Patrick S. Moore

Last updated
Patrick Moore
Patrick S. Moore 2017-01.JPG
Moore in 2017
Born (1956-10-21) October 21, 1956 (age 67)
Seattle, Washington, U.S.
NationalityAmerican
Education Westminster College
Stanford University
University of Utah
University of California, Berkeley
Known forDiscovery of the human cancer viruses KSHV and MCV
Spouse Yuan Chang
Awards Meyenburg Prize (1997)
Robert Koch Prize (1998)
Charles S. Mott Prize (2003)
Passano Award (2017)
Paul Ehrlich and Ludwig Darmstaedter Prize (2017)
Clarivate Citation Laureates (2017)
Scientific career
Fields Cancer, Microbiology, Epidemiology
Institutions UPMC Hillman Cancer Center University of Pittsburgh

Patrick S. Moore (born October 21, 1956) is an American virologist and epidemiologist who co-discovered together with his wife, Yuan Chang, two different human viruses causing the AIDS-related cancer Kaposi's sarcoma and the skin cancer Merkel cell carcinoma. Moore and Chang have discovered two of the seven known human viruses causing cancer. The couple met while in medical school together and were married in 1989 while they pursued fellowships at different universities.

Contents

Education and career

Moore received a Bachelor of Science in chemistry and biology from Westminster College in Salt Lake City, an M.S. degree from Stanford University, and M.D. and MPhil degrees from the University of Utah, and an M.P.H. degree from the University of California, Berkeley. As an epidemiologist working at the US Centers for Disease Control and Prevention (CDC), he developed widely used international guidelines to control meningococcal meningitis epidemics [1] [2] and led a team of CDC epidemiologists during the 1992 Somali Civil War. Civilian death rates documented during this civil war-famine were among the highest ever reported. [3] [4] The extreme mortality statistics helped to solidify international support behind the US-led military intervention Operation Restore Hope. [5] He received the 1989 CDC Langmuir Prize for his work on epidemic meningitis control.

After leaving the CDC, Moore served briefly as a New York City epidemiologist but quit to search for new human viruses with his wife, Yuan Chang who was then a newly appointed assistant professor at Columbia University. [6] Unemployed, he worked in his wife's laboratory, allowing him to rapidly pick up training in molecular biology. Despite having no research funding, Moore and Chang used a new molecular biology technique, representational difference analysis, to search for a virus causing Kaposi's sarcoma, the most common malignancy among AIDS patients. [7] In 1994, they discovered a new human herpesvirus, KSHV, in a KS tumor and along with several collaborators showed that it was the etiologic agent of Kaposi's sarcoma, primary effusion lymphoma, and some forms of multicentric Castleman's disease. [8] [9] [10] Moore was hired onto the faculty at Columbia and the Chang-Moore Laboratory secured research funding to investigate this new virus. They subsequently sequenced KSHV, [11] identified oncogenes encoded by the virus, [12] demonstrated transmission during transplantation and developed diagnostic tests to detect infection. [13] [14] In 2002, he moved his laboratory to the University of Pittsburgh where he served as founding director of the Cancer Virology Program at the UPMC Hillman Cancer Center r until 2018. Chang and Moore jointly developed a new technique to find human tumor viruses called digital transcriptome subtraction (DTS). [15] Using this approach, they identified the most recently discovered cancer virus, a new human polyomavirus infecting Merkel carcinoma cells in 2008. [16] This virus causes of 50-80% of Merkel cell carcinomas [17] and hence is named Merkel cell polyomavirus. His laboratory currently seeks to understand the role of tumor virus immunoevasion of the innate immune system as a cause for viral tumorigenesis. [18] [19] [20] [21] They have also discovered another polyomavirus (Human polyomavirus 7) as a cause of skin disease in transplant patients, [22] the generation of viral circular RNAs in KSHV, EBV and MCV, [23] the role of CDK1 in controlling protein translation during mitosis [24] and they defined the clonal mutation pattern of Merkel cell polyomavirus in cancers [25] as well as its oncogenes. [26]

Awards

Related Research Articles

<i>Polyomaviridae</i> Family of viruses

Polyomaviridae is a family of viruses whose natural hosts are primarily mammals and birds. As of 2024, there are eight recognized genera. 14 species are known to infect humans, while others, such as Simian Virus 40, have been identified in humans to a lesser extent. Most of these viruses are very common and typically asymptomatic in most human populations studied. BK virus is associated with nephropathy in renal transplant and non-renal solid organ transplant patients, JC virus with progressive multifocal leukoencephalopathy, and Merkel cell virus with Merkel cell cancer.

<span class="mw-page-title-main">Kaposi's sarcoma-associated herpesvirus</span> Species of virus

Kaposi's sarcoma-associated herpesvirus (KSHV) is the ninth known human herpesvirus; its formal name according to the International Committee on Taxonomy of Viruses (ICTV) is Human gammaherpesvirus 8, or HHV-8 in short. Like other herpesviruses, its informal names are used interchangeably with its formal ICTV name. This virus causes Kaposi's sarcoma, a cancer commonly occurring in AIDS patients, as well as primary effusion lymphoma, HHV-8-associated multicentric Castleman's disease and KSHV inflammatory cytokine syndrome. It is one of seven currently known human cancer viruses, or oncoviruses. Even after many years since the discovery of KSHV/HHV8, there is no known cure for KSHV associated tumorigenesis.

<span class="mw-page-title-main">Oncovirus</span> Viruses that can cause cancer

An oncovirus or oncogenic virus is a virus that can cause cancer. This term originated from studies of acutely transforming retroviruses in the 1950–60s, when the term "oncornaviruses" was used to denote their RNA virus origin. With the letters "RNA" removed, it now refers to any virus with a DNA or RNA genome causing cancer and is synonymous with "tumor virus" or "cancer virus". The vast majority of human and animal viruses do not cause cancer, probably because of longstanding co-evolution between the virus and its host. Oncoviruses have been important not only in epidemiology, but also in investigations of cell cycle control mechanisms such as the retinoblastoma protein.

<span class="mw-page-title-main">Merkel-cell carcinoma</span> Rare and highly aggressive skin cancer

Merkel-cell carcinoma (MCC) is a rare and aggressive skin cancer occurring in about three people per million members of the population. It is also known as cutaneous APUDoma, primary neuroendocrine carcinoma of the skin, primary small cell carcinoma of the skin, and trabecular carcinoma of the skin. Factors involved in the development of MCC include the Merkel cell polyomavirus, a weakened immune system, and exposure to ultraviolet radiation. Merkel-cell carcinoma usually arises on the head, neck, and extremities, as well as in the perianal region and on the eyelid. It is more common in people over sixty years old, Caucasian people, and males. MCC is less common in children.

<span class="mw-page-title-main">Primary effusion lymphoma</span> Medical condition

Primary effusion lymphoma (PEL) is classified as a diffuse large B cell lymphoma. It is a rare malignancy of plasmablastic cells that occurs in individuals that are infected with the Kaposi's sarcoma-associated herpesvirus. Plasmablasts are immature plasma cells, i.e. lymphocytes of the B-cell type that have differentiated into plasmablasts but because of their malignant nature do not differentiate into mature plasma cells but rather proliferate excessively and thereby cause life-threatening disease. In PEL, the proliferating plasmablastoid cells commonly accumulate within body cavities to produce effusions, primarily in the pleural, pericardial, or peritoneal cavities, without forming a contiguous tumor mass. In rare cases of these cavitary forms of PEL, the effusions develop in joints, the epidural space surrounding the brain and spinal cord, and underneath the capsule which forms around breast implants. Less frequently, individuals present with extracavitary primary effusion lymphomas, i.e., solid tumor masses not accompanied by effusions. The extracavitary tumors may develop in lymph nodes, bone, bone marrow, the gastrointestinal tract, skin, spleen, liver, lungs, central nervous system, testes, paranasal sinuses, muscle, and, rarely, inside the vasculature and sinuses of lymph nodes. As their disease progresses, however, individuals with the classical effusion-form of PEL may develop extracavitary tumors and individuals with extracavitary PEL may develop cavitary effusions.

<span class="mw-page-title-main">Yuan Chang</span> American virologist and pathologist

Yuan Chang is a Taiwanese-born American virologist and pathologist who co-discovered together with her husband, Patrick S. Moore, the Kaposi's sarcoma-associated herpesvirus (KSHV) and Merkel cell polyomavirus, two of the seven known human oncoviruses.

<span class="mw-page-title-main">Interferon regulatory factors</span> Protein family

Interferon regulatory factors (IRF) are proteins which regulate transcription of interferons. Interferon regulatory factors contain a conserved N-terminal region of about 120 amino acids, which folds into a structure that binds specifically to the IRF-element (IRF-E) motifs, which is located upstream of the interferon genes. Some viruses have evolved defense mechanisms that regulate and interfere with IRF functions to escape the host immune system. For instance, the remaining parts of the interferon regulatory factor sequence vary depending on the precise function of the protein. The Kaposi sarcoma herpesvirus, KSHV, is a cancer virus that encodes four different IRF-like genes; including vIRF1, which is a transforming oncoprotein that inhibits type 1 interferon activity. In addition, the expression of IRF genes is under epigenetic regulation by promoter DNA methylation.

A transmissible cancer is a cancer cell or cluster of cancer cells that can be transferred between individuals without the involvement of an infectious agent, such as an Oncovirus. The evolution of transmissible cancer has occurred naturally in other animal species, but human cancer transmission is rare. This transfer is typically between members of the same species or closely related species.

<span class="mw-page-title-main">CD200</span> Protein-coding gene in the species Homo sapiens

OX-2 membrane glycoprotein, also named CD200 is a human protein encoded by the CD200 gene. CD200 gene is in human located on chromosome 3 in proximity to genes encoding other B7 proteins CD80/CD86. In mice CD200 gene is on chromosome 16.

Murid gammaherpesvirus 68 (MuHV-68) is an isolate of the virus species Murid gammaherpesvirus 4, a member of the genus Rhadinovirus. It is a member of the subfamily Gammaherpesvirinae in the family of Herpesviridae. MuHV-68 serves as a model for study of human gammaherpesviruses which cause significant human disease including B-cell lymphoma and Kaposi's sarcoma. The WUMS strain of MuHV-68 was fully sequenced and annotated in 1997, and the necessity of most of its genes in viral replication was characterized by random transposon mutagenesis.

Merkel cell polyomavirus was first described in January 2008 in Pittsburgh, Pennsylvania. It was the first example of a human viral pathogen discovered using unbiased metagenomic next-generation sequencing with a technique called digital transcriptome subtraction. MCV is one of seven currently known human oncoviruses. It is suspected to cause the majority of cases of Merkel cell carcinoma, a rare but aggressive form of skin cancer. Approximately 80% of Merkel cell carcinoma (MCC) tumors have been found to be infected with MCV. MCV appears to be a common—if not universal—infection of older children and adults. It is found in respiratory secretions, suggesting that it might be transmitted via a respiratory route. However, it has also been found elsewhere, such as in shedded healthy skin and gastrointestinal tract tissues, thus its precise mode of transmission remains unknown. In addition, recent studies suggest that this virus may latently infect the human sera and peripheral blood mononuclear cells.

The latency-associated nuclear antigen (LANA-1) or latent nuclear antigen is a Kaposi's sarcoma-associated herpesvirus (KSHV) latent protein initially found by Moore and colleagues as a speckled nuclear antigen present in primary effusion lymphoma cells that reacts with antibodies from patients with KS. It is the most immunodominant KSHV protein identified by Western-blotting as 222–234 kDa double bands migrate slower than the predicted molecular weight. LANA has been suspected of playing a crucial role in modulating viral and cellular gene expression. It is commonly used as an antigen in blood tests to detect antibodies in persons that have been exposed to KSHV.

<span class="mw-page-title-main">Kaposi's sarcoma</span> Cancer of the skin, integumentary lymph nodes, or other organs

Kaposi's sarcoma (KS) is a type of cancer that can form masses in the skin, in lymph nodes, in the mouth, or in other organs. The skin lesions are usually painless, purple and may be flat or raised. Lesions can occur singly, multiply in a limited area, or may be widespread. Depending on the sub-type of disease and level of immune suppression, KS may worsen either gradually or quickly. Except for Classical KS where there is generally no immune suppression, KS is caused by a combination of immune suppression and infection by Human herpesvirus 8.

VG-1 is a B cell line which was derived from primary effusion lymphoma (PEL). It was first established in 2000 by David T. Scadden’s group at Massachusetts General Hospital. It is infected with Kaposi's sarcoma-associated herpesvirus (KSHV), but negative with Epstein–Barr virus (EBV).

<span class="mw-page-title-main">Infectious causes of cancer</span>

Estimates place the worldwide risk of cancers from infectious causes at 16.1%. Viral infections are risk factors for cervical cancer, 80% of liver cancers, and 15–20% of the other cancers. This proportion varies in different regions of the world from a high of 32.7% in Sub-Saharan Africa to 3.3% in Australia and New Zealand.

<span class="mw-page-title-main">Digital transcriptome subtraction</span>

Digital transcriptome subtraction (DTS) is a bioinformatics method to detect the presence of novel pathogen transcripts through computational removal of the host sequences. DTS is the direct in silico analogue of the wet-lab approach representational difference analysis (RDA), and is made possible by unbiased high-throughput sequencing and the availability of a high-quality, annotated reference genome of the host. The method specifically examines the etiological agent of infectious diseases and is best known for discovering Merkel cell polyomavirus, the suspect causative agent in Merkel-cell carcinoma.

Large B-cell lymphoma arising in HHV8-associated multicentric Castleman's disease is a type of large B-cell lymphoma, recognized in the WHO 2008 classification. It is sometimes called the plasmablastic form of multicentric Castleman disease. It has sometimes been confused with plasmablastic lymphoma in the literature, although that is a dissimilar specific entity. It has variable CD20 expression and unmutated immunoglobulin variable region genes.

Eva Henriette Gottwein is a virologist and Associate Professor of Microbiology-Immunology at Northwestern University Feinberg School of Medicine in Chicago, Illinois. The main focus of her research is the role of viral miRNAs involved in herpesviral oncogenesis. Gottwein is member of Robert H. Lurie Comprehensive Cancer Center of Northwestern University. Her contributions as a member include the focus on how encoded miRNAs target and function in the human oncogenic herpesvirus Kaposi's sarcoma-associated herpesvirus known as KSHV.

<span class="mw-page-title-main">Large tumor antigen</span>

The large tumor antigen is a protein encoded in the genomes of polyomaviruses, which are small double-stranded DNA viruses. LTag is expressed early in the infectious cycle and is essential for viral proliferation. Containing four well-conserved protein domains as well as several intrinsically disordered regions, LTag is a fairly large multifunctional protein; in most polyomaviruses, it ranges from around 600-800 amino acids in length. LTag has two primary functions, both related to replication of the viral genome: it unwinds the virus's DNA to prepare it for replication, and it interacts with proteins in the host cell to dysregulate the cell cycle so that the host's DNA replication machinery can be used to replicate the virus's genome. Some polyomavirus LTag proteins - most notably the well-studied SV40 large tumor antigen from the SV40 virus - are oncoproteins that can induce neoplastic transformation in the host cell.

<span class="mw-page-title-main">Small tumor antigen</span>

The small tumor antigen is a protein encoded in the genomes of polyomaviruses, which are small double-stranded DNA viruses. STag is expressed early in the infectious cycle and is usually not essential for viral proliferation, though in most polyomaviruses it does improve replication efficiency. The STag protein is expressed from a gene that overlaps the large tumor antigen (LTag) such that the two proteins share an N-terminal DnaJ-like domain but have distinct C-terminal regions. STag is known to interact with host cell proteins, most notably protein phosphatase 2A (PP2A), and may activate the expression of cellular proteins associated with the cell cycle transition to S phase. In some polyomaviruses - such as the well-studied SV40, which natively infects monkeys - STag is unable to induce neoplastic transformation in the host cell on its own, but its presence may increase the transforming efficiency of LTag. In other polyomaviruses, such as Merkel cell polyomavirus, which causes Merkel cell carcinoma in humans, STag appears to be important for replication and to be an oncoprotein in its own right.

References

  1. ↑ Moore, Patrick S. (1992). "Meningococcal meningitis in sub-Saharan Africa: a model for the epidemic process". Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America. 14 (2): 515–525. doi:10.1093/clinids/14.2.515. ISSN   1058-4838. PMID   1554841.
  2. ↑ Moore, P. S.; Broome, C. V. (1994). "Cerebrospinal meningitis epidemics". Scientific American. 271 (5): 38–45. Bibcode:1994SciAm.271e..38M. doi:10.1038/scientificamerican1194-38. ISSN   0036-8733. PMID   7997865.
  3. ↑ Centers for Disease Control (CDC) (December 11, 1992). "Population-based mortality assessment--Baidoa and Afgoi, Somalia, 1992". MMWR. Morbidity and Mortality Weekly Report. 41 (49): 913–917. ISSN   0149-2195. PMID   1448038.
  4. ↑ Moore, P. S.; Marfin, A. A.; Quenemoen, L. E.; Gessner, B. D.; Ayub, Y. S.; Miller, D. S.; Sullivan, K. M.; Toole, M. J. (April 10, 1993). "Mortality rates in displaced and resident populations of central Somalia during 1992 famine". Lancet. 341 (8850): 935–938. doi:10.1016/0140-6736(93)91223-9. ISSN   0140-6736. PMID   8096276. S2CID   38013442.
  5. ↑ "1992: American marines land in Somalia". On This Day . BBC. December 9, 1992. Retrieved July 21, 2009.
  6. ↑ Schmidt C (April 2008). "Yuan Chang and Patrick Moore: teaming up to hunt down cancer-causing viruses". Journal of the National Cancer Institute. 100 (8): 524–5, 529. doi: 10.1093/jnci/djn122 . PMID   18398088.
  7. ↑ Chang, Y.; Cesarman, E.; Pessin, M. S.; Lee, F.; Culpepper, J.; Knowles, D. M.; Moore, P. S. (December 16, 1994). "Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma". Science. 266 (5192): 1865–1869. Bibcode:1994Sci...266.1865C. doi:10.1126/science.7997879. ISSN   0036-8075. PMID   7997879. S2CID   29977325.
  8. ↑ Cesarman, E.; Chang, Y.; Moore, P. S.; Said, J. W.; Knowles, D. M. (May 4, 1995). "Kaposi's sarcoma-associated herpesvirus-like DNA sequences in AIDS-related body-cavity-based lymphomas". The New England Journal of Medicine. 332 (18): 1186–1191. doi:10.1056/NEJM199505043321802. ISSN   0028-4793. PMID   7700311.
  9. ↑ Parravicini, C.; Corbellino, M.; Paulli, M.; Magrini, U.; Lazzarino, M.; Moore, P. S.; Chang, Y. (1997). "Expression of a virus-derived cytokine, KSHV vIL-6, in HIV-seronegative Castleman's disease". The American Journal of Pathology. 151 (6): 1517–1522. ISSN   0002-9440. PMC   1858372 . PMID   9403701.
  10. ↑ Adler, T. (December 17, 1994). "Scientists Link New Herpesvirus to Cancer". Science News. 146 (25): 405. doi:10.2307/3978785. JSTOR   3978785.
  11. ↑ Russo, J. J.; Bohenzky, R. A.; Chien, M. C.; Chen, J.; Yan, M.; Maddalena, D.; Parry, J. P.; Peruzzi, D.; Edelman, I. S.; Chang, Y.; Moore, P. S. (December 10, 1996). "Nucleotide sequence of the Kaposi sarcoma-associated herpesvirus (HHV8)". Proceedings of the National Academy of Sciences of the United States of America. 93 (25): 14862–14867. Bibcode:1996PNAS...9314862R. doi: 10.1073/pnas.93.25.14862 . ISSN   0027-8424. PMC   26227 . PMID   8962146.
  12. ↑ Moore, P. S.; Boshoff, C.; Weiss, R. A.; Chang, Y. (December 6, 1996). "Molecular mimicry of human cytokine and cytokine response pathway genes by KSHV". Science. 274 (5293): 1739–1744. Bibcode:1996Sci...274.1739M. doi:10.1126/science.274.5293.1739. ISSN   0036-8075. PMID   8939871. S2CID   29713179.
  13. ↑ Moore, P. S.; Gao, S. J.; Dominguez, G.; Cesarman, E.; Lungu, O.; Knowles, D. M.; Garber, R.; Pellett, P. E.; McGeoch, D. J.; Chang, Y. (January 1996). "Primary characterization of a herpesvirus agent associated with Kaposi's sarcoma". Journal of Virology. 70 (1): 549–558. doi:10.1128/JVI.70.1.549-558.1996. ISSN   0022-538X. PMC   189843 . PMID   8523568.
  14. ↑ Gao, S. J.; Kingsley, L.; Hoover, D. R.; Spira, T. J.; Rinaldo, C. R.; Saah, A.; Phair, J.; Detels, R.; Parry, P.; Chang, Y.; Moore, P. S. (July 25, 1996). "Seroconversion to antibodies against Kaposi's sarcoma-associated herpesvirus-related latent nuclear antigens before the development of Kaposi's sarcoma". The New England Journal of Medicine. 335 (4): 233–241. doi:10.1056/NEJM199607253350403. ISSN   0028-4793. PMID   8657239.
  15. ↑ Feng H, Taylor JL, Benos PV, et al. (October 2007). "Human transcriptome subtraction by using short sequence tags to search for tumor viruses in conjunctival carcinoma". Journal of Virology. 81 (20): 11332–40. doi:10.1128/JVI.00875-07. PMC   2045575 . PMID   17686852.
  16. ↑ Feng H, Shuda M, Chang Y, Moore PS (February 2008). "Clonal integration of a polyomavirus in human Merkel cell carcinoma". Science. 319 (5866): 1096–100. Bibcode:2008Sci...319.1096F. doi:10.1126/science.1152586. PMC   2740911 . PMID   18202256.
  17. ↑ Becker, Jürgen C.; Stang, Andreas; DeCaprio, James A.; Cerroni, Lorenzo; Lebbé, Celeste; Veness, Michael; Nghiem, Paul (October 26, 2017). "Merkel cell carcinoma". Nature Reviews. Disease Primers. 3: 17077. doi:10.1038/nrdp.2017.77. ISSN   2056-676X. PMC   6054450 . PMID   29072302.
  18. ↑ Moore, P. S.; Chang, Y. (1998). "Antiviral activity of tumor-suppressor pathways: clues from molecular piracy by KSHV". Trends in Genetics. 14 (4): 144–150. doi:10.1016/s0168-9525(98)01408-5. ISSN   0168-9525. PMID   9594662.
  19. ↑ Chatterjee, Malini; Osborne, Julie; Bestetti, Giovanna; Chang, Yuan; Moore, Patrick S. (November 15, 2002). "Viral IL-6-induced cell proliferation and immune evasion of interferon activity". Science. 298 (5597): 1432–1435. Bibcode:2002Sci...298.1432C. doi:10.1126/science.1074883. ISSN   1095-9203. PMID   12434062. S2CID   23133493.
  20. ↑ Moore, Patrick S.; Chang, Yuan (2003). "Kaposi's sarcoma-associated herpesvirus immunoevasion and tumorigenesis: two sides of the same coin?". Annual Review of Microbiology. 57: 609–639. doi:10.1146/annurev.micro.57.030502.090824. ISSN   0066-4227. PMC   3732455 . PMID   14527293.
  21. ↑ Moore, Patrick S.; Chang, Yuan (2010). "Why do viruses cause cancer? Highlights of the first century of human tumour virology". Nature Reviews. Cancer. 10 (12): 878–889. doi:10.1038/nrc2961. ISSN   1474-1768. PMC   3718018 . PMID   21102637.
  22. ↑ Ho, J.; Jedrych, J. J.; Feng, H.; Natalie, A. A.; Grandinetti, L.; Mirvish, E.; Crespo, M. M.; Yadav, D.; Fasanella, K. E.; Proksell, S.; Kuan, S.-F.; Pastrana, D. V.; Buck, C. B.; Shuda, Y.; Moore, P. S. (September 17, 2014). "Human Polyomavirus 7-Associated Pruritic Rash and Viremia in Transplant Recipients". Journal of Infectious Diseases. 211 (10): 1560–1565. doi:10.1093/infdis/jiu524. ISSN   0022-1899. PMC   4425822 . PMID   25231015.
  23. ↑ Toptan, Tuna; Abere, Bizunesh; Nalesnik, Michael A.; Swerdlow, Steven H.; Ranganathan, Sarangarajan; Lee, Nara; Shair, Kathy H.; Moore, Patrick S.; Chang, Yuan (August 27, 2018). "Circular DNA tumor viruses make circular RNAs". Proceedings of the National Academy of Sciences. 115 (37): E8737–E8745. Bibcode:2018PNAS..115E8737T. doi: 10.1073/pnas.1811728115 . ISSN   0027-8424. PMC   6140489 . PMID   30150410.
  24. ↑ Shuda, Masahiro; Velásquez, Celestino; Cheng, Erdong; Cordek, Daniel G.; Kwun, Hyun Jin; Chang, Yuan; Moore, Patrick S. (April 16, 2015). "CDK1 substitutes for mTOR kinase to activate mitotic cap-dependent protein translation". Proceedings of the National Academy of Sciences. 112 (19): 5875–5882. Bibcode:2015PNAS..112.5875S. doi: 10.1073/pnas.1505787112 . ISSN   0027-8424. PMC   4434708 . PMID   25883264.
  25. ↑ Shuda, Masahiro; Feng, Huichen; Kwun, Hyun Jin; Rosen, Steven T.; Gjoerup, Ole; Moore, Patrick S.; Chang, Yuan (October 21, 2008). "T antigen mutations are a human tumor-specific signature for Merkel cell polyomavirus". Proceedings of the National Academy of Sciences. 105 (42): 16272–16277. Bibcode:2008PNAS..10516272S. doi: 10.1073/pnas.0806526105 . ISSN   0027-8424. PMC   2551627 . PMID   18812503.
  26. ↑ "Merkel Cell Polyomavirus", Definitions, Qeios, February 7, 2020, doi: 10.32388/iwhh3w
  27. ↑ Spice, Byron (June 10, 2003). "Pitt couple wins top prize for cancer research". Pittsburgh Post-Gazette . Retrieved July 21, 2009.

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