Module 1:cancer Flashcards

(27 cards)

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

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
p53 Tumor suppressor gene
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
Paraneoplastic syndrome
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
Tumor markers
DO NOT USE IN SCREENING | Diagnose, detect, manage some CAs