Douglas D. Taylor

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Douglas D. Taylor is an entrepreneur and former academic researcher in the field of extracellular vesicles.

Taylor attained a bachelor's degree from the University of Richmond and a Ph.D. from Wake Forest University. He was a post-doctoral fellow at Boston University. [1] Taylor was a professor and Vice Chair for Research in the Department of Obstetrics, Gynecology, and Women's Healthheld at the University of Louisville in Kentucky. [1] [ when? ] He was also on the faculty of the University of California, Davis. [2] [ when? ] From 2013 to 2015, he was the Chief Scientific Officer of Aethlon Medical's wholly owned subsidiary, Exosome Sciences. [3] [4]

Taylor first described exosomes in the 1980s, originally believing them to be cell fragments. [5] He later wrote in a now retracted paper that exosomes could potentially be used as biomarkers for profiling in ovarian cancer biopsies, and could extend their utility to screening other asymptomatic areas. [6] What constitutes exosomes has not been defined; specifically, markers of exosomes do not exist. [7]

In 2015, the Journal of Immunology retracted a paper it published in 2006 and which Taylor had co-written [8] after an "institutional research misconduct investigation committee determined that multiple figures in the...paper were falsified". [9] [10] Taylor responded to the retraction on the blog Retraction Watch, disputing various aspects of the retraction, and stating that he sent "copies of the original data so that the [journal's] editor could independently verify that no falsification or fabrication occurred". [10]

Related Research Articles

In academic publishing, a retraction is a mechanism by which a published paper in an academic journal is flagged for being seriously flawed to the extent that their results and conclusions can no longer be relied upon. Retracted articles are not removed from the published literature but marked as retracted. In some cases it may be necessary to remove an article from publication, such as when the article is clearly defamatory, violates personal privacy, is the subject of a court order, or might pose a serious health risk to the general public.

Robert Allan Weinberg is an American biologist, Daniel K. Ludwig Professor for Cancer Research at Massachusetts Institute of Technology (MIT), director of the Ludwig Center of the MIT, and American Cancer Society Research Professor. His research is in the area of oncogenes and the genetic basis of human cancer.

Early prostate cancer antigen-2 (EPCA-2) is a protein of which blood levels are elevated in prostate cancer. It appears to provide more accuracy in identifying early prostate cancer than the standard prostate cancer marker, PSA.

<span class="mw-page-title-main">Interleukin 21</span> Mammalian protein found in humans

Interleukin 21 (IL-21) is a protein that in humans is encoded by the IL21 gene.

<span class="mw-page-title-main">CXCL9</span> Mammalian protein found in Homo sapiens

Chemokine ligand 9 (CXCL9) is a small cytokine belonging to the CXC chemokine family that is also known as monokine induced by gamma interferon (MIG). The CXCL9 is one of the chemokine which plays role to induce chemotaxis, promote differentiation and multiplication of leukocytes, and cause tissue extravasation.

<span class="mw-page-title-main">Toll-like receptor 5</span> Protein found in humans

Toll-like receptor 5, also known as TLR5, is a protein which in humans is encoded by the TLR5 gene. It is a member of the toll-like receptor (TLR) family. TLR5 is known to recognize bacterial flagellin from invading mobile bacteria. It has been shown to be involved in the onset of many diseases, including Inflammatory bowel disease due to the high expression of TLR in intestinal lamina propria dendritic cells. Recent studies have also shown that malfunctioning of TLR5 is likely related to rheumatoid arthritis, osteoclastogenesis, and bone loss. Abnormal TLR5 functioning is related to the onset of gastric, cervical, endometrial and ovarian cancers.

<span class="mw-page-title-main">CD9</span> Human protein-encoding gene

CD9 is a gene encoding a protein that is a member of the transmembrane 4 superfamily also known as the tetraspanin family. It is a cell surface glycoprotein that consists of four transmembrane regions and has two extracellular loops that contain disulfide bonds which are conserved throughout the tetraspanin family. Also containing distinct palmitoylation sites that allows CD9 to interact with lipids and other proteins.

<span class="mw-page-title-main">C-C chemokine receptor type 7</span> Protein-coding gene in the species Homo sapiens

C-C chemokine receptor type 7 is a protein that in humans is encoded by the CCR7 gene. Two ligands have been identified for this receptor: the chemokines ligand 19 (CCL19/ELC) and ligand 21 (CCL21). The ligands have similar affinity for the receptor, though CCL19 has been shown to induce internalisation of CCR7 and desensitisation of the cell to CCL19/CCL21 signals. CCR7 is a transmembrane protein with 7 transmembrane domains, which is coupled with heterotrimeric G proteins, which transduce the signal downstream through various signalling cascades. The main function of the receptor is to guide immune cells to immune organs by detecting specific chemokines, which these tissues secrete.

<span class="mw-page-title-main">C5AR2</span> Protein-coding gene in the species Homo sapiens

Complement component 5a receptor 2 is a protein of the complement system that in humans is encoded by the C5AR2 gene. It is highly expressed in the blood and spleen, predominantly by myeloid cells.

<i>CD82</i> (gene) Mammalian protein found in humans

CD82, or KAI1, is a human protein encoded by the CD82 gene.

<span class="mw-page-title-main">PRDM1</span> Protein-coding gene in the species Homo sapiens

PR domain zinc finger protein 1, or B lymphocyte-induced maturation protein-1 (BLIMP-1), is a protein in humans encoded by the gene PRDM1 located on chromosome 6q21. BLIMP-1 is considered a 'master regulator' of hematopoietic stem cells, and plays a critical role in the development of plasma B cells, T cells, dendritic cells (DCs), macrophages, and osteoclasts. Pattern Recognition Receptors (PRRs) can activate BLIMP-1, both as a direct target and through downstream activation. BLIMP-1 is a transcription factor that triggers expression of many downstream signaling cascades. As a fine-tuned and contextual rheostat of the immune system, BLIMP-1 up- or down-regulates immune responses depending on the precise scenarios. BLIMP-1 is highly expressed in exhausted T-cells – clones of dysfunctional T-cells with diminished functions due to chronic immune response against cancer, viral infections, or organ transplant.

<span class="mw-page-title-main">IL13RA2</span> Protein-coding gene in the species Homo sapiens

Interleukin-13 receptor subunit alpha-2 (IL-13Rα2), also known as CD213A2, is a membrane bound protein that in humans is encoded by the IL13RA2 gene.

<span class="mw-page-title-main">VTCN1</span> Protein-coding gene in the species Homo sapiens

V-set domain-containing T-cell activation inhibitor 1 is a protein that in humans is encoded by the VTCN1 gene.

<span class="mw-page-title-main">Lymphocyte-activation gene 3</span> Protein-coding gene in the species Homo sapiens

Lymphocyte-activation gene 3, also known as LAG-3, is a protein which in humans is encoded by the LAG3 gene. LAG3, which was discovered in 1990 and was designated CD223 after the Seventh Human Leucocyte Differentiation Antigen Workshop in 2000, is a cell surface molecule with diverse biological effects on T cell function but overall has an immune inhibitory effect. It is an immune checkpoint receptor and as such is the target of various drug development programs by pharmaceutical companies seeking to develop new treatments for cancer and autoimmune disorders. In soluble form it is also being developed as a cancer drug in its own right.

<span class="mw-page-title-main">Trogocytosis</span>

Trogocytosis is when a cell nibbles another cell. It is a process whereby lymphocytes conjugated to antigen-presenting cells extract surface molecules from these cells and express them on their own surface. The molecular reorganization occurring at the interface between the lymphocyte and the antigen-presenting cell during conjugation is also called "immunological synapse".

<span class="mw-page-title-main">Clear-cell adenocarcinoma</span> Type of adenocarcinoma that shows clear cells

Clear-cell adenocarcinoma is a rare and aggressive form of cancer that typically arises in the female reproductive organs, particularly the ovaries and the endometrium as well as the kidneys and is characterized by the presence of clear, glycogen-rich cells. Specific criteria must be met for a tumor to be classified as clear cell adenocarcinoma. According to the WHO, these criteria include polygonal or hobnail or cells with clear or eosinophilic/oxyphilic cytoplasm and nuclear atypia, with different architectural patterns of growth, such as papillary, tubulocystic, or solid.

mir-31

miR-31 has been characterised as a tumour suppressor miRNA, with its levels varying in breast cancer cells according to the metastatic state of the tumour. From its typical abundance in healthy tissue is a moderate decrease in non-metastatic breast cancer cell lines, and levels are almost completely absent in mouse and human metastatic breast cancer cell lines. Mir-31-5p has also been observed upregulated in Zinc Deficient rats compared to normal in ESCC and in other types of cancers when using this animal model. There has also been observed a strong encapsulation of tumour cells expressing miR-31, as well as a reduced cell survival rate. miR-31's antimetastatic effects therefore make it a potential therapeutic target for breast cancer. However, these two papers were formally retracted by the authors in 2015.

Scientific Reports is a peer-reviewed open-access scientific mega journal published by Nature Portfolio, covering all areas of the natural sciences. The journal was established in 2011. The journal states that their aim is to assess solely the scientific validity of a submitted paper, rather than its perceived importance, significance, or impact.

Anil Potti is a physician and former Duke University associate professor and cancer researcher, focusing on oncogenomics. He, along with Joseph Nevins, are at the center of a research fabrication scandal at Duke University. On 9 November 2015, the Office of Research Integrity (ORI) found that Potti had engaged in research misconduct. According to Potti's voluntary settlement agreement with ORI, Potti can continue to perform research with the requirement of supervision until year 2020, while he "neither admits nor denies ORI's findings of research misconduct." As of 2024 Potti, who is employed at the Cancer Center of North Dakota, has had 11 of his research publications retracted, one publication has received an expression of concern, and two others have been corrected.

References

  1. 1 2 "Aethlon Medical Appoints Douglas Taylor to Exosome Sciences Advisory Board". PR Newswire (Press release). Retrieved August 31, 2016.
  2. UC Davis Health System, Department of Public Affairs and Marketing. "UC Davis Health System Feature Story: Cancer in the crosshairs". ucdavis.edu. Retrieved 15 July 2015.
  3. "Aethlon Medical Announces Dr. Douglas Taylor as Chief Scientific Officer of Exosome Sciences, Inc". PR Newswire (Press release). Retrieved August 31, 2016.
  4. "Executive Team". Exosome Sciences. Archived from the original on August 17, 2015. Retrieved March 3, 2016.
  5. Todd S. Ing, et al, Dialysis: History, Development and Promise (Hackensack, New Jersey: World Scientific Publishing, 2012), p. 843
  6. Taylor, Douglas (July 2008). "MicroRNA signatures of tumor-derived exosomes as diagnostic biomarkers of ovarian cancer". Gynecologic Oncology. 110 (1): 13–21. doi:10.1016/j.ygyno.2008.04.033. PMID   18589210. (Retracted, see doi:10.1016/j.ygyno.2023.06.002, PMID   37479418,  Retraction Watch)
  7. Edgar, James (2016). "Q&A: What are exosomes, exactly?". BMC Biology. 14 (1): 46. doi: 10.1186/s12915-016-0268-z . PMC   4906597 . PMID   27296830.
  8. Taylor, DD; Akyol, S; Gercel-Taylor, C (2006). "Pregnancy-associated exosomes and their modulation of T cell signaling". J Immunol. 176 (3): 1534–42. doi: 10.4049/jimmunol.176.3.1534 . PMID   16424182. (Retracted, see doi:10.4049/jimmunol.1500893, PMID   26048967,  Retraction Watch)
  9. "Retraction: Pregnancy-Associated Exosomes and Their Modulation of T Cell Signaling," Journal of Immunology, June 15, 2015, vol. 194 no. 12 6190.(subscription required)
  10. 1 2 Bernès, Sylvain (June 10, 2015). "Exosome pioneer's paper retracted after investigation finds "multiple" faked figures". Retraction Watch . Retrieved January 7, 2016.