Findings of Research Misconduct, 62803-62807 [2023-19779]
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—Figure 2B, b-actin panel, representing
b-actin expression in different cells
with different treatments:
D Left middle b-actin panel and right
middle b-actin panel are duplicated by
reusing the same source images with
manipulation
—Figures 3A and 3B, b-actin panels,
representing b-actin expression in
different cells with different
treatments:
D Left top b-actin panel in Figure 3A
and left top b-actin panel in Figure 3B
are identical
D Right top b-actin panel in Figure 3A
and left bottom b-actin panel in Figure
3B are duplicated by reusing the same
source images with manipulation
D Right bottom b-actin panel in Figure
3A and right bottom b-actin panel in
Figure 3B are identical
• Cancer Prev Res. 2011:
—Figure 3A, representing expression of
different proteins with different
treatments:
D Lane 1, aP2 panel, is falsified and/
or fabricated
D Lanes 3 and 5, aP2 panel, and lanes
1–6, 18S rRNA panel, are identical
• Cancer Prev Res. 2012a:
—Figure 4A, representing input
expression treated with different
doses of Zyflamend with or without
17–AAG:
D Lanes 1–5 are identical
D Lanes 6–7 are identical
—Figure 4B, representing input
expression treated with different
doses of carnosol with or without 17–
AAG:
D Lanes 1–5 are identical
• Cancer Prev Res. 2012b:
—Figure 2, representing expression of
different proteins under different
experimental conditions:
D Lane 1, 15–PGDH panel in Figure
2B and lanes 3–4, b-Actin panel in
Figure 2E are duplicated by reusing a
same source band with manipulation
D Lane 2, b-Actin panel in Figure 2B
and lane 1, Snail panel in Figure 2E are
duplicated by reusing a same source
band with manipulation
D Lane 3, Snail panel in Figure 2G
and lane 1, 15–PGDH panel in Figure
2H are duplicated by reusing a same
source band with manipulation
D Lanes 1 and 2, b-Actin panel in
Figure 2H are duplicated by reusing a
same source band with manipulation
D Lanes 1–3, b-Actin panel in Figure
2J and lanes 1–2, b-Actin panel in
Figure 2K are duplicated by reusing a
same source band with manipulation
—Figure 4E, b-Actin panel, representing
b-actin expression in control and
pioglitazone samples:
D Lanes 1 and 2 are identical
• Cancer Prev Res. 2013:
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—Figure 3, representing binding of
nuclear protein from mammary glands
of mice with different treatments:
D Lanes 7–9 (first three empty lanes
are counted also) and lanes 13–15 are
identical
• Cancer Prev Res. 2014:
—Figures 5A and 5C, representing
expression of different proteins with
different treatments:
D Lanes 2–3, CYP1A1 panel, and
lanes 2–3, CYP1B1 panel, in Figure 5A
and lane 3, CYP1B1 panel, in Figure 5C
are duplicated by reusing a same source
band with manipulation
—Figure 5B, b-actin panel, representing
b-actin expression in different cells
with different treatments:
D Lanes 2–4 are identical
—Figure 5D, b-actin panel, representing
b-actin expression in different cells
with different treatments:
D Lanes 1–4 are duplicated by reusing
a same source band with manipulation
• Cancer Prev Res. 2015:
—Figure 3A, b-actin panel, representing
b-actin expression in DLD–1 treated
with different doses of PGE2:
D Lanes 1, 3, and 5 are identical
D Lanes 2 and 4 are identical
Respondent entered into a Voluntary
Exclusion Agreement (Agreement) and
voluntarily agreed to the following:
(1) Respondent will exclude himself
voluntarily for a period of seven (7)
years beginning on August 16, 2023 (the
‘‘Exclusion Period’’), from any
contracting or subcontracting with any
agency of the United States Government
and from eligibility for or involvement
in nonprocurement or procurement
transactions referred to as ‘‘covered
transactions’’ in 2 CFR parts 180 and
376 (collectively the ‘‘Debarment
Regulations’’).
(2) During the Exclusion Period,
Respondent will exclude himself
voluntarily from serving in any advisory
or consultant capacity to PHS including,
but not limited to, service on any PHS
advisory committee, board, and/or peer
review committee.
Dated: September 8, 2023.
Sheila Garrity,
Director, Office of Research Integrity, Office
of the Assistant Secretary for Health.
[FR Doc. 2023–19780 Filed 9–12–23; 8:45 am]
BILLING CODE 4150–31–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Office of the Secretary
Findings of Research Misconduct
Office of the Secretary, HHS.
Notice.
AGENCY:
ACTION:
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Sfmt 4703
62803
Findings of research
misconduct have been made against
Andrew Dannenberg, M.D.
(Respondent), who was a Professor of
Medicine, Department of Medicine,
Weill Cornell Medical College (WCMC).
Respondent engaged in research
misconduct in research supported by
U.S. Public Health Service (PHS) funds,
specifically National Cancer Institute
(NCI), National Institutes of Health
(NIH), grants P01 CA077839, P01
CA106451, R01 CA108773, R01
CA154481, T32 CA009685, R25
CA105012, and N01 CN43302, National
Institute on Deafness and Other
Communication Disorders (NIDCD),
NIH, grant T32 DC000027, and National
Center for Advancing Translational
Sciences (NCATS), NIH, grant UL1
TR000457. The administrative actions,
including supervision for a period of
seven (7) years, were implemented
beginning on August 14, 2023, and are
detailed below.
FOR FURTHER INFORMATION CONTACT:
Sheila Garrity, JD, MPH, MBA, Director,
Office of Research Integrity, 1101
Wootton Parkway, Suite 240, Rockville,
MD 20852, (240) 453–8200.
SUPPLEMENTARY INFORMATION: Notice is
hereby given that the Office of Research
Integrity (ORI) has taken final action in
the following case:
Andrew Dannenberg, M.D., Weill
Cornell Medical College (WCMC): Based
on the report of an investigation
conducted by WCMC and additional
analysis conducted by ORI in its
oversight review, ORI found that
Andrew Dannenberg, former Professor
of Medicine, Department of Medicine,
WCMC, engaged in research misconduct
in research supported by PHS funds,
specifically NCI, NIH, grants P01
CA077839, P01 CA106451, R01
CA108773, R01 CA154481, T32
CA009685, R25 CA105012, and N01
CN43302, NIDCD, NIH, grant T32
DC000027, and NCATS, NIH, grant UL1
TR000457.
ORI found that Respondent engaged
in research misconduct by recklessly
reporting falsified and/or fabricated data
in the following twelve (12) published
papers:
• Increased levels of COX–2 and
prostaglandin E2 contribute to elevated
aromatase expression in inflamed breast
tissue of obese women. Cancer Discov.
2012 Apr;2(4):356–65. doi: 10.1158/
2159–8290.CD–11–0241 (hereafter
referred to as ‘‘Cancer Discov. 2012’’).
Retraction in: Cancer Discov. 2021
May;11(5):1306. doi: 10.1158/2159–
8290.CD–21–0224.
• EP2 and EP4 receptors regulate
aromatase expression in human
SUMMARY:
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adipocytes and breast cancer cells.
Evidence of a BRCA1 and p300
exchange. J Biol Chem. 2008 Feb
8;283(6):3433–44. doi: 10.1074/
jbc.M705409200 (hereafter referred to as
‘‘J Biol Chem. 2008’’). Retraction in: J
Biol Chem. 2020 Jan 3; 295(1):295. doi:
10.1074/jbc.W119.012140.
• HDAC6 modulates Hsp90
chaperone activity and regulates
activation of aryl hydrocarbon receptor
signaling. J Biol Chem. 2009 Mar 20;
284(12):7436–45. doi: 10.1074/
jbc.M808999200 (hereafter referred to as
‘‘J Biol Chem. 2009’’). Retraction in: J
Biol Chem. 2020 Jan 3; 295(1):297. doi:
10.1074/jbc.W119.012142.
• p53 protein regulates Hsp90
ATPase activity and thereby Wnt
signaling by modulating Aha1
expression. J Biol Chem. 2014 Mar
7;289(10):6513–25. doi: 10.1074/
jbc.M113.532523 (hereafter referred to
as ‘‘J Biol Chem. 2014’’). Retraction in:
J Biol Chem. 2020 Jan 3; 295(1):289. doi:
10.1074/jbc.W119.012134.
• Hsp90 and PKM2 drive the
expression of aromatase in Li-Fraumeni
syndrome breast adipose stromal cells. J
Biol Chem. 2016 Jul 29;291(31):16011–
23. doi: 10.1074/jbc.M115.698902
(hereafter referred to as ‘‘J Biol Chem.
2016’’). Retraction in: J Biol Chem. 2020
Jan 3; 295(1):290. doi: 10.1074/
jbc.W119.012135.
• Heat shock protein 90 inhibitors
suppress aryl hydrocarbon receptormediated activation of CYP1A1 and
CYP1B1 transcription and DNA adduct
formation. Cancer Prev Res (Phila). 2008
Nov;1(6):485–93. doi: 10.1158/1940–
6207.CAPR–08–0149 (hereafter referred
to as ‘‘Cancer Prev Res. 2008’’).
Retraction in: Cancer Prev Res (Phila).
2022 Jun 2;15(6):415. doi: 10.1158/
1940–6207.CAPR–22–0200.
• Obesity is associated with
inflammation and elevated aromatase
expression in the mouse mammary
gland. Cancer Prev Res (Phila). 2011
Mar;4(3):329–46. doi: 10.1158/1940–
6207.CAPR–10–0381 (hereafter referred
to as ‘‘Cancer Prev Res. 2011’’).
Retraction in: Cancer Prev Res (Phila).
2022 Jun 2; 15(6):413. doi: 10.1158/
1940–6207.CAPR–22–0202.
• Carnosol, a constituent of
Zyflamend, inhibits aryl hydrocarbon
receptor-mediated activation of CYP1A1
and CYP1B1 transcription and
mutagenesis. Cancer Prev Res (Phila).
2012 Apr;5(4):593–602. doi: 10.1158/
1940–6207.CAPR–12–0002 (hereafter
referred to as ‘‘Cancer Prev Res. 2012a’’).
Retraction in: Cancer Prev Res (Phila).
2022 Jun 2;15(6):412. doi: 10.1158/
1940–6207.CAPR–22–0203.
• Pioglitazone, a PPARg agonist,
suppresses CYP19 transcription:
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evidence for involvement of 15hydroxyprostaglandin dehydrogenase
and BRCA1. Cancer Prev Res (Phila).
2012 Oct;5(10):1183–94. doi: 10.1158/
1940–6207.CAPR–12–0201 (hereafter
referred to as ‘‘Cancer Prev Res.
2012b’’). Retraction in: Cancer Prev Res
(Phila). 2022 Jun 2;15(6):411. doi:
10.1158/1940–6207.CAPR–22–0204.
• Caloric restriction reverses obesityinduced mammary gland inflammation
in mice. Cancer Prev Res (Phila). 2013
Apr;6(4):282–9. doi: 10.1158/1940–
6207.CAPR–12–0467 (hereafter referred
to as ‘‘Cancer Prev Res. 2013’’).
Retraction in: Cancer Prev Res (Phila).
2022 Jun 2; 15(6):410. doi: 10.1158/
1940–6207.CAPR–22–0205.
• p53 modulates Hsp90 ATPase
activity and regulates aryl hydrocarbon
receptor signaling. Cancer Prev Res
(Phila). 2014 Jun;7(6):596–606. doi:
10.1158/1940–6207.CAPR–14–0051
(hereafter referred to as ‘‘Cancer Prev
Res. 2014’’). Retraction in: Cancer Prev
Res (Phila). 2022 Jun 2;15(6):408. doi:
10.1158/1940–6207.CAPR–22–0207.
• Id1 deficiency protects against
tumor formation in Apc(Min/+) mice
but not in a mouse model of colitisassociated colon cancer. Cancer Prev
Res (Phila). 2015 Apr;8(4):303–11. doi:
10.1158/1940–6207.CAPR–14–0411
(hereafter referred to as ‘‘Cancer Prev
Res. 2015’’). Retraction in: Cancer Prev
Res (Phila). 2022 Jun 2;15(6):407. doi:
10.1158/1940–6207.CAPR–22–0208.
Respondent recklessly reported
falsified and/or fabricated Western blot
image data that were reused, with or
without manipulation to conceal their
similarities, and falsely relabeled as data
representing different experiments or
proteins in sixty (60) figure panels
included in twelve (12) published
papers. In the absence of reliable image
and numerical data, the figures,
statistical analyses, and related text also
are false.
Specifically, Respondent reported
Western blot images that were reused
from the same source and falsely
relabeled to represent different proteins
and/or experimental results in:
• Cancer Discov. 2012:
—Figure 2B, b-Actin panel, representing
b-Actin expression in inflamed
breast tissue with different levels of
inflammation:
D All lanes are duplicated by reusing
a same source band with
manipulation
—Figure 4C, representing the expression
of progesterone receptor (PR) and bActin in inflamed breast tissue with
different levels of inflammation:
D PR panel: Lanes 1, 2, and 14–16 are
duplicated by reusing a same source
PO 00000
Frm 00035
Fmt 4703
Sfmt 4703
band with manipulation; lanes 3, 6–
9, 13, and 17 are duplicated by
reusing a same source band with
manipulation
D b-Actin panel: All lanes are
duplicated by reusing a same source
band with manipulation
—Figure 5H, b-Actin panel, representing
b-Actin expression in macrophages
with different treatments:
D Lane 2 and lane 4 are identical
• J Biol Chem. 2008:
—Figure 2B, lanes 1–3, Aromatase
panel, representing aromatase
expression in adipocytes treated
with PGE1 alcohol, and Figure 2E,
lanes 2–4, Aromatase panel,
representing aromatase expression
in adipocytes treated with PGE2
with or without ONO, are
duplicated by reusing the same
source images with manipulation
—Figure 3B, 18S rRNA panel,
representing 18S rRNA expression
in adipocytes with different
treatments:
D Lanes 2 and 6 are identical
D Lanes 3 and 7 are identical
—Figure 5A, 18S rRNA panel,
representing 18S rRNA expression
in adipocytes treated with different
doses of PGE2:
D Lanes 1 and 5 are identical
D Lanes 2 and 6 are identical
—Figure 5B, b-actin panel, representing
b-actin expression in adipocytes
treated with different doses of PGE2:
D Lanes 1, 3, and 4 are identical
—Figure 6D, BRCA1 and Aromatase
panels, representing expression of
both BRCA1 and aromatase in
SKBR3 cells treated with different
doses of PGE1 alcohol:
D Lanes 3–4, BRCA1 panel and lanes
1–2, Aromatase panel are
duplicated by reusing the same
source images with manipulation
—Figure 5A, BRCA1 panel, representing
BRCA1 expression in adipocytes
treated with different doses of PGE2:
D Lanes 3–6 are falsified and/or
fabricated
—Figure 5C, 18S rRNA panel,
representing 18S rRNA expression
in adipocytes treated with different
doses of butaprost:
D Entire 18S rRNA panel is falsified
and/or fabricated
—Figure 5E:
D Lane 4, BRCA1 panel and lane 1,
18S rRNA panel are identical
—Figures 6C, 6D, 6E, and 6F:
D Images used in the following figures
are duplicated by reusing the same
source images with manipulation:
➢ Figure 6C, lane 1, BRCA1 panel,
representing BRCA1 expression in
control sample without treatment of
butaprost
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➢ Figure 6C, lane 3, Aromatase panel,
representing aromatase expression
with 0.25 mM butaprost treatment
➢ Figure 6D, lane 1, BRCA1 panel,
representing BRCA1 expression in
control sample without treatment of
PGE1 alcohol
➢ Figure 6F, lane 1, BRCA1 panel,
representing BRCA1 expression in
control sample without treatment of
PGE2 and ONO
D Images used in the following figures
are duplicated by reusing the same
source images with manipulation:
➢ Figure 6C, lane 2, BRCA1 panel,
representing BRCA1 expression in
sample treated with 0.10 mM
butaprost
➢ Figure 6D, lane 3, Aromatase panel,
representing aromatase expression
in sample treated with 0.25 mM
PGE1 alcohol
D Images used in the following figures
are duplicated by reusing the same
source images with manipulation:
➢ Figure 6C, lane 3, BRCA1 panel,
representing BRCA1 expression in
sample treated with 0.25 mM
butaprost
➢Figure 6D, lane 3, BRCA1 panel,
representing BRCA1 expression in
sample treated with 0.25 mM PGE1
alcohol
➢Figure 6D, lane 2, Aromatase panel,
representing aromatase expression
in sample treated with 0.10 mM
PGE1 alcohol
D Images used in the following figures
are duplicated by reusing the same
source images with manipulation:
➢Figure 6C, lane 4, BRCA1 panel,
representing BRCA1 expression in
sample treated with 0.50 mM
butaprost
➢Figure 6C, lane 1, Aromatase panel,
representing aromatase expression
in control sample without treatment
of butaprost
➢Figure 6D, lane 1, Aromatase panel,
representing aromatase expression
in control sample without treatment
of PGE1 alcohol
➢Figure 6E, lane 2, BRCA1 panel,
representing BRCA1 expression in
sample treated with PGE2 without
AH6809
D Images used in the following figures
are duplicated by reusing the same
source images with manipulation:
➢Figure 6C, lane 2, Aromatase panel,
representing aromatase expression
in sample treated with 0.10 mM
butaprost
➢Figure 6E, lane 3, BRCA1 panel,
representing BRCA1 expression in
sample treated with PGE2 and 25
mM AH6809
➢Figure 6F, lane 2, BRCA1 panel,
representing BRCA1 expression in
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sample treated with PGE2 but
without ONO
D Images used in the following figures
are duplicated by reusing the same
source images with manipulation:
➢Figure 6C, lane 4, Aromatase panel,
representing aromatase expression
in sample treated with 0.50 mM
butaprost
➢Figure 6D, lane 2, BRCA1 panel,
representing BRCA1 expression in
sample treated with 0.10 mM PGE1
alcohol
➢Figure 6E, lane 4, BRCA1 panel,
representing BRCA1 expression in
sample treated with PGE2 and 50
mM AH6809
➢Figure 6F, lane 3, BRCA1 panel,
representing BRCA1 expression in
sample treated with PGE2 and 0.10
mM ONO
D Images used in the following figures
are duplicated by reusing the same
source images with manipulation:
➢Figure 6D, 18S rRNA panel,
representing 18S rRNA expression
in samples treated with different
doses of PGE1 alcohol
➢Figure 6F, 18S rRNA panel,
representing 18S rRNA expression
in samples treated with different
doses of PGE2 and ONO
• J Biol Chem. 2009:
—Figures 2A and 2B, b-actin panels,
representing b-actin expression in
KYSE450 cells and MSK-Leuk1
cells, respectively:
D The two panels are identical
—Figure 3B, representing protein
expression at two different time
points:
D Column 4, 1-hour panel, and
column 2, 3-hour panel, are
duplicated by reusing the same
source images with resizing
—Figure 6H, representing expression of
different proteins with different
treatments:
D Column 1, Control group and
column 3, Control siRNA group are
identical
—Figure 6I, representing expression of
different proteins with different
treatments:
D Lanes 2 and 5, column 1 are
identical
D Lane 3, column 1 and lane 5,
column 2 are identical
—Figure 8G, Input panel, representing
input protein expression in A549
cells with different treatments:
D Lanes 2 and 3 are identical
—Figure 9B, Input panel, representing
input protein expression in
different samples:
D Lanes 2 and 3 are identical
—Figures 8E and 9D:
D Images used in the following figures
are duplicated by reusing a same
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Sfmt 4703
62805
source band with resizing:
➢Figure 8E, lane 2, AhR panel,
representing AhR expression in
sample treated with B[a]P
➢Figure 9D, lane 3, b-actin panel,
representing b-actin expression in
K/R sample treated with TS
—Figure 9D, b-actin panel, representing
b-actin expression under different
experimental conditions:
D Lane 1 is falsified and/or fabricated
—Figure 9C, Input panel, representing
input protein expression in K/A
sample:
D Lane 5 is falsified and/or fabricated
—Figure S1A, p23 panel, representing
p23 expression in MSK-Leuk1 cells
and A549 cells:
D Lanes 1 and 2 are identical
—Figure S1C, XAP–2 panel,
representing XAP–2 expression in
control and sample treated with
HDAC6 KD:
D Lanes 1 and 2 are identical
—Figure S1B, representing expression
of different proteins in MSK-Leuk1
cells with different treatments:
D Lanes 3 and 4, Hsp90 panel are
identical
D Lanes 1 and 2, AhR panel are
identical
D Lanes 1 and 2, b-actin panel are
identical
D Lanes 3 and 4, b-actin panel are
identical
—Figure S1E, representing expression of
different proteins in MSK-Leuk1
cells with different treatments:
D Lane 1, Hsp90 panel, and lanes 1
and 2, HDAC6 panel, are identical
D Lane 3, Hsp90 panel, and lane 3,
XAP–2 panel, are identical
—Figure S2, representing expression of
different proteins in MSK-Leuk1
cells with different treatments:
D Last lane, IB AcK panel, and lanes
3 and 5, IB HSP90 panel, are
duplicated with resizing
D Lane 4, IB AcK panel, and lanes 1,
4, and 6, IB HSP90 panel, are
duplicated with resizing
D Lane 4, IB AcK panel, is falsified
and/or fabricated
• J Biol Chem. 2014:
—Figure 1D, representing expression of
different proteins treated with
control or p53 siRNA:
D Lane 1, p53 panel, and lanes 1 and
2, b-actin panel, are duplicated by
reusing a same source band with
manipulation
—Figure 2B, b-actin panel, representing
b-actin expression in HCT–15 cells
treated with different doses of CP–
31398:
D Lane 1 and lane 5 are identical
D Lane 2 and lane 6 are identical
—Figure 4K, p23 panel, representing
p23 expression in samples treated
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with different doses of CP–31398 in
HCT–15 cells:
D Lanes 2–4 are identical
—Figures 4H, 4I, and 4L, b-actin panels,
representing b-actin expression
under different experimental
conditions:
D b-actin panels in Figures 4H and 4I,
and lanes 3–4, b-actin panel in
Figure 4L are duplicated by reusing
the same source images with
manipulation
—Figures 4J, 4K, and 4L, representing
expression of HOP (Figure 4J) and
b-actin (Figures 4K and 4L) under
different experimental conditions:
D Lanes 1–2, HOP panel in Figure 4J,
lanes 3–4, b-actin panel in Figure
4K, and lanes 1–2, b-actin panel in
Figure 4L are duplicated by reusing
the same source images with
manipulation
—Figures 5A and 5B, b-actin panels,
representing b-actin expression in
both HCT–15 cells and EB–1 cells,
are identical
—Figure 5H, c-Myc panel and Naked-1
panel, representing expression of cMyc and Naked-1 in EB–1 cells, are
duplicated with resizing
—Figures 10A and 10B, representing bactin (Figure 10A) and Aha1 (Figure
10B) expression:
D Lanes 2–3, b-actin panel in Figure
10A and lanes 2–3, Aha1 panel in
Figure 10B are duplicated with
resizing
• J Biol Chem. 2016:
—Figures 1C and 7A, b-actin panels,
representing b-actin expression in
different cells:
D Lanes 1–2, b-actin panel in Figure
1C and lanes 2–3, b-actin panel in
Figure 7A are duplicated by reusing
the same source images with
manipulation
—Figure 5B, representing expression of
different proteins with different
treatments:
D Lane 6, PKM2 panel, and lane 5,
Hsp90 panel, are identical
—Figure 5A, representing expression of
different proteins with different
treatments:
D Lane 2, HIF–1a panel, and lane 1,
b-actin panel, are identical
• Cancer Prev Res. 2008:
—Figure 2B, b-actin panel, representing
b-actin expression in different cells
with different treatments:
D Left middle b-actin panel and right
middle b-actin panel are duplicated
by reusing the same source images
with manipulation
—Figures 3A and 3B, b-actin panels,
representing b-actin expression in
different cells with different
treatments:
D Left top b-actin panel in Figure 3A
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and left top b-actin panel in Figure
3B are identical
D Right top b-actin panel in Figure 3A
and left bottom b-actin panel in
Figure 3B are duplicated by reusing
the same source images with
manipulation
D Right bottom b-actin panel in Figure
3A and right bottom b-actin panel
in Figure 3B are identical
• Cancer Prev Res. 2011:
—Figure 3A, representing expression of
different proteins with different
treatments:
D Lane 1, aP2 panel, is falsified and/
or fabricated
D Lanes 3 and 5, aP2 panel, and lanes
1–6, 18S rRNA panel, are identical
• Cancer Prev Res. 2012a:
—Figure 4A, representing input
expression treated with different
doses of Zyflamend with or without
17–AAG:
D Lanes 1–5 are identical
D Lanes 6–7 are identical
—Figure 4B, representing input
expression treated with different
doses of carnosol with or without
17–AAG:
D Lanes 1–5 are identical
• Cancer Prev Res. 2012b:
—Figure 2, representing expression of
different proteins under different
experimental conditions:
D Lane 1, 15–PGDH panel in Figure
2B and lanes 3–4, b-Actin panel in
Figure 2E are duplicated by reusing
a same source band with
manipulation
D Lane 2, b-Actin panel in Figure 2B
and lane 1, Snail panel in Figure 2E
are duplicated by reusing a same
source band with manipulation
D Lane 3, Snail panel in Figure 2G
and lane 1, 15–PGDH panel in
Figure 2H are duplicated by reusing
a same source band with
manipulation
D Lanes 1 and 2, b-Actin panel in
Figure 2H are duplicated by reusing
a same source band with
manipulation
D Lanes 1–3, b-Actin panel in Figure
2J and lanes 1–2, b-Actin panel in
Figure 2K are duplicated by reusing
a same source band with
manipulation
—Figure 4E, b-Actin panel, representing
b-actin expression in control and
pioglitazone samples:
D Lanes 1 and 2 are identical
• Cancer Prev Res. 2013:
—Figure 3, representing binding of
nuclear protein from mammary
glands of mice with different
treatments:
D Lanes 7–9 (first three empty lanes
are counted also) and lanes 13–15
are identical
PO 00000
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• Cancer Prev Res. 2014:
—Figures 5A and 5C, representing
expression of different proteins
with different treatments:
D Lanes 2–3, CYP1A1 panel, and
lanes 2–3, CYP1B1 panel, in Figure
5A and lane 3, CYP1B1 panel, in
Figure 5C are duplicated by reusing
a same source band with
manipulation
—Figure 5B, b-actin panel, representing
b-actin expression in different cells
with different treatments:
D Lanes 2–4 are identical
—Figure 5D, b-actin panel, representing
b-actin expression in different cells
with different treatments:
D Lanes 1–4 are duplicated by reusing
a same source band with
manipulation
• Cancer Prev Res. 2015:
—Figure 3A, b-actin panel, representing
b-actin expression in DLD–1 treated
with different doses of PGE2:
D Lanes 1, 3, and 5 are identical
D Lanes 2 and 4 are identical
Respondent entered into a Voluntary
Settlement Agreement (Agreement) and
voluntarily agreed to the following:
(1) Respondent will have his research
supervised for a period of seven (7)
years beginning on August 14, 2023 (the
‘‘Supervision Period’’). Prior to the
submission of an application for PHS
support for a research project on which
Respondent’s participation is proposed
and prior to Respondent’s participation
in any capacity in PHS-supported
research, Respondent will submit a plan
for supervision of Respondent’s duties
to ORI for approval. The supervision
plan must be designed to ensure the
integrity of Respondent’s research.
Respondent will not participate in any
PHS-supported research until such a
supervision plan is approved by ORI.
Respondent will comply with the
agreed-upon supervision plan.
(2) The requirements for Respondent’s
supervision plan are as follows:
i. A committee of 2 senior faculty
members at the institution who are
familiar with Respondent’s field of
research, but not including
Respondent’s supervisor or
collaborators, will provide oversight and
guidance for a period of seven (7) years
from the effective date of the
Agreement. The committee will review
primary data from Respondent’s
laboratory on a quarterly basis and
submit a report to ORI at six (6) month
intervals setting forth the committee
meeting dates and Respondent’s
compliance with appropriate research
standards and confirming the integrity
of Respondent’s research.
ii. The committee will conduct an
advance review of each application for
E:\FR\FM\13SEN1.SGM
13SEN1
Federal Register / Vol. 88, No. 176 / Wednesday, September 13, 2023 / Notices
PHS funds, or report, manuscript, or
abstract involving PHS-supported
research in which Respondent is
involved. The review will include a
discussion with Respondent of the
primary data represented in those
documents and will include a
certification to ORI that the data
presented in the proposed application,
report, manuscript, or abstract are
supported by the research record.
(3) During the Supervision Period,
Respondent will ensure that any
institution employing him submits, in
conjunction with each application for
PHS funds, or report, manuscript, or
abstract involving PHS-supported
research in which Respondent is
involved, a certification to ORI that the
data provided by Respondent are based
on actual experiments or are otherwise
legitimately derived and that the data,
procedures, and methodology are
accurately reported and not plagiarized
in the application, report, manuscript,
or abstract.
(4) If no supervision plan is provided
to ORI, Respondent will provide
certification to ORI at the conclusion of
the Supervision Period that his
participation was not proposed on a
research project for which an
application for PHS support was
submitted and that he has not
participated in any capacity in PHSsupported research.
(5) During the Supervision Period,
Respondent will exclude himself
voluntarily from serving in any advisory
or consultant capacity to PHS including,
but not limited to, service on any PHS
advisory committee, board, and/or peer
review committee.
Dated: September 8, 2023.
Sheila Garrity,
Director, Office of Research Integrity, Office
of the Assistant Secretary for Health.
[FR Doc. 2023–19779 Filed 9–12–23; 8:45 am]
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DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
ddrumheller on DSK120RN23PROD with NOTICES1
National Institute on Drug Abuse;
Notice of Closed Meetings
Pursuant to section 1009 of the
Federal Advisory Committee Act, as
amended, notice is hereby given of the
following meetings.
The meetings will be closed to the
public in accordance with the
provisions set forth in sections
552b(c)(4) and 552b(c)(6), Title 5 U.S.C.,
as amended. The grant applications
and/or contract proposals and the
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discussions could disclose confidential
trade secrets or commercial property
such as patentable material, and
personal information concerning
individuals associated with the grant
applications and/or contract proposals,
the disclosure of which would
constitute a clearly unwarranted
invasion of personal privacy.
Name of Committee: National Institute on
Drug Abuse Special Emphasis Panel;
Assessment of Potential Substance Abuse
Treatment Medications in Nonhuman
Primate Models.
Date: October 26, 2023.
Time: 12:00 p.m. to 1:00 p.m.
Agenda: To review and evaluate contract
proposals.
Place: National Institute of Health,
National Institute on Drug Abuse, 301 North
Stonestreet Avenue, Bethesda, MD 20892
(Virtual Meeting).
Contact Person: Soyoun Cho, Ph.D.,
Scientific Review Officer, Scientific Review
Branch, Division of Extramural Research,
National Institute on Drug Abuse, NIH, 301
North Stonestreet Avenue, MSC 6021,
Bethesda, MD 20892, (301) 594–9460,
Soyoun.cho@nih.gov.
Name of Committee: National Institute on
Drug Abuse Special Emphasis Panel;
Accelerating the Pace of Drug Abuse
Research Using Existing Data.
Date: November 2, 2023.
Time: 10:00 a.m. to 6:00 p.m.
Agenda: To review and evaluate grant
applications.
Place: National Institute of Health,
National Institute on Drug Abuse, 301 North
Stonestreet Avenue, Bethesda, MD 20892
(Virtual Meeting).
Contact Person: Li Rebekah Feng, Ph.D.,
Scientific Review Officer, Scientific Review
Branch, National Institute on Drug Abuse,
NIH, 301 North Stonestreet Avenue, MSC
6021, Bethesda, MD 20892, (301) 827–7245,
rebekah.feng@nih.gov.
(Catalogue of Federal Domestic Assistance
Program Nos. 93.277, Drug Abuse Scientist
Development Award for Clinicians, Scientist
Development Awards, and Research Scientist
Awards; 93.278, Drug Abuse National
Research Service Awards for Research
Training; 93.279, Drug Abuse and Addiction
Research Programs, National Institutes of
Health, HHS)
Dated: September 7, 2023.
Tyeshia M. Roberson-Curtis,
Program Analyst, Office of Federal Advisory
Committee Policy.
[FR Doc. 2023–19724 Filed 9–12–23; 8:45 am]
BILLING CODE 4140–01–P
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62807
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
National Institutes of Health
National Eye Institute; Notice of
Meeting
Pursuant to section 1009 of the
Federal Advisory Committee Act, as
amended, notice is hereby given of a
meeting of the National Advisory Eye
Council.
The meeting will be open to the
public as indicated below, with
attendance limited to space available.
Individuals who plan to attend and
need special assistance, such as sign
language interpretation or other
reasonable accommodations, should
notify the Contact Person listed below
in advance of the meeting. The open
session will be videocast and can be
accessed from the NIH Videocasting and
Podcasting website (https://
videocast.nih.gov/watch=52408).
The meeting will be closed to the
public in accordance with the
provisions set forth in sections
552b(c)(4) and 552b(c)(6), title 5 U.S.C.,
as amended. The intramural programs
and projects as well as the grant
applications and/or contract proposals
and the discussions could disclose
confidential trade secrets or commercial
property such as patentable material,
and personal information concerning
individuals associated with the grant
applications and/or contract proposals,
the disclosure of which would
constitute a clearly unwarranted
invasion of personal privacy.
Name of Committee: National Advisory
Eye Council.
Date: October 13, 2023.
Open: 8:30 a.m. to 3:00 p.m.
Agenda: Presentation of the NEI Director’s
report, discussion of NEI programs, and
concept clearances.
Place: National Eye Institute, 6700B
Rockledge Drive, Bethesda, MD 20892
Closed: 3:15 p.m. to 5:00 p.m.
Agenda: To review and evaluate grant
applications and/or proposals.
Place: National Eye Institute, 6700B
Rockledge Drive, Bethesda, MD 20892.
Contact Person: Kathleen C. Anderson,
Ph.D., Director, Division of Extramural
Activities, National Eye Institute, 6700B
Rockledge Drive, Room 3440, Bethesda, MD
20892, (301) 451–2020, kanders1@
nei.nih.gov.
Any interested person may file written
comments with the committee by forwarding
the statement to the contact person listed
above before the meeting or within 15 days
after the meeting. The statement should
include the name, address, telephone number
and when applicable, the business or
professional affiliation of the interested
person.
E:\FR\FM\13SEN1.SGM
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Agencies
[Federal Register Volume 88, Number 176 (Wednesday, September 13, 2023)]
[Notices]
[Pages 62803-62807]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2023-19779]
-----------------------------------------------------------------------
DEPARTMENT OF HEALTH AND HUMAN SERVICES
Office of the Secretary
Findings of Research Misconduct
AGENCY: Office of the Secretary, HHS.
ACTION: Notice.
-----------------------------------------------------------------------
SUMMARY: Findings of research misconduct have been made against Andrew
Dannenberg, M.D. (Respondent), who was a Professor of Medicine,
Department of Medicine, Weill Cornell Medical College (WCMC).
Respondent engaged in research misconduct in research supported by U.S.
Public Health Service (PHS) funds, specifically National Cancer
Institute (NCI), National Institutes of Health (NIH), grants P01
CA077839, P01 CA106451, R01 CA108773, R01 CA154481, T32 CA009685, R25
CA105012, and N01 CN43302, National Institute on Deafness and Other
Communication Disorders (NIDCD), NIH, grant T32 DC000027, and National
Center for Advancing Translational Sciences (NCATS), NIH, grant UL1
TR000457. The administrative actions, including supervision for a
period of seven (7) years, were implemented beginning on August 14,
2023, and are detailed below.
FOR FURTHER INFORMATION CONTACT: Sheila Garrity, JD, MPH, MBA,
Director, Office of Research Integrity, 1101 Wootton Parkway, Suite
240, Rockville, MD 20852, (240) 453-8200.
SUPPLEMENTARY INFORMATION: Notice is hereby given that the Office of
Research Integrity (ORI) has taken final action in the following case:
Andrew Dannenberg, M.D., Weill Cornell Medical College (WCMC):
Based on the report of an investigation conducted by WCMC and
additional analysis conducted by ORI in its oversight review, ORI found
that Andrew Dannenberg, former Professor of Medicine, Department of
Medicine, WCMC, engaged in research misconduct in research supported by
PHS funds, specifically NCI, NIH, grants P01 CA077839, P01 CA106451,
R01 CA108773, R01 CA154481, T32 CA009685, R25 CA105012, and N01
CN43302, NIDCD, NIH, grant T32 DC000027, and NCATS, NIH, grant UL1
TR000457.
ORI found that Respondent engaged in research misconduct by
recklessly reporting falsified and/or fabricated data in the following
twelve (12) published papers:
Increased levels of COX-2 and prostaglandin E2 contribute
to elevated aromatase expression in inflamed breast tissue of obese
women. Cancer Discov. 2012 Apr;2(4):356-65. doi: 10.1158/2159-8290.CD-
11-0241 (hereafter referred to as ``Cancer Discov. 2012''). Retraction
in: Cancer Discov. 2021 May;11(5):1306. doi: 10.1158/2159-8290.CD-21-
0224.
EP2 and EP4 receptors regulate aromatase expression in
human
[[Page 62804]]
adipocytes and breast cancer cells. Evidence of a BRCA1 and p300
exchange. J Biol Chem. 2008 Feb 8;283(6):3433-44. doi: 10.1074/
jbc.M705409200 (hereafter referred to as ``J Biol Chem. 2008'').
Retraction in: J Biol Chem. 2020 Jan 3; 295(1):295. doi: 10.1074/
jbc.W119.012140.
HDAC6 modulates Hsp90 chaperone activity and regulates
activation of aryl hydrocarbon receptor signaling. J Biol Chem. 2009
Mar 20; 284(12):7436-45. doi: 10.1074/jbc.M808999200 (hereafter
referred to as ``J Biol Chem. 2009''). Retraction in: J Biol Chem. 2020
Jan 3; 295(1):297. doi: 10.1074/jbc.W119.012142.
p53 protein regulates Hsp90 ATPase activity and thereby
Wnt signaling by modulating Aha1 expression. J Biol Chem. 2014 Mar
7;289(10):6513-25. doi: 10.1074/jbc.M113.532523 (hereafter referred to
as ``J Biol Chem. 2014''). Retraction in: J Biol Chem. 2020 Jan 3;
295(1):289. doi: 10.1074/jbc.W119.012134.
Hsp90 and PKM2 drive the expression of aromatase in Li-
Fraumeni syndrome breast adipose stromal cells. J Biol Chem. 2016 Jul
29;291(31):16011-23. doi: 10.1074/jbc.M115.698902 (hereafter referred
to as ``J Biol Chem. 2016''). Retraction in: J Biol Chem. 2020 Jan 3;
295(1):290. doi: 10.1074/jbc.W119.012135.
Heat shock protein 90 inhibitors suppress aryl hydrocarbon
receptor-mediated activation of CYP1A1 and CYP1B1 transcription and DNA
adduct formation. Cancer Prev Res (Phila). 2008 Nov;1(6):485-93. doi:
10.1158/1940-6207.CAPR-08-0149 (hereafter referred to as ``Cancer Prev
Res. 2008''). Retraction in: Cancer Prev Res (Phila). 2022 Jun
2;15(6):415. doi: 10.1158/1940-6207.CAPR-22-0200.
Obesity is associated with inflammation and elevated
aromatase expression in the mouse mammary gland. Cancer Prev Res
(Phila). 2011 Mar;4(3):329-46. doi: 10.1158/1940-6207.CAPR-10-0381
(hereafter referred to as ``Cancer Prev Res. 2011''). Retraction in:
Cancer Prev Res (Phila). 2022 Jun 2; 15(6):413. doi: 10.1158/1940-
6207.CAPR-22-0202.
Carnosol, a constituent of Zyflamend, inhibits aryl
hydrocarbon receptor-mediated activation of CYP1A1 and CYP1B1
transcription and mutagenesis. Cancer Prev Res (Phila). 2012
Apr;5(4):593-602. doi: 10.1158/1940-6207.CAPR-12-0002 (hereafter
referred to as ``Cancer Prev Res. 2012a''). Retraction in: Cancer Prev
Res (Phila). 2022 Jun 2;15(6):412. doi: 10.1158/1940-6207.CAPR-22-0203.
Pioglitazone, a PPAR[gamma] agonist, suppresses CYP19
transcription: evidence for involvement of 15-hydroxyprostaglandin
dehydrogenase and BRCA1. Cancer Prev Res (Phila). 2012 Oct;5(10):1183-
94. doi: 10.1158/1940-6207.CAPR-12-0201 (hereafter referred to as
``Cancer Prev Res. 2012b''). Retraction in: Cancer Prev Res (Phila).
2022 Jun 2;15(6):411. doi: 10.1158/1940-6207.CAPR-22-0204.
Caloric restriction reverses obesity-induced mammary gland
inflammation in mice. Cancer Prev Res (Phila). 2013 Apr;6(4):282-9.
doi: 10.1158/1940-6207.CAPR-12-0467 (hereafter referred to as ``Cancer
Prev Res. 2013''). Retraction in: Cancer Prev Res (Phila). 2022 Jun 2;
15(6):410. doi: 10.1158/1940-6207.CAPR-22-0205.
p53 modulates Hsp90 ATPase activity and regulates aryl
hydrocarbon receptor signaling. Cancer Prev Res (Phila). 2014
Jun;7(6):596-606. doi: 10.1158/1940-6207.CAPR-14-0051 (hereafter
referred to as ``Cancer Prev Res. 2014''). Retraction in: Cancer Prev
Res (Phila). 2022 Jun 2;15(6):408. doi: 10.1158/1940-6207.CAPR-22-0207.
Id1 deficiency protects against tumor formation in
Apc(Min/+) mice but not in a mouse model of colitis-associated colon
cancer. Cancer Prev Res (Phila). 2015 Apr;8(4):303-11. doi: 10.1158/
1940-6207.CAPR-14-0411 (hereafter referred to as ``Cancer Prev Res.
2015''). Retraction in: Cancer Prev Res (Phila). 2022 Jun 2;15(6):407.
doi: 10.1158/1940-6207.CAPR-22-0208.
Respondent recklessly reported falsified and/or fabricated Western
blot image data that were reused, with or without manipulation to
conceal their similarities, and falsely relabeled as data representing
different experiments or proteins in sixty (60) figure panels included
in twelve (12) published papers. In the absence of reliable image and
numerical data, the figures, statistical analyses, and related text
also are false.
Specifically, Respondent reported Western blot images that were
reused from the same source and falsely relabeled to represent
different proteins and/or experimental results in:
Cancer Discov. 2012:
--Figure 2B, [beta]-Actin panel, representing [beta]-Actin expression
in inflamed breast tissue with different levels of inflammation:
[ssquf] All lanes are duplicated by reusing a same source band with
manipulation
--Figure 4C, representing the expression of progesterone receptor (PR)
and [beta]-Actin in inflamed breast tissue with different levels of
inflammation:
[ssquf] PR panel: Lanes 1, 2, and 14-16 are duplicated by reusing a
same source band with manipulation; lanes 3, 6-9, 13, and 17 are
duplicated by reusing a same source band with manipulation
[ssquf] [beta]-Actin panel: All lanes are duplicated by reusing a
same source band with manipulation
--Figure 5H, [beta]-Actin panel, representing [beta]-Actin expression
in macrophages with different treatments:
[ssquf] Lane 2 and lane 4 are identical
J Biol Chem. 2008:
--Figure 2B, lanes 1-3, Aromatase panel, representing aromatase
expression in adipocytes treated with PGE1 alcohol, and Figure 2E,
lanes 2-4, Aromatase panel, representing aromatase expression in
adipocytes treated with PGE2 with or without ONO, are
duplicated by reusing the same source images with manipulation
--Figure 3B, 18S rRNA panel, representing 18S rRNA expression in
adipocytes with different treatments:
[ssquf] Lanes 2 and 6 are identical
[ssquf] Lanes 3 and 7 are identical
--Figure 5A, 18S rRNA panel, representing 18S rRNA expression in
adipocytes treated with different doses of PGE2:
[ssquf] Lanes 1 and 5 are identical
[ssquf] Lanes 2 and 6 are identical
--Figure 5B, [beta]-actin panel, representing [beta]-actin expression
in adipocytes treated with different doses of PGE2:
[ssquf] Lanes 1, 3, and 4 are identical
--Figure 6D, BRCA1 and Aromatase panels, representing expression of
both BRCA1 and aromatase in SKBR3 cells treated with different doses of
PGE1 alcohol:
[ssquf] Lanes 3-4, BRCA1 panel and lanes 1-2, Aromatase panel are
duplicated by reusing the same source images with manipulation
--Figure 5A, BRCA1 panel, representing BRCA1 expression in adipocytes
treated with different doses of PGE2:
[ssquf] Lanes 3-6 are falsified and/or fabricated
--Figure 5C, 18S rRNA panel, representing 18S rRNA expression in
adipocytes treated with different doses of butaprost:
[ssquf] Entire 18S rRNA panel is falsified and/or fabricated
--Figure 5E:
[ssquf] Lane 4, BRCA1 panel and lane 1, 18S rRNA panel are
identical
--Figures 6C, 6D, 6E, and 6F:
[ssquf] Images used in the following figures are duplicated by
reusing the same source images with manipulation:
[rtarr8] Figure 6C, lane 1, BRCA1 panel, representing BRCA1
expression in control sample without treatment of butaprost
[[Page 62805]]
[rtarr8] Figure 6C, lane 3, Aromatase panel, representing aromatase
expression with 0.25 [mu]M butaprost treatment
[rtarr8] Figure 6D, lane 1, BRCA1 panel, representing BRCA1
expression in control sample without treatment of PGE1 alcohol
[rtarr8] Figure 6F, lane 1, BRCA1 panel, representing BRCA1
expression in control sample without treatment of PGE2 and
ONO
[ssquf] Images used in the following figures are duplicated by
reusing the same source images with manipulation:
[rtarr8] Figure 6C, lane 2, BRCA1 panel, representing BRCA1
expression in sample treated with 0.10 [mu]M butaprost
[rtarr8] Figure 6D, lane 3, Aromatase panel, representing aromatase
expression in sample treated with 0.25 [mu]M PGE1 alcohol
[ssquf] Images used in the following figures are duplicated by
reusing the same source images with manipulation:
[rtarr8] Figure 6C, lane 3, BRCA1 panel, representing BRCA1
expression in sample treated with 0.25 [mu]M butaprost
[rtarr8]Figure 6D, lane 3, BRCA1 panel, representing BRCA1
expression in sample treated with 0.25 [mu]M PGE1 alcohol
[rtarr8]Figure 6D, lane 2, Aromatase panel, representing aromatase
expression in sample treated with 0.10 [mu]M PGE1 alcohol
[ssquf] Images used in the following figures are duplicated by
reusing the same source images with manipulation:
[rtarr8]Figure 6C, lane 4, BRCA1 panel, representing BRCA1
expression in sample treated with 0.50 [mu]M butaprost
[rtarr8]Figure 6C, lane 1, Aromatase panel, representing aromatase
expression in control sample without treatment of butaprost
[rtarr8]Figure 6D, lane 1, Aromatase panel, representing aromatase
expression in control sample without treatment of PGE1 alcohol
[rtarr8]Figure 6E, lane 2, BRCA1 panel, representing BRCA1
expression in sample treated with PGE2 without AH6809
[ssquf] Images used in the following figures are duplicated by
reusing the same source images with manipulation:
[rtarr8]Figure 6C, lane 2, Aromatase panel, representing aromatase
expression in sample treated with 0.10 [mu]M butaprost
[rtarr8]Figure 6E, lane 3, BRCA1 panel, representing BRCA1
expression in sample treated with PGE2 and 25 [mu]M AH6809
[rtarr8]Figure 6F, lane 2, BRCA1 panel, representing BRCA1
expression in sample treated with PGE2 but without ONO
[ssquf] Images used in the following figures are duplicated by
reusing the same source images with manipulation:
[rtarr8]Figure 6C, lane 4, Aromatase panel, representing aromatase
expression in sample treated with 0.50 [mu]M butaprost
[rtarr8]Figure 6D, lane 2, BRCA1 panel, representing BRCA1
expression in sample treated with 0.10 [mu]M PGE1 alcohol
[rtarr8]Figure 6E, lane 4, BRCA1 panel, representing BRCA1
expression in sample treated with PGE2 and 50 [mu]M AH6809
[rtarr8]Figure 6F, lane 3, BRCA1 panel, representing BRCA1
expression in sample treated with PGE2 and 0.10 [mu]M ONO
[ssquf] Images used in the following figures are duplicated by
reusing the same source images with manipulation:
[rtarr8]Figure 6D, 18S rRNA panel, representing 18S rRNA expression
in samples treated with different doses of PGE1 alcohol
[rtarr8]Figure 6F, 18S rRNA panel, representing 18S rRNA expression
in samples treated with different doses of PGE2 and ONO
J Biol Chem. 2009:
--Figures 2A and 2B, [beta]-actin panels, representing [beta]-actin
expression in KYSE450 cells and MSK-Leuk1 cells, respectively:
[ssquf] The two panels are identical
--Figure 3B, representing protein expression at two different time
points:
[ssquf] Column 4, 1-hour panel, and column 2, 3-hour panel, are
duplicated by reusing the same source images with resizing
--Figure 6H, representing expression of different proteins with
different treatments:
[ssquf] Column 1, Control group and column 3, Control siRNA group
are identical
--Figure 6I, representing expression of different proteins with
different treatments:
[ssquf] Lanes 2 and 5, column 1 are identical
[ssquf] Lane 3, column 1 and lane 5, column 2 are identical
--Figure 8G, Input panel, representing input protein expression in A549
cells with different treatments:
[ssquf] Lanes 2 and 3 are identical
--Figure 9B, Input panel, representing input protein expression in
different samples:
[ssquf] Lanes 2 and 3 are identical
--Figures 8E and 9D:
[ssquf] Images used in the following figures are duplicated by
reusing a same source band with resizing:
[rtarr8]Figure 8E, lane 2, AhR panel, representing AhR expression
in sample treated with B[a]P
[rtarr8]Figure 9D, lane 3, [beta]-actin panel, representing [beta]-
actin expression in K/R sample treated with TS
--Figure 9D, [beta]-actin panel, representing [beta]-actin expression
under different experimental conditions:
[ssquf] Lane 1 is falsified and/or fabricated
--Figure 9C, Input panel, representing input protein expression in K/A
sample:
[ssquf] Lane 5 is falsified and/or fabricated
--Figure S1A, p23 panel, representing p23 expression in MSK-Leuk1 cells
and A549 cells:
[ssquf] Lanes 1 and 2 are identical
--Figure S1C, XAP-2 panel, representing XAP-2 expression in control and
sample treated with HDAC6 KD:
[ssquf] Lanes 1 and 2 are identical
--Figure S1B, representing expression of different proteins in MSK-
Leuk1 cells with different treatments:
[ssquf] Lanes 3 and 4, Hsp90 panel are identical
[ssquf] Lanes 1 and 2, AhR panel are identical
[ssquf] Lanes 1 and 2, [beta]-actin panel are identical
[ssquf] Lanes 3 and 4, [beta]-actin panel are identical
--Figure S1E, representing expression of different proteins in MSK-
Leuk1 cells with different treatments:
[ssquf] Lane 1, Hsp90 panel, and lanes 1 and 2, HDAC6 panel, are
identical
[ssquf] Lane 3, Hsp90 panel, and lane 3, XAP-2 panel, are identical
--Figure S2, representing expression of different proteins in MSK-Leuk1
cells with different treatments:
[ssquf] Last lane, IB AcK panel, and lanes 3 and 5, IB HSP90 panel,
are duplicated with resizing
[ssquf] Lane 4, IB AcK panel, and lanes 1, 4, and 6, IB HSP90
panel, are duplicated with resizing
[ssquf] Lane 4, IB AcK panel, is falsified and/or fabricated
J Biol Chem. 2014:
--Figure 1D, representing expression of different proteins treated with
control or p53 siRNA:
[ssquf] Lane 1, p53 panel, and lanes 1 and 2, [beta]-actin panel,
are duplicated by reusing a same source band with manipulation
--Figure 2B, [beta]-actin panel, representing [beta]-actin expression
in HCT-15 cells treated with different doses of CP-31398:
[ssquf] Lane 1 and lane 5 are identical
[ssquf] Lane 2 and lane 6 are identical
--Figure 4K, p23 panel, representing p23 expression in samples treated
[[Page 62806]]
with different doses of CP-31398 in HCT-15 cells:
[ssquf] Lanes 2-4 are identical
--Figures 4H, 4I, and 4L, [beta]-actin panels, representing [beta]-
actin expression under different experimental conditions:
[ssquf] [beta]-actin panels in Figures 4H and 4I, and lanes 3-4,
[beta]-actin panel in Figure 4L are duplicated by reusing the same
source images with manipulation
--Figures 4J, 4K, and 4L, representing expression of HOP (Figure 4J)
and [beta]-actin (Figures 4K and 4L) under different experimental
conditions:
[ssquf] Lanes 1-2, HOP panel in Figure 4J, lanes 3-4, [beta]-actin
panel in Figure 4K, and lanes 1-2, [beta]-actin panel in Figure 4L are
duplicated by reusing the same source images with manipulation
--Figures 5A and 5B, [beta]-actin panels, representing [beta]-actin
expression in both HCT-15 cells and EB-1 cells, are identical
--Figure 5H, c-Myc panel and Naked-1 panel, representing expression of
c-Myc and Naked-1 in EB-1 cells, are duplicated with resizing
--Figures 10A and 10B, representing [beta]-actin (Figure 10A) and Aha1
(Figure 10B) expression:
[ssquf] Lanes 2-3, [beta]-actin panel in Figure 10A and lanes 2-3,
Aha1 panel in Figure 10B are duplicated with resizing
J Biol Chem. 2016:
--Figures 1C and 7A, [beta]-actin panels, representing [beta]-actin
expression in different cells:
[ssquf] Lanes 1-2, [beta]-actin panel in Figure 1C and lanes 2-3,
[beta]-actin panel in Figure 7A are duplicated by reusing the same
source images with manipulation
--Figure 5B, representing expression of different proteins with
different treatments:
[ssquf] Lane 6, PKM2 panel, and lane 5, Hsp90 panel, are identical
--Figure 5A, representing expression of different proteins with
different treatments:
[ssquf] Lane 2, HIF-1[alpha] panel, and lane 1, [beta]-actin panel,
are identical
Cancer Prev Res. 2008:
--Figure 2B, [beta]-actin panel, representing [beta]-actin expression
in different cells with different treatments:
[ssquf] Left middle [beta]-actin panel and right middle [beta]-
actin panel are duplicated by reusing the same source images with
manipulation
--Figures 3A and 3B, [beta]-actin panels, representing [beta]-actin
expression in different cells with different treatments:
[ssquf] Left top [beta]-actin panel in Figure 3A and left top
[beta]-actin panel in Figure 3B are identical
[ssquf] Right top [beta]-actin panel in Figure 3A and left bottom
[beta]-actin panel in Figure 3B are duplicated by reusing the same
source images with manipulation
[ssquf] Right bottom [beta]-actin panel in Figure 3A and right
bottom [beta]-actin panel in Figure 3B are identical
Cancer Prev Res. 2011:
--Figure 3A, representing expression of different proteins with
different treatments:
[ssquf] Lane 1, aP2 panel, is falsified and/or fabricated
[ssquf] Lanes 3 and 5, aP2 panel, and lanes 1-6, 18S rRNA panel,
are identical
Cancer Prev Res. 2012a:
--Figure 4A, representing input expression treated with different doses
of Zyflamend with or without 17-AAG:
[ssquf] Lanes 1-5 are identical
[ssquf] Lanes 6-7 are identical
--Figure 4B, representing input expression treated with different doses
of carnosol with or without 17-AAG:
[ssquf] Lanes 1-5 are identical
Cancer Prev Res. 2012b:
--Figure 2, representing expression of different proteins under
different experimental conditions:
[ssquf] Lane 1, 15-PGDH panel in Figure 2B and lanes 3-4, [beta]-
Actin panel in Figure 2E are duplicated by reusing a same source band
with manipulation
[ssquf] Lane 2, [beta]-Actin panel in Figure 2B and lane 1, Snail
panel in Figure 2E are duplicated by reusing a same source band with
manipulation
[ssquf] Lane 3, Snail panel in Figure 2G and lane 1, 15-PGDH panel
in Figure 2H are duplicated by reusing a same source band with
manipulation
[ssquf] Lanes 1 and 2, [beta]-Actin panel in Figure 2H are
duplicated by reusing a same source band with manipulation
[ssquf] Lanes 1-3, [beta]-Actin panel in Figure 2J and lanes 1-2,
[beta]-Actin panel in Figure 2K are duplicated by reusing a same source
band with manipulation
--Figure 4E, [beta]-Actin panel, representing [beta]-actin expression
in control and pioglitazone samples:
[ssquf] Lanes 1 and 2 are identical
Cancer Prev Res. 2013:
--Figure 3, representing binding of nuclear protein from mammary glands
of mice with different treatments:
[ssquf] Lanes 7-9 (first three empty lanes are counted also) and
lanes 13-15 are identical
Cancer Prev Res. 2014:
--Figures 5A and 5C, representing expression of different proteins with
different treatments:
[ssquf] Lanes 2-3, CYP1A1 panel, and lanes 2-3, CYP1B1 panel, in
Figure 5A and lane 3, CYP1B1 panel, in Figure 5C are duplicated by
reusing a same source band with manipulation
--Figure 5B, [beta]-actin panel, representing [beta]-actin expression
in different cells with different treatments:
[ssquf] Lanes 2-4 are identical
--Figure 5D, [beta]-actin panel, representing [beta]-actin expression
in different cells with different treatments:
[ssquf] Lanes 1-4 are duplicated by reusing a same source band with
manipulation
Cancer Prev Res. 2015:
--Figure 3A, [beta]-actin panel, representing [beta]-actin expression
in DLD-1 treated with different doses of PGE2:
[ssquf] Lanes 1, 3, and 5 are identical
[ssquf] Lanes 2 and 4 are identical
Respondent entered into a Voluntary Settlement Agreement
(Agreement) and voluntarily agreed to the following:
(1) Respondent will have his research supervised for a period of
seven (7) years beginning on August 14, 2023 (the ``Supervision
Period''). Prior to the submission of an application for PHS support
for a research project on which Respondent's participation is proposed
and prior to Respondent's participation in any capacity in PHS-
supported research, Respondent will submit a plan for supervision of
Respondent's duties to ORI for approval. The supervision plan must be
designed to ensure the integrity of Respondent's research. Respondent
will not participate in any PHS-supported research until such a
supervision plan is approved by ORI. Respondent will comply with the
agreed-upon supervision plan.
(2) The requirements for Respondent's supervision plan are as
follows:
i. A committee of 2 senior faculty members at the institution who
are familiar with Respondent's field of research, but not including
Respondent's supervisor or collaborators, will provide oversight and
guidance for a period of seven (7) years from the effective date of the
Agreement. The committee will review primary data from Respondent's
laboratory on a quarterly basis and submit a report to ORI at six (6)
month intervals setting forth the committee meeting dates and
Respondent's compliance with appropriate research standards and
confirming the integrity of Respondent's research.
ii. The committee will conduct an advance review of each
application for
[[Page 62807]]
PHS funds, or report, manuscript, or abstract involving PHS-supported
research in which Respondent is involved. The review will include a
discussion with Respondent of the primary data represented in those
documents and will include a certification to ORI that the data
presented in the proposed application, report, manuscript, or abstract
are supported by the research record.
(3) During the Supervision Period, Respondent will ensure that any
institution employing him submits, in conjunction with each application
for PHS funds, or report, manuscript, or abstract involving PHS-
supported research in which Respondent is involved, a certification to
ORI that the data provided by Respondent are based on actual
experiments or are otherwise legitimately derived and that the data,
procedures, and methodology are accurately reported and not plagiarized
in the application, report, manuscript, or abstract.
(4) If no supervision plan is provided to ORI, Respondent will
provide certification to ORI at the conclusion of the Supervision
Period that his participation was not proposed on a research project
for which an application for PHS support was submitted and that he has
not participated in any capacity in PHS-supported research.
(5) During the Supervision Period, Respondent will exclude himself
voluntarily from serving in any advisory or consultant capacity to PHS
including, but not limited to, service on any PHS advisory committee,
board, and/or peer review committee.
Dated: September 8, 2023.
Sheila Garrity,
Director, Office of Research Integrity, Office of the Assistant
Secretary for Health.
[FR Doc. 2023-19779 Filed 9-12-23; 8:45 am]
BILLING CODE 4150-31-P