[Federal Register Volume 89, Number 158 (Thursday, August 15, 2024)]
[Notices]
[Pages 66420-66422]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2024-18289]


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DEPARTMENT OF HEALTH AND HUMAN SERVICES

Office of the Secretary


Findings of Research Misconduct

AGENCY: Office of the Secretary, HHS.

ACTION: Notice.

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SUMMARY: Findings of research misconduct have been made against Richard 
L. Eckert, Ph.D. (Respondent), who was a Professor, Chair of the 
Department of Biochemistry and Molecular Biology, and Deputy Director 
of the University of Maryland and Stewart Greenebaum Comprehensive 
Cancer Center, University of Maryland, Baltimore (UMB). 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 R01 CA211909, R01 
CA184027, R01 CA131074, R01 CA131064, R01 CA092201, R01 CA109196, P30 
CA134274, and P30 CA043703, National Institute of Arthritis and 
Musculoskeletal and Skin Diseases (NIAMS), NIH, grants R21 AR065266, 
R01 AR046494, R01 AR053851, R01 AR060388, P30 AR039750, R01 AR041456, 
R01 AR049713, and R01 AR045357, National Eye Institute (NEI), NIH, 
grants P30 EY011373 and T32 EY007157, and National Institute of General 
Medical Sciences (NIGMS), NIH, grant R01 GM043751. The questioned 
research was included in two (2) grant applications submitted for PHS 
funds, specifically R01 CA233450-01 and R01 CA233450-01A1 submitted to 
NCI, NIH. The administrative actions, including debarment for a period 
of eight (8) years, were implemented beginning on August 1, 2024, 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:
    Richard L. Eckert, Ph.D., University of Maryland, Baltimore (UMB): 
Based on the report of an investigation conducted by UMB and additional 
analysis conducted by ORI in its oversight review, ORI found that Dr. 
Richard L. Eckert (Respondent), former Professor, Chair of the 
Department of Biochemistry and Molecular Biology, and Deputy Director 
of the University of Maryland and Stewart Greenebaum Comprehensive 
Cancer Center, UMB, engaged in research misconduct in research 
supported by PHS funds, specifically NCI, NIH, grants R01 CA211909, R01 
CA184027, R01 CA131074, R01 CA131064, R01 CA092201, R01 CA109196, P30 
CA134274, and P30 CA043703, NIAMS, NIH, grants R21 AR065266, R01 
AR046494, R01 AR053851, R01 AR060388, P30 AR039750, R01 AR041456, R01 
AR049713, and R01 AR045357, NEI, NIH, grants P30 EY011373 and T32 
EY007157, and NIGMS, NIH, grant R01 GM043751. The questioned research 
was included in two (2) grant applications submitted for PHS funds, 
specifically R01 CA233450-01 and R01 CA233450-01A1 submitted to NCI, 
NIH.
    ORI found that Respondent engaged in research misconduct by 
intentionally, knowingly, or recklessly falsifying and/or fabricating 
data in the following thirteen (13) published papers and two (2) PHS 
grant applications:
     Inhibition of YAP function overcomes BRAF inhibitor 
resistance in melanoma cancer stem cells. Oncotarget. 2017 Nov 22; 
8(66):110257-110272. doi: 10.18632/oncotarget.22628 (hereafter referred 
to as ``Oncotarget 2017'').
     The Bmi-1 helix-turn and ring finger domains are required 
for Bmi-1 antagonism of (-) epigallocatechin-3-gallate suppression of 
skin cancer cell survival. Cell Signal. 2015 Jul;27(7):1336-44. doi: 
10.1016/j.cellsig.2015.03.021 (hereafter referred to as ``Cell Signal 
2015''). Erratum in: Cell Signal. 2021 Jun;82:109952. doi: 10.1016/
j.cellsig.2021.109952.
     P38[delta] regulates p53 to control p21Cip1 expression in 
human epidermal keratinocytes. J Biol Chem. 2014 Apr 18; 289(16):11443-
11453. doi: 10.1074/jbc.M113.543165 (hereafter referred to as ``J Biol 
Chem. 2014'').

[[Page 66421]]

     Methylosome protein 50 and PKC[delta]/p38[delta] protein 
signaling control keratinocyte proliferation via opposing effects on 
p21Cip1 gene expression. J Biol Chem. 2015 May 22;290(21):13521-30. 
doi: 10.1074/jbc.M115.642868 (hereafter referred to as ``J Biol Chem. 
2015'').
     Transamidase site-targeted agents alter the conformation 
of the transglutaminase cancer stem cell survival protein to reduce GTP 
binding activity and cancer stem cell survival. Oncogene. 2017 May 
25;36(21):2981-2990. doi: 10.1038/onc.2016.452 (hereafter referred to 
as ``Oncogene 2017''). Erratum in: Oncogene. 2021 Apr;40(13):2479-2481. 
doi: 10.1038/s41388-021-01709-5.
     Suppression of AP1 transcription factor function in 
keratinocyte suppresses differentiation. PLoS One. 2012;7(5):e36941. 
doi: 10.1371/journal.pone.0036941 (hereafter referred to as ``PLoS One 
2012''). Retraction in: PLoS One. 2021 Feb 11;16(2):e0247222. doi: 
10.1371/journal.pone.0247222.
     Suppressing AP1 factor signaling in the suprabasal 
epidermis produces a keratoderma phenotype. J Invest Dermatol. 2015 
Jan;135(1):170-180. doi: 10.1038/jid.2014.310 (hereafter referred to as 
``J Invest Dermatol. 2015''). Erratum in: J Invest Dermatol. 2021 Jul; 
141(7):1862. doi: 10.1016/j.jid.2021.05.008.
     Protein kinase C (PKC) delta suppresses keratinocyte 
proliferation by increasing p21(Cip1) level by a KLF4 transcription 
factor-dependent mechanism. J Biol Chem. 2011 Aug 19; 286(33):28772-
28782. doi: 10.1074/jbc.M110.205245 (hereafter referred to as ``J Biol 
Chem. 2011'').
     The Bmi-1 polycomb protein antagonizes the (-)-
epigallocatechin-3-gallate-dependent suppression of skin cancer cell 
survival. Carcinogenesis. 2010 Mar;31(3):496-503. doi: 10.1093/carcin/
bgp314 (hereafter referred to as ``Carcinogenesis 2010'').
     PKC-delta and -eta, MEKK-1, MEK-6, MEK-3, and p38-delta 
are essential mediators of the response of normal human epidermal 
keratinocytes to differentiating agents. J Invest Dermatol. 2010 
Aug;130(8):2017-30. doi: 10.1038/jid.2010.108 (hereafter referred to as 
``J Invest Dermatol. 2010'').
     Sulforaphane suppresses PRMT5/MEP50 function in epidermal 
squamous cell carcinoma leading to reduced tumor formation. 
Carcinogenesis. 2017 Aug 1;38(8):827-836. doi: 10.1093/carcin/bgx044 
(hereafter referred to as ``Carcinogenesis 2017''). Erratum in: 
Carcinogenesis. 2023 Oct 20;44(7):626-627. doi: 10.1093/carcin/bgad044.
     Localization of the TIG3 transglutaminase interaction 
domain and demonstration that the amino-terminal region is required for 
TIG3 function as a keratinocyte differentiation regulator. J Invest 
Dermatol. 2008 Mar;128(3):517-29. doi: 10.1038/sj.jid.5701035 
(hereafter referred to as ``J Invest Dermatol. 2008'').
     Transglutaminase interaction with [alpha]6/[beta]4-
integrin stimulates YAP1-Dependent [Delta]Np63[alpha] stabilization and 
leads to enhanced cancer stem cell survival and tumor formation. Cancer 
Res. 2016 Dec 15;76(24):7265-7276. doi: 10.1158/0008-5472.CAN-16-2032 
(hereafter referred to as ``Cancer Res. 2016'').
     R01 CA233450-01, ``Sulforaphane suppression of PRMT5 
epigenetics to reduce cancer stem cell survival,'' submitted to NCI, 
NIH, on 01/26/2018, administratively withdrawn by NCI on 07/01/2020
     R01 CA233450-01A1, ``Sulforaphane suppression of PRMT5 
epigenetics to reduce cancer stem cell survival,'' submitted to NCI, 
NIH, on 10/30/2018, administratively withdrawn by NCI on 03/01/2021
    Specifically, ORI found that Respondent intentionally, knowingly, 
or recklessly falsified and/or fabricated Western blot image data and 
microscopy image data by:
     using images representing unrelated experiments, with or 
without manipulating them, and falsely relabeling them as data 
representing different proteins and/or experimental results as follows:

--In Figure 3F of Oncotarget 2017, the bands in rows 4 and 7 of the 
A375-PLX-R right-side panel, representing expression of TAZ-P (row 4) 
and ERK1/2 (row 7), are falsified and/or fabricated by using unrelated 
bands from a source image representing different proteins in an 
unrelated experiment
--In Figure 2B of J Biol Chem. 2014, the bands in row 2 in the top 
panel, representing MEK3 expression in normal human keratinocytes 
(KERn) infected with Ad5-EV, Ad5-MEK3, and Ad5-PKC[delta] (from left to 
right), are falsified and/or fabricated by compiling unrelated bands 
from a source image representing p44 expression in an unrelated 
experiment
--In Figure 2B of J Biol Chem. 2014, the bands in row 3 in the top 
panel, representing p38[delta] expression in KERn infected with Ad5-EV, 
Ad5-MEK3, and Ad5-PKC[delta] (from left to right), are falsified and/or 
fabricated by compiling unrelated bands from a source image 
representing [beta]-actin expression in an unrelated experiment
--In Figure 1B of J Biol Chem. 2015, the bands in rows 1-3 in the upper 
panel, representing expression of MEP50 (row 1), FLAG (row 2), and 
[beta]-actin (row 3), are falsified and/or fabricated by compiling 
different bands from source images representing expression of different 
proteins in unrelated experiments
--In Figure 7C of J Biol Chem. 2011, the bands in row 2 in the right 
panel, representing p21\Cip1\ expression under treatments of Control-
siRNA or hKLF4-siRNA, are falsified and/or fabricated by using 
unrelated bands from a source image representing p21 expression in 
cells treated with Ad5-EV or Ad5-PKCd
--In Figure 1B of PLoS One 2012, the bands in row 1, representing 
TAM67-FLAG expression, are falsified and/or fabricated by using 
unrelated bands from a source image representing CyclinA expression
--In Figure 2C of PLoS One 2012, the bands in rows 3 and 4, 
representing negative expression of junB (row 3) and junD (row 4), are 
falsified and/or fabricated by using blank areas that were far from the 
target molecular weight in a source image
--In Figure 6a of J Invest Dermatol. 2015, the bands 1-4 in the bottom 
row, representing [beta]-Actin expression under treatments of Loricrin, 
TAM67-rTA, and/or Dox, are falsified and/or fabricated by:
--[rtarr8] using 3 bands from a source image representing [beta]-actin 
expression in an unrelated experiment for bands 1-3
--[rtarr8] duplicating band 3 to create band 4
--In Figure 1B of Carcinogenesis 2010, the bands in rows 1, 2, and 5 in 
the left panel, representing expression of Ezh2 (row 1), H3 K27-3M (row 
2), and [beta]-actin (row 5) in two different cell types treated with 
60 [micro]M EGCG, are falsified and/or fabricated by using unrelated 
bands from a source image representing expression of the same proteins 
under an unrelated experiment
--In Carcinogenesis 2010, the bands in row 3 in the right panel of 
Figure 1B and the bands 1-5 in row 3 in the upper panel of Figure 2A 
are falsified and/or fabricated by using unrelated bands from a source 
image. Specifically:
--[rtarr8] the bands 1-4 in the upper panel of Figure 2A, representing 
Ezh2 expression treated with 0, 10, 20, and 40 [micro]M EGCG are used 
from the bands representing the same protein

[[Page 66422]]

but treated with different doses of EGCG in the source image
--[rtarr8] the bands 1 and 5 in the upper panel of Figure 2A, 
representing Ezh2 expression, are reused and relabeled in the bands in 
Figure 1B, row 3 in the right panel to represent Suz12 expression
--In Figure 4A of Carcinogenesis 2010, the bands in rows 6 and 7, 
representing expression of cyclin E (row 6) and cyclin A (row 7) in 
cells treated with 60 [micro]m EGCG plus other reagents, are falsified 
and/or fabricated by reusing and relabeling the bands from a source 
image representing cyclin E expression in cells treated with 150 
[micro]m EGCG plus other reagents
--In Figure 7a of J Invest Dermatol. 2008:
--[rtarr8] bands 1 and 5 (including the empty lanes) in the COX4 panel, 
representing expression of COX4 treated with EV (band 1) and TIG3 1-134 
(band 5), are falsified and/or fabricated by reusing a band labeled as 
TGI C377 sample 3 from the primary data
--[rtarr8] band 8 (including the empty lanes) in the Cytochrome c 
panel, representing expression of Cytochrome c treated with TIG3 124-
164, is falsified and/or fabricated by using an unrelated band from 
unknown source

     reusing the same source images, with or without 
manipulating them to conceal their similarities, and falsely relabeling 
them as data representing different proteins or experimental results as 
follows:

--In Figure 2 of Cell Signal 2015, two control samples in the bottom 
panel, representing cells in tAd5-FLAG-hBmi[Delta]RF condition (left) 
and tAd5-FLAG-hBmi-1[Delta]HT condition (right), are reused from 
different fields of a same source image
--In J Biol Chem. 2014, Figure 2B, bands 2 and 3 in row 1 of 3rd panel, 
representing ATF2-P expression, and Figure 6C, bands 1 and 2 in row 2 
of the 3rd panel, representing p38[alpha] expression, are identical
--In J Biol Chem. 2014, Figure 2C, bands 1 and 3 in row 3 of the upper 
panel, representing MEK3 expression, and Figure 6C, bands 1 and 2 in 
row 2 of the top panel, representing p38[alpha] expression, are 
identical
--In Figure 3C of Oncogene 2017, band 9, representing TG2 expression 
treated with total CP4d, is falsified and/or fabricated by reusing and 
relabeling band 3, representing TG2 expression treated with NC9 (total) 
in the same figure
--In Carcinogenesis 2010, Figure 3C, the bands in row 2, representing 
[beta]-actin expression, and Figure 4C, the bands in row 3, 
representing procaspase 9 expression, are identical
--In Figure 7b of J Invest Dermatol. 2010, the bands in the upper 
panel, representing expression of MEKK1 and its [beta]-Actin control, 
are falsified and/or fabricated by reusing and relabeling the bands in 
the middle panel, representing expression of MEK6 and its
--[beta]-Actin control in the same figure
--In Figure 1D of Carcinogenesis 2017, Figure 5B of R01 CA233450-01 and 
Figure 3B of R01 CA233450-01A1, the bands in rows 3 in both the upper 
and bottom panels, representing H4 expression, are falsified and/or 
fabricated by reusing and relabeling the same source images that are 
used for the bands in row 2 in Figure 3J of Carcinogenesis 2017, 
representing PRMT5 expression
--In Figure 1c of J Invest Dermatol. 2008, the background area between 
molecular weight 20-45 in the TIG3 (41-164) lanes of the right panel is 
falsified and/or fabricated by reusing and relabeling the background 
area of TIG3 WT group with flipping
--In Figure 1c of J Invest Dermatol. 2008, the bands in lanes 7-8 of 
the left panel, representing expression of TIG3 monomer under TIG3 
(100-164) condition, are falsified and/or fabricated by reusing and 
relabeling the bands in lanes 9-10 of the left panel, representing 
expression of TIG3 monomer under TIG3 (41-164) condition
--In Cancer Res. 2016, bands 2-3 in the bottom row in Figure 3C, 
representing [beta]-actin expression treated with Integrin [alpha]6-
siRNA (band 2) and Integrin [beta]4-siRNA (band 3), and bands 1-2 in 
the bottom row in Figure 3D, representing [beta]-actin expression 
treated with Control-siRNA (band 1) and FAK-siRNA (band 2), are 
identical
     manipulating the data to exclude the band from a source 
image to falsely show a favorable result in Figure 2C of PLoS One 2012 
by erasing the band in the left lane of the top row to falsely 
represent a lack of TAM67-FLAG expression
    Respondent entered into a Voluntary Exclusion Agreement (Agreement) 
and voluntarily agreed to the following:
    (1) Respondent will exclude himself voluntarily for a period of 
eight (8) years beginning on August 1, 2024 (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 not apply for, 
permit his name to be used on an application for, receive, or be 
supported by funds of the United States Government and its agencies 
made available through contracts, subcontracts, or covered 
transactions.
    (3) 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.
    (4) Respondent will request that the following papers be corrected 
or retracted:
     Oncotarget 2017 Nov 22;8(66):110257-110272. doi: 10.18632/
oncotarget.22628.
     J Biol Chem. 2014 Apr 18;289(16):11443-11453. doi: 
10.1074/jbc.M113.543165.
     J Biol Chem. 2015 May 22;290(21):13521-30. doi: 10.1074/
jbc.M115.642868.
     J Biol Chem. 2011 Aug 19;286(33):28772-28782. doi: 
10.1074/jbc.M110.205245.
     Carcinogenesis 2010 Mar;31(3):496-503. doi: 10.1093/
carcin/bgp314.
     J Invest Dermatol. 2008 Mar; 128(3):517-29. doi: l 0.1038/
sj.jid.5701035.
     J Invest Dermatol. 2010 Aug;130(8):2017-30. doi: 10.1038/
jid.2010.108.
     Cancer Res. 2016 Dec 15;76(24):7265-7276. doi: 10.1158/
0008-5472.CAN-16-2032.
    Respondent will copy ORI and the Research Integrity Officer at UMB 
on the correspondence with the journals.

    Dated: August 12, 2024.
Sheila Garrity,
Director, Office of Research Integrity, Office of the Assistant 
Secretary for Health.
[FR Doc. 2024-18289 Filed 8-14-24; 8:45 am]
BILLING CODE 4150-31-P