[Federal Register Volume 80, Number 17 (Tuesday, January 27, 2015)]
[Notices]
[Pages 4267-4268]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2015-01427]


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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: Notice is hereby given that the Office of Research Integrity 
(ORI) has taken final action in the following case:
    Dong Xiao, Ph.D., University of Pittsburgh: Based on the report of 
an inquiry conducted by the University of Pittsburgh (UP), additional 
analysis conducted by ORI in its oversight review, and an admission by 
the Respondent that he had ``intentionally fabricated data contained in 
a paper entitled `Guggulsterone inhibits prostate cancer growth via 
inactivation of Akt regulated by ATP citrate signaling,' specifically 
Figure 6G,'' ORI found that Dr. Dong Xiao, former Research Assistant 
Professor, Department of Urology, UP, engaged in research misconduct in 
research supported by National Cancer Institute (NCI), National 
Institutes of Health (NIH), grant R01 CA157477.
    ORI found that Respondent engaged in research misconduct by 
reporting falsified data in Figures 1, 4, 5, S2, and S3 in the 
following paper published online:
     Gao, Y., Zeng, Y., Tian, J., Kslam, M.S., Jiang, G., & 
Xiao, D., ``Gugglesterone inhibits prostate cancer growth via 
inactivation of Akt regulated by ATP citrate signaling.'' Oncotarget, 
June 26, 2014 [Epub ahead of print], PMID: 24980815; hereafter referred 
to as the ``Oncotarget paper.''
    Specifically, in the Oncotarget paper, Respondent:

 Falsely stated that 10 mice per group were used to obtain data 
for tumor volume (Figure 1A) and tumor weight (Figure 1B) when data for 
only four mice per group were available
 falsified the results for C-caspase 3 and phosphorylated Akt 
in the Western blots presented in Figure 1D to claim that treatment of 
tumor bearing mice with Z-Gug significantly enhanced C-capase 3 
activity and significantly inhibited Akt phorphorylation, while the 
original data showed no significant effect for either activity
 falsified Figure 4C by manipulating p-Akt bands to show that 
Z-Gug alone and in combination with PHTM significantly inhibited Akt 
phosphorylation in PC3 and LNCaP human prostate cancer cell lines; the

[[Page 4268]]

numbers above each band representing the fold change human prostate 
cancer cell lines; the numbers above each band representing the fold 
change in expression relative to the DMSO control also were falsified 
for p-ACLY (LNCaP cell line) and p-Akt (PC3 and LNCaP cell lines) 
compared to the values provided to the Respondent
 falsified Figure 4D by substituting bands for p-ACLY for those 
provided to him to allow Respondent to claim that Z-Gug significantly 
inhibited phosphorylation of ACLY in lysates of prostate tumors 
obtained from mice, when the original data showed no effect
 falsified Figures 5C and 5D to show that treatment of PC3 and 
LNCaP cells with Z-Gug alone and with Z-Gug plus si-RNA targets to ACLY 
stimulated Caspase 3/7 activity, when the original data provided to him 
showed no significant effect of either treatment in PC3 cells and no 
effect of Z-Gug alone in LNCaP cells
 falsified Figures 6G and 6H; these figures purported to show 
that N-acetyl-L-cysteine (NAC), an inhibitor of reactive oxygen species 
(ROS), reversed the inhibition of Akt phosphorylation caused by Z-Gug 
in PC3 cells (Figure 6G) and LNCaP cells (Figure 6G) when no Akt data 
for this protocol was available to the Respondent; Respondent admitted 
to falsifying Figure 6G
 falsified Figures S2B and S3B by altering data provided to 
him; these experiments are complementary to those shown in Figures 5C 
and 5D, except that the effect of Z-Gug and Z-gug plus si-RNA on 
Caspase 3/7 activity utilized on si-RNA was directed to Akt activity. 
The original data showed no significant effect of either treatment in 
PC3 cells and no effect of Z-Gug on LNCaP cells, while both treatments 
were claimed to be significant inducers of caspase activity in both 
cell lines in the published figures.

    Dr. Xiao has entered into a Voluntary Settlement Agreement 
(Agreement) and has voluntarily agreed for a period of three (3) years, 
beginning on December 23, 2014:
    (1) To have his research supervised; Respondent agreed to ensure 
that prior to the submission of an application for U.S. Public Health 
Service (PHS) support for a research project on which the Respondent's 
participation is proposed and prior to Respondent's participation in 
any capacity on PHS-supported research, the institution employing him 
must submit a plan for supervision of his duties to ORI for approval; 
the plan for supervision must be designed to ensure the scientific 
integrity of Respondent's research contribution; Respondent agreed that 
he will not participate in any PHS-supported research until such a 
supervision plan is submitted to and approved by ORI; Respondent agreed 
to maintain responsibility for compliance with the agreed upon plan for 
supervision;
    (2) that any institution employing him must submit, 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 in the 
application, report, manuscript, or abstract; and
    (3) to exclude himself voluntarily from serving in any advisory 
capacity to PHS including, but not limited to, service on any PHS 
advisory committee, board, and/or peer review committee, or as a 
consultant.

FOR FURTHER INFORMATION CONTACT: Acting Director, Office of Research 
Integrity, 1101 Wootton Parkway, Suite 750, Rockville, MD 20852, (240) 
453-8200.

Donald Wright,
Acting Director, Office of Research Integrity.
[FR Doc. 2015-01427 Filed 1-26-15; 8:45 am]
BILLING CODE 4150-31-P