Findings of Research Misconduct C, 90833-90834 [2024-26756]
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Federal Register / Vol. 89, No. 222 / Monday, November 18, 2024 / Notices
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Affected Public: Individuals or
Households.
Estimated Annual Burden: 10,833.
Estimated Average Burden per
Respondent: 1 minute.
Frequency of Response: One time.
Estimated Number of Respondents:
650,000.
(Authority: 44 U.S.C. 3501 et seq.)
Maribel Aponte,
VA PRA Clearance Officer, Office of
Enterprise and Integration, Data Governance
Analytics, Department of Veterans Affairs.
[FR Doc. 2024–26803 Filed 11–15–24; 8:45 am]
BILLING CODE 8320–01–P
DEPARTMENT OF VETERANS
AFFAIRS
Findings of Research MisconductC
Department of Veterans Affairs.
Notice.
AGENCY:
ACTION:
The Department of Veterans
Affairs (VA), gives notice, pursuant to
Veterans Health Administration (VHA)
Directive 1058.02 ‘‘Research
Misconduct’’ section 8.l, that the
Department has made findings of
research misconduct against Alan
Lichtenstein, M.D. (‘‘Respondent’’), a
former staff physician at the VA Greater
Los Angeles Healthcare System, Los
Angeles, CA. The Respondent did not
appeal the findings or corrective actions
against him.
FOR FURTHER INFORMATION CONTACT:
Shara Kabak, Research Misconduct
Officer, Office of Research Oversight
(10RO), 810 Vermont Avenue NW,
Washington, DC 20420, (202) 632–7620
(this is not a toll-free number).
lotter on DSK11XQN23PROD with NOTICES1
SUMMARY:
VerDate Sep<11>2014
17:17 Nov 15, 2024
Jkt 265001
VA has
made final findings of research
misconduct against Alan Lichtenstein,
M.D. (‘‘Respondent’’), a former staff
physician at the VA Greater Los Angeles
Healthcare System in Los Angeles, CA.
Based on the recommended findings
of a joint investigation conducted by VA
Greater Los Angeles Healthcare System
and University of California, Los
Angeles School of Medicine, the
Department found that the Respondent
engaged in research misconduct by
recklessly falsifying data included in at
least ten of the following thirteen
published papers:
• DEPTOR is linked to a TORC1-p21
survival proliferation pathway in
multiple myeloma. Genes & Cancer.
2014 Nov;5(11–12):407–19. doi:
10.18632/genesandcancer.44 (hereafter,
‘‘Genes Cancer 2014’’).
• Cytotoxic properties of a DEPTORmTOR inhibitor in multiple myeloma
cells. Cancer Research. 2016 Oct
1;76(19):5822–5831. doi: 10.1158/0008–
5472. CAN–16–1019 (hereafter, ‘‘Cancer
Res. 2016’’).
• Interleukin-6 activates
phosphoinositol-3 kinase in multiple
myeloma tumor cells by signaling
through RAS-dependent and, separately,
through p85-dependent pathways.
Oncogene. 2004 Apr 22;23(19):3368–75.
doi: 10.1038/sj.onc.1207459 (hereafter,
‘‘Oncogene 2004’’).
• MNK1-induced eIF–4E
phosphorylation in myeloma cells: a
pathway mediating IL–6-induced
expansion and expression of genes
involved in metabolic and proteotoxic
responses. PLoS One. 2014 Apr
8;9(4):e94011. doi: 10.1371/
journal.pone.0094011 (hereafter, ‘‘PLoS
One 2014’’). Retraction in: PLoS One.
2023 Sep 8;18(9):e0291491. doi:
10.1371/journal.pone.0291491.
• Mammalian target of rapamycin
inhibitors activate the AKT kinase in
multiple myeloma cells by up-regulating
the insulin-like growth factor receptor/
insulin receptor substrate-1/
phosphatidylinositol 3-kinase cascade.
Molecular Cancer Therapeutics. 2005
Oct;4(10):1533–40. doi: 10.1158/1535–
7163.MCT–05–0068 (hereafter, ‘‘Mol
Cancer Ther. 2005’’).
• Inhibition of SAPK2/p38 enhances
sensitivity to mTORC1 inhibition by
blocking IRES-mediated translation
initiation in glioblastoma. Molecular
Cancer Therapeutics. 2011 10:2244–
2256 Dec;10(12):2244–56. doi: 10.1158/
1535–7163.MCT–11–0478 (hereafter,
‘‘Mol Cancer Ther. 2011’’).
• Specific blockade of Rictor-mTOR
association inhibits mTORC2 activity
and is cytotoxic in glioblastoma. PLoS
One. 2017; Apr 28;12(4):e0176599. doi:
SUPPLEMENTARY INFORMATION:
PO 00000
Frm 00171
Fmt 4703
Sfmt 4703
90833
10.1371/journal.pone.0176599
(hereafter, ‘‘PLoS One 2017’’).
Correction in: PLoS One. 2019 Feb
6;14(2):e0212160. doi: 10.1371/
journal.pone.0212160. Retraction in:
PLoS One. 2023 Sep 8;18(9):e0291490.
doi: 10.1371/journal.pone.0291490.
• MNK kinases facilitate c-myc IRES
activity in rapamycin-treated multiple
myeloma. Oncogene. 2013 Jan
10;32(2):190–7. doi: 10.1038/
onc.2012.43 (hereafter, ‘‘Oncogene
2013’’). Expression of Concern in:
Oncogene. 2023 Oct;42(41):3088. doi:
10.1038/s41388–023–02818–z.
• The PP242 mammalian target of
rapamycin (mTOR) inhibitor activates
extracellular signal-regulated kinase
(ERK) in multiple myeloma cells via a
target of rapamycin complex 1 (TORC1)/
eukaryotic translation initiation factor
4E (eIF–4E)/RAF pathway and
activation is a mechanism of resistance.
Journal of Biological Chemistry. 2012
Jun 22;287(26):21796–805. doi: 10.1074/
jbc.M111.304626 (hereafter, ‘‘J Biol
Chem. 2012’’).
• Therapeutic potential of targeting
IRES-dependent c-myc translation in
multiple myeloma cells during ER
stress. Oncogene. 2016 Feb
25;35(8):1015–24. doi: 10.1038/
onc.2015.156 (hereafter, ‘‘Oncogene
2016’’). Retraction in: Oncogene. 2023
Sep;42(40):3016. doi: 10.1038/s41388–
023–02820–5.
• SGK kinase activity in multiple
myeloma cells protects against ER stress
apoptosis via a SEK-dependent
mechanism. Molecular Cancer
Research. 2016 Apr;14(4):397–407. doi:
10.1158/1541–7786.MCR–15–0422
(hereafter, ‘‘Mol Cancer Res. 2016’’).
• A novel therapeutic induces
DEPTOR degradation in multiple
myeloma cells with resulting tumor
cytotoxicity. Molecular Cancer
Therapeutics. 2019 Oct;18(10):1822–
1831. doi: 10.1158/1535–7163.MCT–19–
0115 (hereafter, ‘‘Mol Cancer Ther.
2019’’).
• Downstream effectors of oncogenic
ras in multiple myeloma cells. Blood.
2003 Apr 15;101(8):3126–35. doi:
10.1182/blood–2002–08–2640
(hereafter, ‘‘Blood 2003’’).
Specifically, the Department found
that the Respondent recklessly
committed research misconduct by
reusing the same Western blot or kinase
assay image to falsely represent the
results related to the following pairs of
experiments such that at least one of the
sets of images in each of the pairs listed
below is inaccurate:
• p-4E–BP1–T37/46, p–4E–BP1–S65
and Tubulin expression in Figure 3B of
Genes Cancer 2014 and Figure 1F of
Cancer Res. 2016.
E:\FR\FM\18NON1.SGM
18NON1
lotter on DSK11XQN23PROD with NOTICES1
90834
Federal Register / Vol. 89, No. 222 / Monday, November 18, 2024 / Notices
• P–AKT–S473 expression in Figure
3C in Genes Cancer 2014 and lanes 1–
4 of DEPTOR expression in Figure 3C of
Cancer Res. 2016 with resizing.
• Lanes 7–9 of p70S6K1 expression in
Figure 1A of Genes Cancer 2014 and
DEPTOR expression in Figure 4C of
Cancer Res. 2016.
• STAT3 associated kinase activity in
Figure 4A and lanes 1–4 of p110 mu
associated kinase activity in Figure 5B
of Oncogene 2004.
• Lanes 7–8 of ACTIN expression in
Figure 1A and lanes 7–8 of ACTIN
expression in Figure 1C of PLoS One
2014.
• Lanes 3–4 of P–MNK and T–MNK
expression in Figure 1C of PloS One
2014 and lanes 1–2 of FKHD–P and
FKHD–T expression (top panels) in
Figure 1B of Mol Cancer Ther. 2005.
• Lanes 4–8 of P–AKT (S473) and
actin expression in Figure 2A of Mol
Cancer Ther. 2011 and AKT and S6K
expression in Figure 1F of PloS One
2017 with a 180 degree rotation of the
P–AKT/AKT panels.
• Lanes 1–2 of T–HSP27 expression
and lanes 4–5 of GAPDH expression in
Figure 2B of Oncogene 2013.
• Lanes 1–3 of p–erk and lanes 2–4 of
t-erk expression in Figure 3B and lanes
1–3 of erk(T202/Y204) and erk
expression in Figure 4A of J Biol Chem.
2012.
• a-tubulin expression in Figure 4D
and 4E of Genes Cancer 2014.
• C-myc expression in Figure 1B and
lanes 1–4 of T-p70 expression in Figure
1E of Oncogene 2016.
• T–4E–BP1 (a, b and g
phosphorylated forms) expression
(middle panel) and lanes 1–4 of T–4E–
BP (a, b and g phosphorylated forms)
expression (right panel) of
Supplemental Figure 2A of Oncogene
2016.
• T–S6 expression and C–myc
expression in Figure 1F of Oncogene
2016.
• Lanes 2–5 of MNK–P and MNK–T
expression (left panel) in Figure 3A and
ERK–T and Hsp–27–T expression in
Figure 4A of Oncogene 2016.
• MNK1, MNK2 and GAPDH
expression in Figure 3E of Oncogene
2016 and MNK1, MNK2 and GAPDH
expression in Figure 3A of PloS One
2014.
• ire–1–total expression (right panel)
in Figure 5B of Mol Cancer Res. 2016
and mTor expression in Figure 8A of
Genes Cancer 2014 with resizing.
• The right panel of ACTIN
expression in Figure 2A and the right
panel of ACTIN expression in Figure 2g
of Mol Cancer Ther. 2019.
• Lanes 1–6 of DEPTOR and mTOR
expression in Figure 1A of Genes
VerDate Sep<11>2014
17:17 Nov 15, 2024
Jkt 265001
Cancer 2014 and DEPTOR and mTor
expression in Figure 6A of Mol Cancer
Ther. 2019.
• IRS–1 expression in lanes 4–5 and
lanes 8–9 in Figure 6B of Mol Cancer
Ther. 2005.
• AKT expression (bottom panel) in
Figure 1Aand lanes 7–9 of IRS–1
expression in Figure 6B of Mol Cancer
Ther. 2005.
• Lanes 4–6 of IGF–R expression and
lanes 4–6 of FLAG expression in Figure
5B of Mol Cancer Ther. 2005 with a 180degree rotation.
• Lanes 2–3 of AKT–T expression
(4th panel) in and lanes 1–2 of AKT–T
expression (6th panel) in Figure 1C of
Mol Cancer Ther. 2005.
• Lanes 1–2 of AKT–P expression
(top panel) and lanes 1–2 of AKT–P
expression (5th panel) in Figure 1E of
Mol Cancer Ther. 2005.
• Lanes 1–3 and lanes 5–7 of FKH–T
expression in Figure 3C of Blood 2003.
• Lane 1 of p70 expression and
Ser411 expression in Figure 4B and lane
4 of Ser411 expression and lanes 1–2 of
Ser411 expression in Figure 4c of Blood
2003.
• Lanes 1 and 3 of ERK–P expression
and lanes 2 and 4 of ERK–T expression
in Figure 2C of Blood 2003.
Based on these findings of research
misconduct, which the Respondent did
not appeal, the Department has imposed
the following corrective actions:
(1) Prohibition from conducting VA
research for at least 2 years;
(2) Notification to the relevant
journals of the research misconduct
findings.
Signing Authority
Denis McDonough, Secretary of
Veterans Affairs, signed and approved
this document on November 12, 2024,
and authorized the undersigned to sign
and submit the document to the Office
of the Federal Register for publication
electronically as an official document of
the Department of Veterans Affairs.
Jeffrey M. Martin,
Assistant Director, Office of Regulation Policy
& Management, Office of General Counsel,
Department of Veterans Affairs.
[FR Doc. 2024–26756 Filed 11–15–24; 8:45 am]
BILLING CODE 8320–01–P
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DEPARTMENT OF VETERANS
AFFAIRS
[OMB Control No. 2900–0012]
Agency Information Collection Activity
Under OMB Review: Application for
Cash Surrender or Policy Loan and
Application for Cash Surrender
(Docusign)
Veterans Benefits
Administration, Department of Veterans
Affairs.
ACTION: Notice.
AGENCY:
In compliance with the
Paperwork Reduction Act (PRA) of
1995, this notice announces that the
Veterans Benefits Administration,
Department of Veterans Affairs, will
submit the collection of information
abstracted below to the Office of
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review and comment. The PRA
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information collection and its expected
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select ‘‘Currently under Review—Open
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Title or ‘‘OMB Control No. 2900–0012.’’
FOR FURTHER INFORMATION CONTACT: VA
PRA information: Maribel Aponte, (202)
461–8900, vacopaperworkreduact@
va.gov.
SUPPLEMENTARY INFORMATION:
Title: Application for Cash Surrender
or Policy Loan (VA Form 29–1546).
Application for Cash Surrender (VA
Form 29–1546e—DocuSign).
OMB Control Number: 2900–0012—
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Type of Review: Extension without
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Abstract: The Application for Cash
Surrender or Policy Loan solicits
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apply for cash surrender value or policy
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29–1546e has been added to this
collection. This is an electronic version
of the 29–1546 but is for cash surrender
only. This form was created so Veterans
can apply for a cash surrender of their
policy online. This will not affect the
number of respondents but will make it
SUMMARY:
E:\FR\FM\18NON1.SGM
18NON1
Agencies
[Federal Register Volume 89, Number 222 (Monday, November 18, 2024)]
[Notices]
[Pages 90833-90834]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2024-26756]
-----------------------------------------------------------------------
DEPARTMENT OF VETERANS AFFAIRS
Findings of Research MisconductC
AGENCY: Department of Veterans Affairs.
ACTION: Notice.
-----------------------------------------------------------------------
SUMMARY: The Department of Veterans Affairs (VA), gives notice,
pursuant to Veterans Health Administration (VHA) Directive 1058.02
``Research Misconduct'' section 8.l, that the Department has made
findings of research misconduct against Alan Lichtenstein, M.D.
(``Respondent''), a former staff physician at the VA Greater Los
Angeles Healthcare System, Los Angeles, CA. The Respondent did not
appeal the findings or corrective actions against him.
FOR FURTHER INFORMATION CONTACT: Shara Kabak, Research Misconduct
Officer, Office of Research Oversight (10RO), 810 Vermont Avenue NW,
Washington, DC 20420, (202) 632-7620 (this is not a toll-free number).
SUPPLEMENTARY INFORMATION: VA has made final findings of research
misconduct against Alan Lichtenstein, M.D. (``Respondent''), a former
staff physician at the VA Greater Los Angeles Healthcare System in Los
Angeles, CA.
Based on the recommended findings of a joint investigation
conducted by VA Greater Los Angeles Healthcare System and University of
California, Los Angeles School of Medicine, the Department found that
the Respondent engaged in research misconduct by recklessly falsifying
data included in at least ten of the following thirteen published
papers:
DEPTOR is linked to a TORC1-p21 survival proliferation
pathway in multiple myeloma. Genes & Cancer. 2014 Nov;5(11-12):407-19.
doi: 10.18632/genesandcancer.44 (hereafter, ``Genes Cancer 2014'').
Cytotoxic properties of a DEPTOR-mTOR inhibitor in
multiple myeloma cells. Cancer Research. 2016 Oct 1;76(19):5822-5831.
doi: 10.1158/0008-5472. CAN-16-1019 (hereafter, ``Cancer Res. 2016'').
Interleukin-6 activates phosphoinositol-3 kinase in
multiple myeloma tumor cells by signaling through RAS-dependent and,
separately, through p85-dependent pathways. Oncogene. 2004 Apr
22;23(19):3368-75. doi: 10.1038/sj.onc.1207459 (hereafter, ``Oncogene
2004'').
MNK1-induced eIF-4E phosphorylation in myeloma cells: a
pathway mediating IL-6-induced expansion and expression of genes
involved in metabolic and proteotoxic responses. PLoS One. 2014 Apr
8;9(4):e94011. doi: 10.1371/journal.pone.0094011 (hereafter, ``PLoS One
2014''). Retraction in: PLoS One. 2023 Sep 8;18(9):e0291491. doi:
10.1371/journal.pone.0291491.
Mammalian target of rapamycin inhibitors activate the AKT
kinase in multiple myeloma cells by up-regulating the insulin-like
growth factor receptor/insulin receptor substrate-1/
phosphatidylinositol 3-kinase cascade. Molecular Cancer Therapeutics.
2005 Oct;4(10):1533-40. doi: 10.1158/1535-7163.MCT-05-0068 (hereafter,
``Mol Cancer Ther. 2005'').
Inhibition of SAPK2/p38 enhances sensitivity to mTORC1
inhibition by blocking IRES-mediated translation initiation in
glioblastoma. Molecular Cancer Therapeutics. 2011 10:2244-2256
Dec;10(12):2244-56. doi: 10.1158/1535-7163.MCT-11-0478 (hereafter,
``Mol Cancer Ther. 2011'').
Specific blockade of Rictor-mTOR association inhibits
mTORC2 activity and is cytotoxic in glioblastoma. PLoS One. 2017; Apr
28;12(4):e0176599. doi: 10.1371/journal.pone.0176599 (hereafter, ``PLoS
One 2017''). Correction in: PLoS One. 2019 Feb 6;14(2):e0212160. doi:
10.1371/journal.pone.0212160. Retraction in: PLoS One. 2023 Sep
8;18(9):e0291490. doi: 10.1371/journal.pone.0291490.
MNK kinases facilitate c-myc IRES activity in rapamycin-
treated multiple myeloma. Oncogene. 2013 Jan 10;32(2):190-7. doi:
10.1038/onc.2012.43 (hereafter, ``Oncogene 2013''). Expression of
Concern in: Oncogene. 2023 Oct;42(41):3088. doi: 10.1038/s41388-023-
02818-z.
The PP242 mammalian target of rapamycin (mTOR) inhibitor
activates extracellular signal-regulated kinase (ERK) in multiple
myeloma cells via a target of rapamycin complex 1 (TORC1)/eukaryotic
translation initiation factor 4E (eIF-4E)/RAF pathway and activation is
a mechanism of resistance. Journal of Biological Chemistry. 2012 Jun
22;287(26):21796-805. doi: 10.1074/jbc.M111.304626 (hereafter, ``J Biol
Chem. 2012'').
Therapeutic potential of targeting IRES-dependent c-myc
translation in multiple myeloma cells during ER stress. Oncogene. 2016
Feb 25;35(8):1015-24. doi: 10.1038/onc.2015.156 (hereafter, ``Oncogene
2016''). Retraction in: Oncogene. 2023 Sep;42(40):3016. doi: 10.1038/
s41388-023-02820-5.
SGK kinase activity in multiple myeloma cells protects
against ER stress apoptosis via a SEK-dependent mechanism. Molecular
Cancer Research. 2016 Apr;14(4):397-407. doi: 10.1158/1541-7786.MCR-15-
0422 (hereafter, ``Mol Cancer Res. 2016'').
A novel therapeutic induces DEPTOR degradation in multiple
myeloma cells with resulting tumor cytotoxicity. Molecular Cancer
Therapeutics. 2019 Oct;18(10):1822-1831. doi: 10.1158/1535-7163.MCT-19-
0115 (hereafter, ``Mol Cancer Ther. 2019'').
Downstream effectors of oncogenic ras in multiple myeloma
cells. Blood. 2003 Apr 15;101(8):3126-35. doi: 10.1182/blood-2002-08-
2640 (hereafter, ``Blood 2003'').
Specifically, the Department found that the Respondent recklessly
committed research misconduct by reusing the same Western blot or
kinase assay image to falsely represent the results related to the
following pairs of experiments such that at least one of the sets of
images in each of the pairs listed below is inaccurate:
p-4E-BP1-T37/46, p-4E-BP1-S65 and Tubulin expression in
Figure 3B of Genes Cancer 2014 and Figure 1F of Cancer Res. 2016.
[[Page 90834]]
P-AKT-S473 expression in Figure 3C in Genes Cancer 2014
and lanes 1-4 of DEPTOR expression in Figure 3C of Cancer Res. 2016
with resizing.
Lanes 7-9 of p70S6K1 expression in Figure 1A of Genes
Cancer 2014 and DEPTOR expression in Figure 4C of Cancer Res. 2016.
STAT3 associated kinase activity in Figure 4A and lanes 1-
4 of p110 mu associated kinase activity in Figure 5B of Oncogene 2004.
Lanes 7-8 of ACTIN expression in Figure 1A and lanes 7-8
of ACTIN expression in Figure 1C of PLoS One 2014.
Lanes 3-4 of P-MNK and T-MNK expression in Figure 1C of
PloS One 2014 and lanes 1-2 of FKHD-P and FKHD-T expression (top
panels) in Figure 1B of Mol Cancer Ther. 2005.
Lanes 4-8 of P-AKT (S473) and actin expression in Figure
2A of Mol Cancer Ther. 2011 and AKT and S6K expression in Figure 1F of
PloS One 2017 with a 180 degree rotation of the P-AKT/AKT panels.
Lanes 1-2 of T-HSP27 expression and lanes 4-5 of GAPDH
expression in Figure 2B of Oncogene 2013.
Lanes 1-3 of p-erk and lanes 2-4 of t-erk expression in
Figure 3B and lanes 1-3 of erk(T202/Y204) and erk expression in Figure
4A of J Biol Chem. 2012.
[alpha]-tubulin expression in Figure 4D and 4E of Genes
Cancer 2014.
C-myc expression in Figure 1B and lanes 1-4 of T-p70
expression in Figure 1E of Oncogene 2016.
T-4E-BP1 ([alpha], [beta] and [gamma] phosphorylated
forms) expression (middle panel) and lanes 1-4 of T-4E-BP ([alpha],
[beta] and [gamma] phosphorylated forms) expression (right panel) of
Supplemental Figure 2A of Oncogene 2016.
T-S6 expression and C-myc expression in Figure 1F of
Oncogene 2016.
Lanes 2-5 of MNK-P and MNK-T expression (left panel) in
Figure 3A and ERK-T and Hsp-27-T expression in Figure 4A of Oncogene
2016.
MNK1, MNK2 and GAPDH expression in Figure 3E of Oncogene
2016 and MNK1, MNK2 and GAPDH expression in Figure 3A of PloS One 2014.
ire-1-total expression (right panel) in Figure 5B of Mol
Cancer Res. 2016 and mTor expression in Figure 8A of Genes Cancer 2014
with resizing.
The right panel of ACTIN expression in Figure 2A and the
right panel of ACTIN expression in Figure 2g of Mol Cancer Ther. 2019.
Lanes 1-6 of DEPTOR and mTOR expression in Figure 1A of
Genes Cancer 2014 and DEPTOR and mTor expression in Figure 6A of Mol
Cancer Ther. 2019.
IRS-1 expression in lanes 4-5 and lanes 8-9 in Figure 6B
of Mol Cancer Ther. 2005.
AKT expression (bottom panel) in Figure 1Aand lanes 7-9 of
IRS-1 expression in Figure 6B of Mol Cancer Ther. 2005.
Lanes 4-6 of IGF-R expression and lanes 4-6 of FLAG
expression in Figure 5B of Mol Cancer Ther. 2005 with a 180-degree
rotation.
Lanes 2-3 of AKT-T expression (4th panel) in and lanes 1-2
of AKT-T expression (6th panel) in Figure 1C of Mol Cancer Ther. 2005.
Lanes 1-2 of AKT-P expression (top panel) and lanes 1-2 of
AKT-P expression (5th panel) in Figure 1E of Mol Cancer Ther. 2005.
Lanes 1-3 and lanes 5-7 of FKH-T expression in Figure 3C
of Blood 2003.
Lane 1 of p70 expression and Ser411 expression in Figure
4B and lane 4 of Ser411 expression and lanes 1-2 of Ser411 expression
in Figure 4c of Blood 2003.
Lanes 1 and 3 of ERK-P expression and lanes 2 and 4 of
ERK-T expression in Figure 2C of Blood 2003.
Based on these findings of research misconduct, which the
Respondent did not appeal, the Department has imposed the following
corrective actions:
(1) Prohibition from conducting VA research for at least 2 years;
(2) Notification to the relevant journals of the research
misconduct findings.
Signing Authority
Denis McDonough, Secretary of Veterans Affairs, signed and approved
this document on November 12, 2024, and authorized the undersigned to
sign and submit the document to the Office of the Federal Register for
publication electronically as an official document of the Department of
Veterans Affairs.
Jeffrey M. Martin,
Assistant Director, Office of Regulation Policy & Management, Office of
General Counsel, Department of Veterans Affairs.
[FR Doc. 2024-26756 Filed 11-15-24; 8:45 am]
BILLING CODE 8320-01-P