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Nutr 4210 > 16. Cancer > Flashcards

16. Cancer Flashcards

(36 cards)

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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

Study These Flashcards
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

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

causes of cachexia

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A

about 1/2 with cachexia weight loss

21
Q

adverse outcomes of cachexia

Study These Flashcards
A

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

22
Q

primary cachexia vs secondary

Study These Flashcards
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

Study These Flashcards
A

proinflammatory cytokines
- TNFa and IL-6

Eicosanoids
- prostoglandins

Tumor derived products
- PIF LMF

24
Q

TNFa and cancer cachexia

Study These Flashcards
A

muscle protein degredation

  • activates NFkB
  • induces ROS

stim lipolysis in adipose

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

Insulin resistance

25
IL-6 and cancer cachexia
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
eiconsanoids
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
PGE2
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
PIF
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
tumor -derived products
proteolysis inducing factor (PIF) | lipid mobalizing factor (LMF)
30
LMF
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
treatment of cachexia
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
Physical acitivity and cachexia
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
types of physical activity
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
n3 and cachexia
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
sarcopenia
severe muscle loss
36
carnatine in cachexia
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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