Module 1:cancer Flashcards

1
Q

Cancer cell biology

A

Lifecycle, growth, proliferation is unregulated Bc not from stem cells
Ignore signals to stop division/trigger apoptosis
Avoid being detected by immune system to keep growing

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2
Q

Tumor marker: Alpha fetoprotein found in

A

Liver or germ cell

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3
Q

Tumor Marker: Carcinoembryonic antigen found in

A

GI, pancreatic,lung, breast

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4
Q

Tumor Marker: Beta human chorionic gonadotropin found in

A

Germ cell, choriocarcinoma

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5
Q

Origin of carcino-/adeno

A

Epithelial

Glandular epithelial

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6
Q

Origin of sarco-

A

Connective tissue

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7
Q

Origin of -oma

A

Tumor or mass

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8
Q

Origin of Carcinoma in situ

A

Very early, preinvasive carcinoma of glandular or squamous epithelial tissue

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9
Q

Origin of Blastoma

A

Nervous tissue/precursor cells

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10
Q

Lung mets

A

Brain+ many others

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11
Q

Colorectal mets

A

Liver and lungs

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12
Q

Testicular mets

A

Lungs, liver, brain

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13
Q

Prostate mets

A

Bone-esp lumbar vertebrae, liver

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14
Q

Breast

A

Bones, lung,liver, brain

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15
Q

Head/neck CA mets

A

Lymphatics, liver, bones

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16
Q

Ovarian mets

A

Peritoneal, diaphragm, omentum, liver

17
Q

Sarcoma mets

A

Lungs

18
Q

Melanoma

A

Lymph,lung,liver, brain, GI tract

19
Q

Cancer mets mechanism

A

Only local invasion possible before Epithelial mesenchymal transition (stimulated by IL8)
Neuroangiogenesis + lymphangiogenesis = Invasion of blood/lymph
Neovascularization gives access to venous/lymph channels

20
Q

TNM staging

A

Tumor-size
Node-degree of involvement
Mets-if distant
^#=^severe

21
Q

Oncogenes

A

Mutated Proto-oncogenes (normally regulate cell div)
No regular cell mechanisms=proliferation
Give ability to secrete growth factors=stimulate own growth (autocrine stimulation)
Activated by point mutations, translocations, gene amplification

22
Q

Tumor suppressors Anti-oncogenes

A

Control proliferation
Stop division in damaged cells+ prevent mutations
2 in each cell
Can mutate and pass thru sperm and egg~~transmission of ca causing genes

23
Q

BRCA gene

A

^ovarian, breast, prostate CA risk

24
Q

Clinical manifestation of CA (condition)

Wasting syndrome

A

Cachexia

Imbalance of energy intake/used
Metabolism^^ in CA
^apoptosis+vCell regeneration

Wasting syndrome-vAppetite, cv atrophy/dysfunction, gut barrier dysfunction, inflammation, acute phase reactants, ^lipolysis,vAlbumin, thermogenesis

25
Q

p53 Tumor suppressor gene

A

Produces p53 protein-monitors cell stress, activates caretaker genes-maintain integrity of genome
Produce proteins that repair dna
Initiates sensescence, apoptosis, suppresses cell division until dna repaired

26
Q

Paraneoplastic syndrome

A

Triggered by release of substances from tumor
Represent earliest sign of unknown CA
Irreversible~death
Ex:carcinoid tumors=serotonin=flushing, diarrhea, wheezing, rapid HR

27
Q

Tumor markers

A

DO NOT USE IN SCREENING

Diagnose, detect, manage some CAs