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Food, Nutrition, Physical
Activity and Cancer Survivors
Food Matters Live
23 November 2016
Martin Wiseman
World Cancer Research Fund International & University
of Southampton
Who we are
AICR (1982)
WCRF UK (1990)
WCRF Netherlands (1994)
WCRF Hong Kong (1997)
WCRF International (1999)
What we do
Fund research on the relationship of
nutrition, physical activity and body
weight to cancer risk
Interpret the accumulated scientific
literature to derive
Recommendations for Cancer
Prevention
Educate people through our national
Health Information programmes
Advocate effective policies to help
people and populations to reduce
their chances of developing cancer
Nutritional influence through the life course
- a fundamental exposure at all stages
Primary
prevention
Secondary
prevention
Premalignant
lesion
Tertiary
prevention
Treatment
Treatment
surgery
chemo/radiotherapy
surgery
chemo/radiotherapy
Cancer
Recurrence
genetic predisposition
Risk of cancer development and/or recurrence
Response to therapeutic prevention strategies
Resilience and Response to surgery
and treatment
Patient quality of life and health status
RESILIENCE
Nutrition and cancer incidence
Global variation in cancer incidence
Colorectum
Breast
http://globocan.iarc.fr/Pages/Map.aspx
Ferlay J, Soerjomataram I, Ervik M, Dikshit R,
Eser S, Mathers C, Rebelo M, Parkin DM,
Forman D, Bray, F.
GLOBOCAN 2012 v1.0,
Cancer Incidence and Mortality Worldwide:
IARC CancerBase No. 11 [Internet].
Lyon,
France: International Agency for Research on
Cancer; 2013. Available from:
http://globocan.iarc.fr, accessed on 18 August
2015
Migration data
Cancer Incidence in Japan*
30
Cancer Incidence
25
Colon
20
Breast
15
10
5
0
1960
1965
1970 '71
1973 '77
1979 '82
* Per 100,000, world population standard
1983 '87
1988 '92
1995
1997
M
m
The WCRF/AICR Continuous
Update Reports
NUTRITION AND CANCERS
ADIPOSITY
BREAST (PM), COLORECTUM, ENDOMETRIUM,
OESOPHAGUS (ADENO), GASTRIC CARDIA, PANCREAS,
GALLBLADDER, LIVER, KIDNEY, OVARY,
PROSTATE (ADVANCED)
PHYSICAL (IN)ACTIVITY
COLON, BREAST, ENDOMETRIUM
MEAT – RED AND PROCESSED
COLORECTAL, STOMACH
ALCOHOL
MPL, BREAST, COLORECTUM, LIVER, OESOPHAGUS (SCC),
STOMACH
PLANT FOODS (F&V, PULSES, WHOLEGRAINS)
MPL, COLORECTAL (DF), LUNG
BREASTFEEDING
BREAST (MOTHER), OBESITY (CHILD)
Estimates of cancer preventability by appropriate
diet, nutrition, physical activity and body fatness
USA
UK
BRAZIL
CHINA
Mouth, pharynx, larynx
63
67
63
44
Oesophagus
63
71
50
33
Lung
36
33
36
38
Stomach
47
45
41
33
Pancreas
19
15
11
8
Gallbladder
21
16
10
6
Liver
15
17
6
6
Colorectum
50
47
41
22
Breast
33
38
22
11
Ovary
5
4
3
1
Endometrium
59
44
37
21
Prostate (advanced)
11
10
5
4
Kidney
24
19
13
8
Total for these cancers
30
32
25
24
Total for all cancers
21
24
17
20
Nutrition and cancer biology
Hallmarks of cancer
Two enabling characteristics for acquiring hallmarks
Hanahan & Weinberg (2011) Cell; Hanahan & Coussens (2012) Cancer Cell
Hallmarks of cancer
Immediate nutritional relevance
Hanahan & Weinberg (2011) Cell; Hanahan & Coussens (2012) Cancer Cell
Two enabling characteristics for acquiring hallmarks
Immediate nutritional relevance
Nutrition and cancer outcome
The Panel emphasises the
importance of not smoking
and of avoiding exposure to
tobacco smoke
Obesity and cancer
progression
Expert US WORKSHOP 2011
Breast cancer
• Normal weight at diagnosis associated with better
outcomes
• Higher (and low) BMI at diagnosis associated with greater
recurrence and death.
• Obesity: 30% increase in mortality
40+% increase in metastases after 10 y
• Importance of physical activity
Institute of Medicine 2011
Obesity and cancer
progression
US Expert WORKSHOP 2011
Prostate cancer
• Sparse and conflicting evidence
Colon cancer
• Limited early evidence only
Institute of Medicine 2011
Pathological features
POSH
Mean tumour size/
mm
Underweight or
Healthy weight
n=1526
(54.0%)
Overweight
n=784
Obese
n=533
(27.6%)
(18.8%)
20
(0-170)
24
(0-199)
26
(0.5-130)
U/H vs. Ov: p<0.0001
U/H vs. Ob: p<0.0001
Multifocal
12 (30.6%)
220 (30.4%)
130 (27.2%)
NS
Grade 3
879 (59.0%)
485 (63.6%)
331 (63.9%)
U/H vs. Ov: p=0.034
U/H vs. Ob: p =0.048
Node positive
736 (49.0%)
419 (54.2%)
284 (54.6%)
U/H vs. Ov: p=0.019
U/H vs. Ob: p=0.027
ER negative
483 (31.7%)
273 (34.9%)
213 (40.1%)
U/H vs Ob: p<0.001
HER 2 positive
381 (28.2%)
180 (26.4%)
129 (27.3%)
NS
ER/ PR/ HER 2
negative
305 (20.8%)
176 (23.4%)
136 (26.8%)
U/H vs. Ob: p=0.005
@NCRI #NCRI2013
conference.ncri.org.uk
Overall survival
POSH
Copson et al. Ann Onc 26: 2015, 101-112
@NCRI #NCRI2013
conference.ncri.org.uk
Obesity and cancer progression
Observational evidence
- Summary
 Although there were significant
associations between BMI (and physical
activity) and outcomes, incomplete
adjustment for potential confounders
restricted the ability to ascribe causality
 CUP Panel concluded that evidence is
limited
WINS and WHEL
WHEL
WINS
Baseline
6 years
975 Int
380 (39%)
1462 Control 648 (44%)
48-79 y, events 1-5y
Baseline
5 years
1537 Int
1308 (85%)
1551 Control 1313 (85%)
18-79, events 2-10 years
Target Achieved
Fat 15%
20%
Stable wt 71kg
Target
Inc F&V
Inc fibre
20% Fat
Stable wt
Control
29%
73kg
Other dietary changes (Fatty
acids, F&V etc)
Borderline primary result,
more in ER/PR -ve
Comparison (I-C)
+3 servings
+5 g/day
-3.5%
+ 0.4kg
No difference
ASCO OBESITY TRIAL
RECOMMENDATIONS
• Large scale randomised trials (energy
balance)
• Multidisciplinary research teams
• Appropriate patient selection
(numbers, recurrence etc)
• Design (power, prognosis/timescale)
• Endpoints (cancer, comorbidities,
economic, biomarkers, feasibility)
BWEL
•
•
•
•
•
Invasive breast cancer
18 y +, HER2-ve
Within 12m diagnosis
10 y invasive disease free
Healthy living program + individual
telephone based weight loss
• Recruiting from end August 2016
External
agents
Protective
factors – ex
and
endogenous
DNA
integrity
Protective
factors endogenous
Endogenous
factors
Growth promoters
eg growth factors, sex
hormones
Time
Ageing
Immunosurveillance
Cancer
cell
Tumour
Loss of capacity
• Cancer cell
• Stroma
• Immune cells
Host Factors – genetic, epigenetic, nutritional/metabolic, immune
micronutrient, macronutrient, energy
What determines variability?
Summary
• Nutrition is an important determinant of risk of several cancers
• we do not yet understand what determines which
individuals will be affected
• Nutrition is an important predictor of outcome after diagnosis
• We do not know what underlies this link
• We understand much of how nutrition can affect cancer
biology
• Nutrition could plausibly contribute to individual varaibility
in progress and response to treatment
• This has not been explored in patient relevant trials
• Patients need and want nutritional advice but the evidence
base is lacking
Improving cancer prevention and care.
For patients. For clinicians. For researchers
•Aim:
to help facilitate translational research in cancer and
nutrition which will generate the evidence to improve cancer
prevention and care
•Objectives:
To bring coherence to existing activities by
–creating a framework as a basis for future research
–establishing better networks for sharing knowledge
between cancer and nutrition stakeholders
• Hosted by Southampton BRC with a range of partners (eg
DH, WCRF, CRUK, BRCs, ECMC, Patient representatives)
•Established March 2014
cancerandnutrition.nihr.ac.uk
NIHR Office for Clinical Research Infrastructure (NOCRI)
Thank you!
www.wcrf.org
@wcrfint
facebook.com/wcrfint
wcrf.org/blog/
linkedin.com