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anatomy > Cancer pt 2 > Flashcards

Cancer pt 2 Flashcards

1
Q

what is cancer? 4

A
  • A collection of over 100 diseases with the potential to invade and spread
  • abnormal growth resulting from uncontrolled
    proliferation
  • Human cells that ignore cell signals > serves no physiologic function
  • Most form tumors
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2
Q

Are all tumors cancer?

A

No, they can be both benign (non-
cancerous) or malignant (cancerous)

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3
Q

BENIGN TUMORS
growth rate
surface
invasive?
spread how?
cell morphology
regrowth?
bleeding?
nomenclature?
pressure?

A
  • slow growing by expansion
  • regular surface, capsulated, not attached to deep structures
  • noninvasive to organs/tissues
  • doesn’t spread/metastasize
  • cells are well-differentiated
  • no recurrence after surgery
  • no bleeding in cut surfaces
  • suffix -oma
  • slight pressure effects on neighboring organs
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4
Q

MALIGNANT TUMORS
growth rate
surface
invasive?
spread how?
cell morphology
regrowth?
bleeding?
nomenclature?
pressure?

A
  • rapidly growing by invasion
  • irregular surface, non-capsulated, attached to deep structures
  • invasive to organs/tissues
  • DOES spread/metastasize
  • cells can be poorly/moderately/well differentiated
  • possible recurrence after surgery
  • bleeding from cut surfaces is common
  • suffix sarcoma/carcinoma
  • heavy pressure effect on neighboring tissue
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5
Q

if a tumor is malignant but still localized, it is called _____

A

“in situ”

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6
Q

How do we detect tumors aside from visible detection and symptoms? 2 EX?

A
  • tumors secrete tumor markers > specific hormones, proteins, antigens, antibodies > can be biologically inactive or active (inactive is safer)
  • EX: Liver tumor cells produce alpha
    fetoprotein > inactive, made in infants
  • EX: Prostate tumor cells produce prostate
    specific antigen
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7
Q

why are tumor markers important

A

Important for diagnosing origin in metastasis as well as recovery

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8
Q

tumors marker for:
ovarian cancer
breast cancer
pancreatic
prostate
colorectal
teratoma
seminoma
choriocarcinoma
SCLC
gastrinoma

A

ovarian: CA, 125
breast: CA 15-3
pancreatic: CA 19-9
prostate: PSA
colorectal: CEA
teratoma: AFP
seminoma: LDH
choriocarcinoma: Beta-hCG
SCLC: NSE
gastrinoma: Gastrin

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9
Q

TRANSFORMATION OF CANCER CELLS
what is it caused by
cell aquires:
no need for:
ignores:
morphology:

A
  • genetic mutations
  • cell acquires “autonomy” > Independence from cellular control mechanisms
  • no need for external growth factors; grow on their own
  • Ignores cell checkpoints when dividing,
    creating daughter cells with the same mutations
  • loss of morphology = no longer perform
    normal function
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10
Q

“wheel” of the hallmarks of cancer 10

A
  1. invasion and metastasis
  2. inflammation
  3. enabling replicative immortality
  4. angiogenesis induction
  5. sustaining proliferative signaling
  6. evading immune destruction
  7. metabolism reprogramming
  8. cell death resistance
  9. evading growth suppressors
  10. genome instability
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11
Q

describe the “invasion and metastasis” hallmark 3

A
  • Cancer cells break off solid tumors and slip into lymph and vasculature by losing their gap junctions & adhesion molecules
  • Cancerous cells are anchorage-independent, meaning they can divide in fluid/blood
  • Cancerous cells have a high degree of proteases meaning they can break down proteins and basement membranes
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12
Q

describe the “inflammation” hallmark 2

A
  • Chronic inflammation is strongly linked to cancer formation
  • The cycle of cell destruction and proliferation increases the likelihood of acquiring mutations
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13
Q

describe the “replicative immortality”

A

active telomerases regenerate telomere caps on the ends of chromosomes

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14
Q

“induction of angiogenesis” hallmark

when does a tumor need its own blood supply
angiogenesis is typically limited to:
tumors secrete:
what does VEGF do?
implications?

A
  • Once it’s over one millimeter in
    diameter
  • wound healing & the uterus
  • angiogenic factors to contribute to angiogenesis (making blood vessels)
  • Vascular endothelial growth factor = proliferation of endothelial cells and recruits stem cells to become endothelial cells
  • promotes sinusoidal vasculature formation; increases the likelyhood of metastasis
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15
Q

describe the “sustaining proliferation” hallmark 4

A
  • can use autocrine signaling for growth factors
  • growth factor receptors are upregulated
  • Gene mutations (point mutations, translocations, etc) contribute to uncontrolled growth.
  • EX: RAS oncogene mutation accelerates proliferation
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16
Q

describe the “evading immune destruction” hallmark 4

A
  • Cancer cells reprogram cells of the immune system to lower T cell destruction/phagocytosis
  • promotes “wound healing” instead of “wound cleaning”
  • Promotes proliferation, angiogenesis, and reduces immune surveillance
  • convert helper T cells to regulatory T cells bc T.reg cells tell the body when to end the immune response (makes body think we are healthy)
17
Q

as part of evading immune destruction, cytokines are released from cancer cells to recruit and create TAMS, what are they and what do they do? 5

A
  • TAMS: Tumor-associated macrophages
  • Different phenotype of normal macrophage
  • Diminished cytotoxic response
  • Can block cytotoxic T cells and NK cells
  • Secrete growth factors and matrix metalloproteinase which promotes matrix degradation
18
Q

describe the “metabolism reprogramming” hallmark 3

A
  • exhibit unique metabolism
  • Shift in main source of ATP production: from Mitochondrial oxidative phosphorylation to just glycolysis
  • Products of glycolysis, (lactate and other
    molecules), are readily used to create more lipids faster
19
Q

describe the “cell death resistance” hallmark 3

A
  • Cancerous cells have increased resistance to cell death pathways (both intrinsic and extrinsic)
  • Many cancers have mutations in their caspase
    genes, resulting in no/faulty caspase proteins
  • failure to undergo apoptosis
20
Q

describe the “evading growth suppressors” hallmark 4

A
  • exhibit inactivation of tumor suppressor genes
  • Regulation of cell cycle, inhibits proliferation when cell is damaged
  • Inactivation = cells can proceed through check
    points unchecked
  • Retinoblastoma (Rb) gene is commonly inactivated in many cancers
21
Q

what is BRCA1 and BRCA2 (4)

A
  • Breast cancer susceptibility genes
    that account for 15-20% of familial cases, 12% gen. pop. cases, 87% of hereditary cases
  • Greatly increases risk of breast and ovarian cancer
  • Deletion of two bases in BRCA1 causes a
    shift in the reading frame, shortens
    protein
  • mutations are autosomal dominant: only 1 allele needs to be affected
22
Q

describe the “genome instability” hallmark of cancer 5

A
  • high degree chromosome instability
  • High rate of chromosome loss
  • translocations
  • loss of allele heterozygosity > they copy and paste the same allele rather than both parents
  • gene amplification > copy and pasting one portion of a gene over and over on ONE chromosome
23
Q

how do we diagnose cancer? 2

A
  • via biopsy, aspiration, or exfoliative cytology
  • Cells are assessed in regards to the size of
    the tumor, the degree to which it has locally
    invaded, and the extent to which it has
    spread/metastasized
24
Q

what are the stages of cancer?

A
  • S1 = cancer is small and confined to the organ
    of origin
  • S2 = locally invasive
  • S3 = spread to regional structures (ie
    nearby lymph nodes)
  • S4 = spread to distant sites
25
Q

treatment for cancer? 6

A
  • treatment is unique
  • Most commonly combinations of
    chemotherapy, radiotherapy, and surgery
  • patient’s emotional state and wishes must be considered
  • Goal is to exploit vulnerabilities, block growth pathways, target cells with high mitotic index
  • hard to treat due to the fact that they are still our own cells
26
Q

acute lymphoid leukemia

found where?
grows?
common in what age?
how many cases per year

A

lymphoid cells
grows quickly
children
6,000/year

27
Q

acute myeloid leukemia

found where
grows how
common in what age
how many cases per year

A

myeloid cells
grows quickly
adults and children
18,000/year

28
Q

chronic lymphoid leukemia

found where
grows how
common in what age
how many cases per year

A

lymphoid cells
grows slowly
adults 55+
15,000/year

29
Q

chronic myeloid leukemia

found where
grows how
common in what age
how many cases per year

A

myeloid cells
grow slowly
adults
6,000/year

30
Q

what are the grades of tumors

A

grade 1: well-differentiated cells
grade 2: moderately differentiated cells
grade 3: poorly differentiated cells
grade 4: un-differentiated cells

31
Q

what is differentiation?
what is stage?
What is grade?

A
  • how abnormal tumors cells look compared to normal cells
  • how far the cancer has traveled/spread
  • how quickly the tumor cells are dividing

anatomy (17 decks)

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