Findings of Research Misconduct, 62800-62803 [2023-19780]
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Federal Register / Vol. 88, No. 176 / Wednesday, September 13, 2023 / Notices
were withdrawn from sale for reasons of
safety or effectiveness.
After considering the citizen petition
and reviewing Agency records and
based on the information we have at this
time, FDA has determined under
§ 314.161 that Oxandrin (oxandrolone)
tablets, 2.5 mg and 10 mg, were
withdrawn for reasons of safety or
effectiveness. We have carefully
reviewed our files for records
concerning the withdrawal of Oxandrin
(oxandrolone) tablets, 2.5 mg and 10 mg,
from sale. We have also independently
evaluated relevant literature and data
for possible postmarketing adverse
events.
Our records show that FDA’s
Endocrinologic and Metabolic Drugs
Advisory Committee met and discussed
anabolic steroids in January 1984. The
advisory committee unanimously
concluded that there was no evidence of
efficacy for oxandrolone.2
As communicated in the product
labeling for Oxandrin (oxandrolone)
tablets, 2.5 mg and 10 mg, multiple
safety warnings and precautions are
associated with the use of this product
including peliosis hepatis, sometimes
associated with liver failure and intraabdominal hemorrhage; liver cell
tumors, sometimes fatal; and blood lipid
changes that are known to be associated
with increased risk of atherosclerosis.3
Per the product labeling, additional
warnings with using this product
include the risks associated with
cholestatic hepatitis, hypercalcemia in
patients with breast cancer, and
increased risk for the development of
prostatic hypertrophy and prostatic
carcinoma in geriatric patients.4
Considering the safety concerns
associated with the use of oxandrolone
noted in the labeling, the Agency
concluded that the benefit-risk profile of
the drug product is unfavorable without
substantial evidence to support
effectiveness.
Based on a thorough evaluation of the
information we have available to us and
an evaluation of the latest version of the
drug products’ approved labeling, we
have determined that the drug products
would not be considered safe and
effective if they were reintroduced to
the market today. New clinical studies
would first need to be conducted to
address the concerns described above.
Thus, after considering the citizen
petition and reviewing Agency records
and based on the information we have
2 See minutes from the January 24 to 25, 1984,
advisory committee meeting discussing anabolic
steroids, at pg. 7.
3 See footnote 1.
4 See footnote 1.
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17:37 Sep 12, 2023
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at this time, FDA has determined under
§ 314.161 that Oxandrin (oxandrolone)
tablets, 2.5 mg and 10 mg, were
withdrawn for reasons of safety or
effectiveness. Accordingly, the Agency
will remove Oxandrin (oxandrolone)
tablets, 2.5 mg and 10 mg, from the list
of drug products published in the
Orange Book per § 314.162. FDA will
not accept or approve ANDAs that refer
to this drug product.
Dated: September 8, 2023.
Lauren K. Roth,
Associate Commissioner for Policy.
[FR Doc. 2023–19796 Filed 9–12–23; 8:45 am]
BILLING CODE 4164–01–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Office of the Secretary
Findings of Research Misconduct
Office of the Secretary, HHS.
Notice.
AGENCY:
ACTION:
Findings of research
misconduct have been made against
Kotha Subbaramaiah, Ph.D.
(Respondent), who was a Professor of
Biochemistry Research in 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
debarment for a period of seven (7)
years, were implemented beginning on
August 16, 2023, and are detailed
below.
SUMMARY:
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:
Kotha Subbaramaiah, Ph.D., Weill
Cornell Medical College: Based on the
report of an investigation conducted by
WCMC and additional analysis
conducted by ORI in its oversight
PO 00000
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review, ORI found that Kotha
Subbaramaiah, Ph.D., former Weill
Cornell Medical College, 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 intentionally,
knowingly, or recklessly falsifying and/
or fabricating data included 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
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
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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:
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.
Specifically, ORI found that
Respondent reused Western blot images
from the same source and falsely
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relabeled them 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
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:
• 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:
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62801
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
➢ 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
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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
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
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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 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:
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—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
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 bactin (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:
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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:
PO 00000
Frm 00034
Fmt 4703
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:
E:\FR\FM\13SEN1.SGM
13SEN1
]]>Agencies
[Federal Register Volume 88, Number 176 (Wednesday, September 13, 2023)]
[Notices]
[Pages 62800-62803]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2023-19780]
-----------------------------------------------------------------------
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 Kotha
Subbaramaiah, Ph.D. (Respondent), who was a Professor of Biochemistry
Research in 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 debarment for
a period of seven (7) years, were implemented beginning on August 16,
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:
Kotha Subbaramaiah, Ph.D., Weill Cornell Medical College: Based on
the report of an investigation conducted by WCMC and additional
analysis conducted by ORI in its oversight review, ORI found that Kotha
Subbaramaiah, Ph.D., former Weill Cornell Medical College, 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
intentionally, knowingly, or recklessly falsifying and/or fabricating
data included 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 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
[[Page 62801]]
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.
Specifically, ORI found that Respondent reused Western blot images
from the same source and falsely relabeled them 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:
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
[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
[[Page 62802]]
[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
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:
[[Page 62803]]
--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 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
