How to present a
scientific paper
Dr. Rebecca B. Riggins
Department of Oncology, Georgetown University
rbr7@georgetown.edu
Outline
• Preliminary thoughts on the assigned
reading
• Typical structure of a scientific paper
– Differences dictated by journal in which it is
published
• Discussion of Zhao et al., with
comparisons to Schafer et al.
• Final thoughts on the assigned reading
Today’s readings
‘A scientific paper is like an hourglass’
Introduction
(Materials and Methods)
Results
Discussion
Abstract = mini hourglass
‘The width of the hourglass is
inversely proportional to importance’
Introduction
(Materials and Methods)
Results
Discussion
• RESULTS and the
HYPOTHESIS/RATI
ONALE are key
when it comes to
presenting a
scientific paper
• The Introduction is
useful for
background
• The Discussion is a
useful summary
Zhao et al.: ErbB2, glycolysis, and
breast cancer growth
• Key words in the title will be better described in the
Introduction section
• This should guide you in preparing 3 or 4 slides to
introduce the paper and why the study is important…
Cancer cell metabolism
• Normal cells and cancer cells differ in how
they derive energy from glucose
• Normal: aerobic
O2+glucose  glycolysis  oxidative phosphorylation  38 ATP
• Cancer: anaerobic
glucose  glycolysis only  2 ATP
• Cancer cell glycolysis dependence =
Warburg effect
• Explain this graphically using simple images
Please DON’T do this
A simple diagram of glycolysis vs.
oxidative phosphorylation
• Multiple molecules and
pathways can regulate
glycolysis
• Some of these include:
• Ras, PI3K, mTOR,
Src
•These are all targets of
the receptor tyrosine
kinase ErbB2
http://www.nutritionaloncology.org/images/aerobicGlycolysis.jpg
Please cite your source!
The full ErbB family signaling pathway
Ereg
Nrg
1,2
Areg
Nrg
3,4
SHC
SOS
PI3K
Nck
PDK1
Ras
PLC-g
Akt/
PKB
FKHR
CDC42
Raf
PAK
Anti-Apoptosis
MKK
3/6
MEK
1/2
mTOR
PKC
GSK3b
p70S6K
JNK
p38
ERKs
Translation
c-Fos
El
k1
C
2009
ProteinLounge.com
c-Jun
Gene Expression
Relevant ErbB family signaling
Ligands
Ereg
Nrg
1,2
Areg
Receptors
SHC
PI3K
SOS
Intracellular
signaling
PDK1
Ras
Akt/
PKB
FKHR
CDC42
Raf
PAK
mTOR
Anti-Apoptosis
MKK
3/6
MEK
1/2
GSK3b
p70S6K
JNK
p38
ERKs
Elk1
c-Fos
c-Jun
C
2009
ProteinLounge.com
Gene Expression
Translation
Translation
How might ErbB2 regulate glycolysis?
• Lactate dehydrogenase A (LDH-A) is a key
glycolytic enzyme, and its expression is
increased in mouse mammary epithelial
cells that overexpress a form of ErbB2
• Heat shock factor 1 (HSF1) is a
transcription factor that regulates glucose
metabolism which is itself regulated by
Ras (a target of ErbB2)
• Does ErbB2 regulate glycolysis through
these molecules?
Experimental results
• Select key figures that illustrate the
important points
– These are often positive, but if there is room
for criticism please provide it
• Do NOT attempt to describe every panel of
every figure
Overexpression of Erb2 promotes
glycolysis in breast cancer cells
O2 consumption
http://www.nutritionaloncology.org/images/aerobicGlycolysis.jpg
Overexpression of ErbB2 increases
LDH-A and HSF1
…and knockdown of ErbB2 reduces LDH-A expression and glycolysis
Downregulation of HSF1 = reduced
LDH-A and glycolysis
Use of Hsf1 -/- cells is a way
to confirm siRNA results
Glycolysis inhibitors, ErbB2, and
cancer
2DG = glucose analog that cannot undergo glycolysis
Oligomycin = inhibitor of oxidative phosphorylation
Oxamate = inhibitor of LDH, which converts pyruvate to lactate
• Are ErbB2
overexpressing cells
more sensitive to
glycolysis inhibitors
(and less sensitive to
oxidative
phosphorylation
inhibitor)?
http://www.nutritionaloncology.org/images/aerobicGlycolysis.jpg
Overexpression of ErbB2 =
sensitivity to glycolysis inhibitors,
and sensitivity to oxidative
phosphorylation inhibitors
Glycolysis inhibitor
Similar results with 2DG in another
cell line overexpressing ErbB2
Oxidative phosphorylation inhibitor
Downregulation HSF1 inhibits ErbB2
effects on glycolysis and sensitivity to
inhibitors
Again, use of Hsf1 -/- cells is a way
to confirm siRNA results
Summary of Results
ErBB2 siRNA
Upregulation of HSF1 protein
HSF1 siRNA
Increased LDH-A expression, enzyme activity
Increased glycolysis
Increased cell growth
Glycolysis inhibitors
Discussion section
• This is a summary of the major findings,
and their importance for the field of study
• The first paragraph is the summary
• Subsequent paragraphs elaborate on the
key findings and place them in context
Schafer et al.: metabolic defects due to
cellular detachment
• Nature papers are ‘different’
Thank you for your attention!
• Questions?
• If you would like an electronic copy of this
presentation, you can download it here:
http://openwetware.org/wiki/Riggins_Lab
• Under Resources, click ‘Lectures’
• Click ‘How to present a scientific paper’