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Pathophys Test 1 > Cancer > Flashcards

Cancer Flashcards

1
Q

What is highest incidence of cancer in males and females?

Main cause of cancer death?

A

Highest incidence- Prostate- men; breat- female

major cause of death= lung cancer in both male and femal

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2
Q

Top 4 incidence for male? Female?

A

Male

  • Prostate
  • Lung and bronchi
  • Colon
  • Urinary bladder

Female

  • Breast
  • Lung and bronchi
  • Colon and rectum
  • uterine corpus
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3
Q

Top 4 Cancer deaths by site male? female?

A

Male

  • lung and bronhus
  • prostate
  • colon
  • pancreas

Female

  • lung and bronchus
  • breast
  • colon
  • pancreas

lung and pancreas fairly virulent/fatal

prostate/breast are very common, but not likely to cause death

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4
Q

What is the cell source for the majority of cancers?

A

Epithelial

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5
Q

What areas of body typically don’t have cancer? Why?

A

Skeletal, cardiomyocytes, neurons

there’s post-mitotic and don’t divide

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6
Q

Cancer incidence increases markedly with ___

A

age

  • childhood Ca very rare and usualyl devleop in utero
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7
Q

What are stroma/stromal cells?

A

support cells in tissue

(Connective tissue, blood vessels)

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8
Q

What are parencyhma/parenchymal cells?

A

special cells uniquely adaped to perform function of organ

(ie hepatocytes, cardiomyocytes, etc)

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9
Q

What are mesenchyme/mesenchymal cells

A

cells of mesodermal or neural crest orgiin

give rise to connective tissue, blood, and muscle

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10
Q

what does- oma mean?

A

benign tumoe

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11
Q

What does -carcinoma mean?

A

malignant tumor of epithelial origin

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12
Q

What does- adenocarinoma mean?

A

malignant tumor of glandular tissue

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13
Q

What does -sarcoma mean?

A

malignant tumor of mesenchymal origin (connective tissue tumor)

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14
Q

What does -blastoma mean?

A

malignant tumor of precursor cells (more common in children)

ex-neuroblastoma

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15
Q

How does a ell become a neoplasm?

A
  • normal tissue has one cell that becomes dysplastic
    • not Ca yet
  • picks up superpower of growth and becomes a neoplasm
    • not yet a Ca
  • Now invades other tissue
    • now Ca and invasive neoplasm

big picture- it starts as one of your cells! Why it’s hard to kill cancer

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16
Q

What does well differentiated/undifferentiated mean?

A

Assigns grading to tumor

  • Well differentiated- Can still detect origin of cell based on where it came from (hepatocyte still looks like hepatocyte)
  • Undifferentiated- does not look like origin site
    • genes randomly turn on/off
      *
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17
Q

What doe TNM stand for?

A
  • T= Tumor
    • T0- no penetration into basement membrane
    • T1) through basement membrane, but still local
    • T4) invasion into other organs/neighboring tissue
  • N= lymph node
    • N0) no lymph node involvement
    • N1) local lymph node involvement
    • N4) extensive lymph node involvement
  • M= metastasis
    • M0) No metastasis
    • m1) metastasis
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18
Q

Characteristics of benign tumor?

A
  • Small
  • Well demarcated
  • slow growing
  • noninvasive
  • nonmetastatic
  • well differentiated
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19
Q

Characteristics of malignant tumor?

A
  • Large
  • poorly demarcated
  • rapidly gorwing with hemorrhage and necrosis
  • locally invasive
  • metastatic
  • poorly differentiated
20
Q

Stages of cancer progression?

A
  • Transformation- carcinogen induced change in a normal cell
  • Progression
    • growing more tumor cells
    • makes multiple mutations
  • Proliferation of genetically unstable cells
  • tumor cell variants heterogeneity
21
Q

What are proto oncogenes?

A
  • better termed “pre” oncogene
  • gene with some normal function
  • usually associated iwth growth
  • easily mutated to make oncogene
  • the oncogene encourages tumor development
  • only need one mutation<– big point
    • mutate either one (either gene) and you have a problem
  • “over activity mutation”- gain of function
22
Q

What is a tumor suppressor gene? Examples?

A
  • suppresses tumors
    • regulates cell cycle
    • if it is inactivated or defective, the cell can proceed to rapid division
  • 2 copies of each
    • lose 1- inactivates tumor suppressor gene
      • NO effect if mutation only in one copy
    • lose 2- eliminates the tumor suppressor gene, stimulating cell proliferation
  • Examples:
    • p53- various ~70% of cancer
    • BRCA 1, BRCA2- breast and ovrian cancer
    • APC- colorectal (adenomatous polyposis coli)
    • RB1- various (retinoblasoma)
    • MSH2- colorectal, endometrial, gastric
    • NF1, NF2- neuroblastoma, etc (neurofibromin)

BOTH GENES MUST BE DEFECTIVE!

23
Q

Proto oncogene vs oncogene protein product?

A

Proto oncogene

  • normal cellular gene
  • can be converted into cancer-promoting oncogene by mutation

Oncogene protein

  • Abnormal activity or
  • is expressed at abnormal levels
    • leads to cell death or gives rise to cancer
24
Q

What are some examples of proto-oncogenes?

A
  • bcl-2 - bcell lymphoma
  • HER2/neu- breast cancer, ovarian cancer, others (epidermal growth factor receptor)
  • n-myc- neuroblastoma
  • c-myc- burkitt lymphoma, others
  • Ras- various, 20-30% of all cancers

only one gene needs to be defective to cause issue!

25
Q

How are chromosomal translocations oncogenic?

A
  1. Change in transcriptional control elements
    • During crossover process, the regulatory domain of the gene expressed at high levels was attached to gene normally expressed at low levels, we have a problem
      • now overproducing something that should be produced at low level, causes issues
  2. Synthesis of a novel fusion protein
    • combine two random axons causing new protein formation
      • might give us a superpower, most of times, it’s bad
26
Q

What is the germline mutation of tumor suppressor gene?

A
  • If mom already defective RB1 (tumor suppressor gene) in egg, then every cell in offspring has one bad tumor suppressor gene
  • Only need 1 more mutation and then you have issues
27
Q

What are six hallmarks of cancer?

A
  • Self sufficiency in growth signals
    • can’t wait for someone to tell it to grow
  • Insensitivity to antigrowth signals
    • needs to do it’s own thing
    • cancer has to be a self-starter
  • Evading apoptosis
    • don’t die
  • limitless replicative potential
    • turn telomerase back on
  • sustained angiogenesis
    • need blood as you grow
  • tissue invasion and metastasis
28
Q

How does RAS affect self-sufficiency in growth signals?

A
  • RAS has GTPase mutation (can’t hydrolyze the GTP–> GDP and stop pathway to encourage growth for cell)
  • Typically, RAS inactivated by GTP–> GDP, however in this mutation, GRP does not get hydrolyzed
  • now, when gorwth factor binds, the cell keeps being stimulaed to grow
  • RAS stays in active form, leading to overgrowth
29
Q

If you have 2 RAS genes, and the one from dad is mutated (during your life), what can happen?

A
  • RAS is protooncogene, so it only needs one mutation (one bad gene) and then the growth pathway stays active
  • GTPase is then mutated and cell will continue to activate MAP kinase pathway for cell growth
30
Q

Examples of how cells maintain insensitivity to anti-growth signals?

A
  • Rb (tumor suppressor gene) is like a gatekeeper for mitosis
    • letting people go through if it is appropriate
    • We have 2 copies of Rb (one mom, one dad)
      • since Rb is like a guard, one is as good as two
      • BUT if 2nd Rb is mutated, then anybody can go through
  • So, if we lose both Rb, we’ve lost a major contorl of the cell cycle and tumor can replicate indefinitely.
31
Q

What is the likelihood of developing retinoblastoma if you start with normal genes and have mutation vs inheriting mutation?

A
  • If you inherit normal genes from parents, then you need 2 spontaneous mutations in the same cell in your livelihood
    • this is VERY unlikely 1/50,000 incidence. Usually when you’re 60/70 yo
  • If you inherit a mutant Rb gene, you only need one more mutation in any cell in order to cause issues
    • nearly 100% incidence of retinoblastoma, and probalby before you’re 1 yo

Mutation in one cell throughout life is likely HOWEVER 2 mutations in the same cell is very unlikely!

32
Q

What is p53 and how does a mutation affect the cell?

A
  • p53 is guardian of DNA. Good p53;
    • asks if you’ve replicated DNA properly?
      • if answer no, p53 will stop process and allow you to fix DNA. If you can’t, p53 will tell you to die or survive, but can’t replicate again
  • If p53 bad
    • nothing to safeguard the cell DNA
    • no cell cycle arrest, no DNA repair, no senesene
    • causes mutant cell to expand and add additional mutations
33
Q

How do cells accomplish limitless replicative potential?

A
  • In cancer, turns back on telomerase enzyme activity
  • this allows telomeres to be maintained and allows cancer cell to replicate indefinitely
34
Q

How do cancer cells sustain angiogensis?

A
  • Tumor needs to secrete tumor agniogenic factors (ie. VEGF- vascular endothlial growth factor)
    • uses normal blood vessel and encourages growth of blood vessels
35
Q

How do tumors invade and metastasize?

A
  • Tumor produces collagenase in order to dissolve basal membrane and separate from neighboring cells
  • then, reaches down to grab fibronectin of basement membrane layer, invading surrounding tissue
36
Q

What is multistep nature of metastasis?

A
  • Primary tumor
  • proliferation/angiogensis
  • detachment/invasion
    • lymphatics, venules, capillaries
  • embolism/circulation
    • interaction with platelets, lymphocytes and other blood components
  • transport
  • arrest in organs
  • adherence ot vesssel wall
  • extravasation
  • establishment of microenvironment
  • proliferation/angiogenesis
  • metastasis
37
Q

What determine where things metastasize

A
  • Cell needs to be able to survive in new organ environment
    • if cell too foreign, then it will die in new organ
  • certain cancers favor certain met spots
    • ie breat–> bone
38
Q

Main sites of blood-borne metastasis?

A
  • Lungs, liver have lots of blood flow, lots of mets
  • However, not many mets to kidney because it’s a bizarre environment for most cells
  • prostate and breast like bone
  • Once cancer metastasizes to brain- game over with mets
  • Also, mets are like cockroaches- once you have one, you have hundreds.
    • mets look like seeds in organ while primary tumors look like one big tumor
39
Q

When does HPV develop from wart to tumor?

A
  • When there’s accidental integration of viral DNA fragment into host chromosome DNA
  • when it’s a benign growth or wart, the viral DNA is still separate from the host DNA
  • Involves binding of E7 and E6 protein to tumor suppressor genes
    • E7 binds to Rb
    • E6 binds to p53
40
Q

What protein does E7 (from HPV) bind to? E6?

What does this do to the cell?

A
  • E7 binds to the retinoblastoma protein ( a tumor suppressor gene)
  • E6 binds to the P53 gene (our most powerful tumor suppressor gene)
  • It doesn’t mutate the gene at all, instead it binds and renders it inactive
  • This makes the cell most susceptible to mutations at a higher rate
    • now cell infected with HPV will more likely become cancerous
41
Q

HPV is responsible for almost ____ % of cervical cancer

A

100%

HPV is also responsible for cancers at other sites

  • strands of HPV are cell-specific and the ones that cause cancer REALLY like cervical cells
42
Q

What are the strands of HPV covered by the HPV vaccine?

A
  • 6, 11, 16, 18
  • By a certain age, you’ve most likely been exposed to them all
  • However, if you’ve only been exposed to say, 18 before the vaccine, then the vaccine will still be effective against 6, 11, and 16
  • Vaccine works like all other vaccines. Antigen from virus is presented to body for B/T cells to find, then your body creates a response to the antigen.
    • next time you’re body is exposed, your immune system can readily fight the virus
43
Q

What is the relationship between tumor cell burden and the phases of cancer treatment?

A
  • Typically, most cancer cells are rejected by natural immune mechanisms (if under 1mm mass)
    • unsure of the exact rate because there’s cancer cells developing all the time in your body
  • When 1 cm mass, then more clinically diagnostic neoplasm. How detectable it is depends on where the tumor is on your body
    • can do surgical debulking, try to remove all tumor but if they don’t remove every cell, then cancer can reoccur
  • Debulking followed by chemo to continue killing cancer cells left behind
44
Q

What are some adverse effects of cancer chemoptherapy?

A
  • Gi tract- particularly mucosa of small intestines
  • bone marrow- all hematopoietic cells are affected
    • anemia, neutropenia- biggest problem
  • hair- hair follicles on head most affected
  • skin- decreased epidermal renewal rate
  • fetus- chemo is strictly contraindicated in pregnancy
    • 1st trimester- absolutely don’t do chemo
    • 2nd and 3rd- maybe ok if absolutely necessary
45
Q

What is actually causing the nasty symptoms of cancer?

A

Immune system response

  • Cytokines and chemokines released causing all the same problems as when you have the flu but at a much higher level
  • often time, no overt organ failure causes death from cancer but instead usually killed by the immune system

Pathophys Test 1 (7 decks)

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