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Nutr 4210 > 16. Cancer > Flashcards

16. Cancer Flashcards

1
Q

3 most common cancers

A
  1. prostate and breast (men vs women)
  2. lung
  3. colorectal
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2
Q

what is cancer

A

abnormal cell growth

- mass of tissue

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3
Q

types of tumors

A

benign

  • non-cancerous
  • rarely threatening
  • dont spread

malignant
- cancerous

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4
Q

spread of cancer cells

A

metastasis

  • development of secondary tumors
  • into blood/lymph system
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5
Q

cancer process

A
  1. initiation
    - DNA damage (ROS)
    - irreversible changes to cells
    - genomic instability -> hyperplasia
  2. promotion
    - evade immune system
    - promote cell survival (proliferation)
    - angiogenesis
    - time of rapid growth
  3. progression
    - metastasis
    - growth, invades surrounding tissue
    - affects normal function
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6
Q

hyperplasia of cancer

A
  1. increase cell proliferation
  2. decrease/block apoptosis

*** 2 seperate processes

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7
Q

abdominal obesity metabolic abnormalities that increase risk

A

Metabolic

  • insulin resistance and hyperinsulinemia
  • hyperglycemia and hyperlipidemia

Altered metabolic hormones

  • increase insulin-like growth factor (IGF-1) (colon)
  • estrogen (breast)

Abnormal adipokine production

  • metabolic signals
  • insulin resistance and high insulin -> risk of some cancers
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8
Q

obestity promote cancer cell survival

A

adipocytes

  • decrease adiponectin
  • increase leptin

macrophages

  • increase IL-6, IL-1beta
  • increase TNFalpha
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9
Q

obesity promote cell proliferation

A

hormones
- estradiole increase (in blood and tumor)

insulin resistance

  • increase insulin and IGF-1
  • adipocytes (adiponectin decrease and leptin increase promote insulin resistance)
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10
Q

obesity promote angiogenesis

A

hormones
- increase estradiol bioavailability

insulin resistance

  • increase insulin and IGF-1
  • adipocytes (adiponectin decrease and leptin increase promote insulin resistance)

adipocytes

  • leptin increase
  • adiponectin decrease
  • directly influence
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11
Q

leptin in caner

A

Promote tumor initiation and Cancel cell proliferation, survival and migration

increase NFkB and STAT3 activation
- increase inflammatory cytokine (TNFa and IL-6 respectively)

promote cell proliferation and cell survival

attract neutrophils and other immune cells

  • into tumor microenvironment (CHEMOTACTIC)
  • increase ROS production -> DNA damage
  • secrete pro-inflam cytokines -> IL-1B, IL-6. IL-8, TNFa

antagonizes anti-inflam mechanisms

  • adiponectin
  • IL-10
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12
Q

adiponectin and cancer

A

reduce cell proliferation and survival

  • inhibits signal pathways
  • reduce cell growth and proliferation

pro-apoptotic

  • activates caspases
  • stims cytochrome C release from mitochondria

anti-inflammatory

  • stim PPARgamma -> block NFkB activation and cytokine production (TNFa)
  • increase IL-10

activates APPL1

  • binds adiponectin receptor
  • reduces ROS production

*** reduced levels in obesity

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13
Q

insulin and cancer

A

hyperinsulinemia

  • increase insulin and free IGF-1
  • increase cell growth and proliferation
  • decrease apoptosis
  • stim VEGF expression and promote angiogenesis
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14
Q

VEGF

A

vascular endtholial growth factor

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15
Q

inflammatory cytokines / transcription factors and cancer

A

IL-6 increases STAT 3 activation

  • active >50% of tumors
  • anti apoptotic (reduce gene expression)
  • promote cell proliferation
  • stim VEGF -> pro angiogetic
  • prolonged NFkB activation

NFkB increases TNFa

  • increase proliferation and angiogenesis
  • increase cIAP (cellular inhibitor of apoptosis)**
  • inhibits caspase activity**
  • promotes cell invasion and metastasis via MMP activation
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16
Q

cancer cachexia

A

body weight loss

  • both skeletal muscle and adipose
  • adequate nutrition

30-80% of cancer patients

  • severe in 15% (10% loss initial body weight)
  • pancreatic, gastric and SI cancers
  • death at 25-30% weight loss
17
Q

cachexia metabolic change associations

A
  • insulin resistance
  • increase glucose production in liver
  • increased lipolysis
18
Q

causes of cachexia

A 
tumor by-products
- inflam cytokines (TNFa, IL-6), and leptin
dysphagia
- difficulty swallowing
gastrointestinal disturbances
- obstruction/constipation
malabsorption
treatment toxicities
- nausea and vomiting 
uncontrolled symptoms
- pain, dyspnea (diff bretahing)
Xerostomia
- dry mouth
19
Q

depletion in muscle mass

A

hypoanabolism

  • hormone change
  • lack amino acids

hypercatabolism

  • proteolytic enzymes
  • proinflam cytokines (TNFa and IL-6)
  • tumor derived catabolic factors

**key distinction for treatment

20
Q

survival rate

A

about 1/2 with cachexia weight loss

21
Q

adverse outcomes of cachexia

A

more complication and death
decrease treatment response
increased therapy toxicity
increased hospotal stal

22
Q

primary cachexia vs secondary

A

primary - cancer mediated

  • metabolic abnormalities
  • extreme muscle tissue loss
  • suffiecient kcal

secondary - not enough kcal

  • anorexia
  • due to treatments
  • dysphagia - swallowing
  • poor oral hygeine
  • gastrointestinal obstruction
23
Q

mediators of cancer cachexia

A

proinflammatory cytokines
- TNFa and IL-6

Eicosanoids
- prostoglandins

Tumor derived products
- PIF LMF

24
Q

TNFa and cancer cachexia

A

muscle protein degredation

  • activates NFkB
  • induces ROS

stim lipolysis in adipose

  • upregulate MAPK and JNK
  • activate PPAR gamma
  • activate NFkB

Insulin resistance

25
Q

IL-6 and cancer cachexia

A

muscle protein degredation

  • activates non-lysosomal (proteosome) pathway
  • activate lysomal (cathepsin) pathway
  • works with TNFa

directly induce acute phase protein respinse to trigger tissue catabolism

upregulate stat3

26
Q

eiconsanoids

A

prostoglandin
PGE2 in colon cancer biopsies

inflam mediators (activate NFkB)
induce peripheral tissue loss
- direct and indirect via acute phase tissue response

produced by tumors

derived from

  • n6 arachidonic acid (proinflammatory)
  • n3 EPA (anti inflammatory)
27
Q

PGE2

A

prostoglandin E2

inhibit apoptosis
- decrease Bcl2 expression
promote proliferation and survival 
- activate B-catenin signal pathway
promote angiogenesis
- VEGF (vascular endothelial growth factor
helps metastasis
- induce MMP - degrades ECM
pro inflammatory
  • one type of prostoglandin -> others not as potenet
  • derived from arachidonic acid N6
  • n3 derived are anti-inflam
28
Q

PIF

A

proteolysis inducing factor (PIF)

  • skeletal muscle and liver
  • in urine of weight loss patients (bio marker)
  • depress prot syn 50%
  • promote prot degredation 50%

activates NFkB -> ROS production
induces IL-6

29
Q

tumor -derived products

A

proteolysis inducing factor (PIF)

lipid mobalizing factor (LMF)

30
Q

LMF

A

tumor derived product

  • lipid mobilizing factor
  • found in urine

identical to - zinc alpha 2 glycoprotein (ZAG) in mice

induce lypolysis (increase lypolytic enzyme expression)

  • UPC-1 and UPC-3 in BAT (brown adipose tissue)
  • increase substrate utilization
  • adipose tissue TAG (ATAG) lipase
  • hormone sensative lipase (HSL)

secreted by adipose and tumor

31
Q

treatment of cachexia

A

1) appetite stimulants (CNS)
- megesterol acetate

2) muscle anabolics
- steroids (oxandrolone, nandrolone)
- AA or protein supplements
- creatine
- exercise**

3) anti- catabolic and anti inflammatory therapies
- NSAIDs
- n3 (EPA)

4) nutritional supplements
- palliative (end of life care)

32
Q

Physical acitivity and cachexia

A

improve cancer related symptoms
- skel muscle loss, improve blood flow, reduce nausea fatigue, quality of life

increase metabolites that reduce inflammation
- IL-10, soluble TNF receptors (binds in blood to deactivate)

increase glut4 synthesis
- glucose transport

increase PI-3-K expression

  • insulin sensitivity
  • glucose transport
  • protein synthesis
33
Q

types of physical activity

A

moderate aerobic

  • 60-75% VO2
  • reduced systemic inflammation
  • increase IL-10 and soluble TNF receptors

strength

  • decrease muscle loss
  • protein syn and reduce degredation
34
Q

n3 and cachexia

A

decrease proinflammatory cytokines

  • impairs PIF
  • tumor associated proteolysis

may improve muscle sensitivity to insulin

  • chemotherapy reduces n3 in blood
  • supplement treats this
  • 69% maintained / gained muscle with treatment
  • only 29% with normal care (other treatments)
  • greatest increases = greatest increases in muscle gain
    EPA -> relationship not yet proven
35
Q

sarcopenia

A

severe muscle loss

36
Q

carnatine in cachexia

A

facilitates transfer of activated long chain FA from cytoplasm to mitochondria

  • 75% diet derived / 25% liver and kidneys
  • from lysine and methionine
  • skel muscle and myocardium are dependent (rq FA ox)

deficient in cachexia
- treatments lower absorption, synthesis and secretion

supplement

  • L-carnitine
  • improves liver lipid metabolism
  • reduced inflam cytokine levels

Nutr 4210 (16 decks)

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