t “die”

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15
Q

4 kinds of genes that can be damaged –> cancer

A

proto-oncogenes (promote growth)
tumor-suppressor genes (inhibit growth)
those that regulate apoptosis
those involved in DNA repair

note: cancers develop in multiple steps

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16
Q

“Cancer genes” cause bad things in cells: (6 things)

A 
Autonomous growth
Insensitivity to growth-inhibitory signals
Evasion of apoptosis
Limitless replication 
Sustained angiogenesis
Invasion and metastasis
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17
Q

proto-oncogene vs. oncogene

A

Proto-oncogene: a normal gene whose product promotes cell growth.
Oncogene: mutated proto-oncogene! Causes cell to grow autonomously!

note: Oncoprotein: the product of an oncogene.

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18
Q

steps leading to cell division (normal cells)

A
  1. Growth factor binds to receptor
  2. Receptor activates signal-transducing protein
  3. Signal-transducing protein activates 2nd messenger
  4. 2nd messenger talks to nuclear transcription factors
  5. Nuclear transcription factors start DNA transcription
  6. Cyclins move the cell through the cell cycle
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19
Q

in cancer cells –> cells divide on their own

what 5 things can happen for this to occur

A

Growth factors may be made by cell itself!
Receptors may be overexpressed or always on
Signal-transducing proteins may always be on
Nuclear transcription factors may always be expressed
Cyclins may be overactive

20
Q

RAS gene: mutation? what does this lead to in cancers and how?

A 
lead to autonomous growth:
RAS is a signal transduction protein
Mutated RAS is always on…
…therefore, always transducing signals…
…therefore, cell is always dividing
21
Q

tumor supressor genes: mutation? what does this lead to in cancers and how?

A

leads to insensitivity to growth-inhibitory signals

Tumor-suppressor genes: normal genes whose products act as “brakes” on the cell cycle.

Mutate these guys, and you lose the brakes!

Gotta lose both copies of the gene to cause tumors.

22
Q

RB gene: mutation? what does this lead to in cancers and how?

A

leads to insensitivity to growth-inhibitory signals

RB gene product stops cells at G1 checkpoint

Mutant RB is inactive; lets cells pass through G1!

Patients with two mutant RB genes have:
increased risk of retinoblastoma
Increased risk of other tumors (sarcoma)

23
Q

p53 gene:
what is its normal function?
if mutated what does this lead to in cancers?

A

leads to insensitivity to growth-inhibitory signals

normal functions:

  • If a cell’s DNA is damaged, p53 causes a pause in the cell cycle (via RB!), so DNA can be repaired.
  • If DNA damage is irreparable, p53 causes the cell to die.

note: most tumors = p53 mutations

24
Q

what important protein is involved in apoptosis?

If genes for these proteins are mutated what happens?

A

“EVASION OF APOPTOSIS”
p53
If genes for these proteins are mutated, the cell becomes immortal.

25
Q

LIMITLESS REPLICATION:
How do tumor cells learn to do?
what enzyme do they have/use to accomplish this?

A

NORMAL cells: Telomeres keep getting shorter leading to cell cycle arrest (via p53 and RB).
HOWEVER,
Stem cells & CANCER CELLS use TELOMERASE enzyme to maintain telomere length and keep replicating

26
Q

sustained angiogenesis: tumor cells must have. how do they do this?

A
  • Tumor cells need blood bc Can’t grow >1-2 cm without new vessels
  • Tumor cells eventually learn how to stimulate angiogenesis
  • Lots of cytokines involved (i.e., VEGF)
  • Tumor vessels are abnormal (grow in evolving network that is unstable and inappropriate to location)
27
Q

to INVADE: what must tumor cells do?

A

Loosen contacts between cells
Degrade extracellular matrix
Migrate away from original site

NOTE: Some tumors:

  • lodge in nearest capillary bed
  • show tropism (preference) (i.e. prostate loves to go to bone)
28
Q

mechanisms which they need to learn how to survive in the blood vessel (see slide 53 of cancer pathogenesis)

A 
might coat themselves with plasma proteins or form a ball to "be sneaky".
clonal growth
metastatic subclone
intravasation
tumor cell embolus
extravasation
29
Q

Examples of hereditary DNA repair defects

A

Hereditary Nonpolyposis Colon Cancer Syndrome

Xeroderma Pigmentosum

30
Q

Hereditary Nonpolyposis Colon Cancer Syndrome

A

failure of mismatch repair (no spellchecker)
inherit one mutation, acquire the other
familial colon cancers

31
Q

Xeroderma Pigmentosum

A

failure of nucleotide excision repair system
small sun exposure leads to skin cancers

UV light can link together pyrimidines
memory point: super sad picture

32
Q

what is the average # of mutations for cancer to arise.

A

90

Normally, body fixes or gets rid of mutated cells (RB, p53)!
sooooo…
For a tumor cell to grow, one of its mutations must be within these checkpoint/guardian genes.

33
Q

if mutation large: what lab procedure is used to find

A

cytogenetics with karyotype

34
Q

if mutation small: what lab procedure is used to find

A

molecular studies like southern blot or PCR

35
Q

karyotypic abnormalities occur predictably in certain tumors. which ones?

A

leukemias, lymphomas

solid tumors

36
Q

how is karyotyping done?

A

DNA probes specific to regions of particular chromosomes are attached to fluorescent markers and hybridized with a chromosome spread. The picture shows a computer-generated “false colour” image in which small variations in fluorescence wavelength among probes are enhanced as distinct primary colours. The combination of probes that hybridize to a particular chromosome produces a unique pattern for each chromosome.

37
Q

balanced translocation: common in what kind of cancers?

A

luekemias and lymphomas
balanced translocation of chromo #9/#22
BRC-ABL hybrid gene –> “bad ass tyrosine kinase”

38
Q

deletions: common in what kind of cancers?
what type of gene mutation is the “usual suspect”?
give a specific example.

A

common in solid tumors
Usually: deletion of a tumor-suppressor gene

Example: del 13q14 in retinoblastoma

39
Q

carcinogenic agents

A

Chemicals
Radiation
Bugs/viruses

40
Q

chemicals: direct-acting agents

A

Carcinogenic as-is
Most are chemotherapy drugs
Cause secondary malignancies (e.g., leukemia)

41
Q

chemical: Indirect-acting agents

examples?

A

Require conversion to become carcinogenic

Examples:
hydrocarbons (in tobacco, charred meats)
aflatoxin B (from Aspergillus-infected grains, nuts)
nitrites (food preservative)

42
Q

what is the biochemical mechanism of chemical carcinogenic agents? i.e. how do they do their damage?
what are the 2 IMPORTANT TARGETS?

A

Highly reactive electrophile groups bind to DNA

Important targets: RAS and p53

43
Q

radiation: Ionizing
radiation: UV light
how does each do it’s damage?
examples?

A

Ionizing radiation: Causes chromosome breakage, translocations

Examples:
Unprotected miners: lung cancer
Atomic bomb survivors: leukemia, other cancers
Therapeutic head/neck radiation: thyroid cancer

UV light: Causes formation of pyrimidine dimers
Repair pathways usually fix – but can become overwhelmed

Examples: squamous cell carcinoma, melanoma

44
Q

staging system for non-small cell cancer

what are the 3 things that are used for “grading”/”staging”?

A

TNM staging system for
T: how big is the tumor (T in situ –> T4)
N: number nodes involved
M: metastasis (yes/no)

diff combinations of these factors determine what “stage” it is.
i.e. stage 4 = distant mets
grading = microscopic
staging = clinical

45
Q

GRADING & STAGING:
what types of tumors is used for?
useful for determining what 2 things?

A

Used for malignant tumors

Useful for determining treatment and prognosis

46
Q

Grading

A

MICROSCOPIC
Tells you how nasty the tumor looks
Pathologic evaluation of tumor (use microscope)
Mitoses, pleomorphism, necrosis, other variables
Somewhat useful

ex: BC = tubules, pleomorphism, mitoses

47
Q

Staging

A 
CLINICAL
Tells you how far the tumor has spread
Clinical evaluation of patient (use imaging, surgery) 
TNM system
Very useful

stage: 0-4

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