Draft:Carlos Rogerio Figueiredo
Submission declined on 9 December 2024 by Ldm1954 (talk).
Where to get help
How to improve a draft
You can also browse Wikipedia:Featured articles and Wikipedia:Good articles to find examples of Wikipedia's best writing on topics similar to your proposed article. Improving your odds of a speedy review To improve your odds of a faster review, tag your draft with relevant WikiProject tags using the button below. This will let reviewers know a new draft has been submitted in their area of interest. For instance, if you wrote about a female astronomer, you would want to add the Biography, Astronomy, and Women scientists tags. Editor resources
|
- Comment: He has made a good start to his career. However, it is very unusual for an assistant professor to be considered to be notable in this Wikipedia. He needs far more, both senior awards and many more publications. I suggest waiting several years. Ldm1954 (talk) 13:58, 9 December 2024 (UTC)
Carlos Rogerio Figueiredo is a Brazilian-Portuguese immunologist and cancer researcher known for his contributions to the field of cancer immunology. His work focuses on understanding the molecular drivers of “cold” tumors to inform the rational development of new combinatorial treatments for cancer immunotherapies. In 2024, he received the Young Investigator Award.[1] from the Scandinavian Society for Immunology for his achievements in immunological research and promotion of the field of immunology.
Early Life and education
[edit]Dr. Figueiredo is both Brazilian and Portuguese by nationality. He earned his bachelor’s degree in Biology from the São Paulo State University (Unesp), followed by a Ph.D. in Immunology and Microbiology from the Paulista School of Medicine (UNIFESP), and a Postdoc training in Clinical and Translational Cancer Medicine at the University of Liverpool and the University of Turku.
Career
[edit]Dr. Figueiredo has experience in cancer research, specializing in the mechanisms underlying tumor escape from immune responses and resistance to immunotherapies. Currently, he serves as an Adjunct Professor and Academy Research Fellow at the University of Turku, funded by the Research Council of Finland. He leads the Medical Immuno-Oncology Research Group (MIORG), a multidisciplinary team focused on understanding the immune landscape of tumors and translating these findings into therapeutic strategies. His work involves close collaboration with clinicians and biobanks to accelerate reverse translational research and identify novel therapeutic targets.
During his career, Dr. Figueiredo has implemented recent technologies such as spatial transcriptomics, high-dimensional single-cell cytometry, mass-cytometry, machine learning, and single-cell sequencing to study cancer immunobiology. His reverse translational approach bridges the gap between preclinical research and clinical applications, contributing to the development of new therapies.
Research contributions
[edit]Dr. Figueiredo has made contributions to understanding immune suppression mechanisms in both cutaneous melanoma and uveal melanoma, with important implications for immunotherapy responses. He identified specific biomarkers and pathways involved in immune suppression, including the role of the BAP1 gene. Using reverse translational approaches and implementing new technologies, he evaluated patient samples to create transcriptomic and proteomic resources. These resources revealed new BAP1-dependent pathways that drive immunosuppression and T-cell dysfunction[2], which were further found to be driven by specific metabolic changes[3]. These discoveries have grounded repurposing clinically approved drugs to counteract these effects in uveal melanoma.
Additionally, Dr. Figueiredo described the impact of the MIF-CD74 axis in metastatic melanoma and its role in the clonal selection of antitumor CD8+ T cells[4]. This finding opened new research avenues at the MD Anderson Cancer Center to develop combinatorial therapies targeting MIF in conjunction with immune checkpoint inhibitors[5]
Dr. Figueiredo has also contributed to the discovery and development of novel antitumor drugs, including natural products, peptides derived from immunoglobulins with demonstrated in vivo antitumor activity[6], and new cytokines involved in cancer immunogenicity[7]. Currently, his research is centered on uncovering key molecular mechanisms involved in the formation of immune desert tumors, validating novel biomarkers and pathways that impact melanoma immunogenicity, and developing therapeutic strategies to inhibit these processes[8]. These efforts aim to enhance the efficacy of immunotherapies, such as anti-PD1 and anti-CTLA4 therapies.
Educational outreach
[edit]In addition to his research, Dr. Figueiredo shares knowledge through digital platforms, developing bilingual lectures and online courses to make advanced immunology and other medical disciplines accessible to a broader audience.
References
[edit]- ^ "Young Investigator Award in immunology to Carlos Rogerio Figueiredo | University of Turku". www.utu.fi. Retrieved 2024-12-04.
- ^ Figueiredo, Carlos R; Kalirai, Helen; Sacco, Joseph J; Azevedo, Ricardo A; Duckworth, Andrew; Slupsky, Joseph R; Coulson, Judy M; Coupland, Sarah E (April 2020). "Loss of BAP1 expression is associated with an immunosuppressive microenvironment in uveal melanoma, with implications for immunotherapy development". The Journal of Pathology. 250 (4): 420–439. doi:10.1002/path.5384. ISSN 0022-3417. PMC 7216965. PMID 31960425.
- ^ Matareed, Maisoon; Maranou, Eleftheria; Koskela, Saara A; Mehmood, Arfa; Kalirai, Helen; Coupland, Sarah E; Figueiredo, Carlos R (June 2023). "Novel prognostication biomarker adipophilin reveals a metabolic shift in uveal melanoma and new therapeutic opportunities". The Journal of Pathology. 260 (2): 203–221. doi:10.1002/path.6076. ISSN 0022-3417. PMID 36825655.
- ^ Figueiredo, Carlos R.; Azevedo, Ricardo A.; Mousdell, Sasha; Resende-Lara, Pedro T.; Ireland, Lucy; Santos, Almudena; Girola, Natalia; Cunha, Rodrigo L. O. R.; Schmid, Michael C.; Polonelli, Luciano; Travassos, Luiz R.; Mielgo, Ainhoa (2018-05-23). "Blockade of MIF–CD74 Signalling on Macrophages and Dendritic Cells Restores the Antitumour Immune Response Against Metastatic Melanoma". Frontiers in Immunology. 9: 1132. doi:10.3389/fimmu.2018.01132. ISSN 1664-3224. PMC 5974174. PMID 29875777.
- ^ de Azevedo, Ricardo A.; Shoshan, Einav; Whang, Shanzhi; Markel, Gal; Jaiswal, Ashvin R.; Liu, Arthur; Curran, Michael A.; Travassos, Luiz R.; Bar-Eli, Menashe (January 2020). "MIF inhibition as a strategy for overcoming resistance to immune checkpoint blockade therapy in melanoma". OncoImmunology. 9 (1). doi:10.1080/2162402X.2020.1846915. ISSN 2162-402X. PMC 7733907. PMID 33344042.
- ^ Figueiredo, Carlos R.; Matsuo, Alisson L.; Azevedo, Ricardo A.; Massaoka, Mariana H.; Girola, Natalia; Polonelli, Luciano; Travassos, Luiz R. (2015-09-22). "A novel microtubule de-stabilizing complementarity-determining region C36L1 peptide displays antitumor activity against melanoma in vitro and in vivo". Scientific Reports. 5 (1): 14310. Bibcode:2015NatSR...514310F. doi:10.1038/srep14310. ISSN 2045-2322. PMC 4585759. PMID 26391685.
- ^ Langguth, Miriam; Maranou, Eleftheria; Koskela, Saara A.; Elenius, Oskar; Kallionpää, Roosa E.; Birkman, Eva-Maria; Pulkkinen, Otto I.; Sundvall, Maria; Salmi, Marko; Figueiredo, Carlos R. (2024-05-22). "TIMP-1 is an activator of MHC-I expression in myeloid dendritic cells with implications for tumor immunogenicity". Genes & Immunity. 25 (3): 188–200. doi:10.1038/s41435-024-00274-7. ISSN 1476-5470. PMC 11178497. PMID 38777826.
- ^ "On the Mission to Unleash the Full Power of ICB in Cancer | University of Turku". www.utu.fi. Retrieved 2024-12-04.
- meet any of the eight academic-specific criteria
- or cite multiple reliable, secondary sources independent of the subject, which cover the subject in some depth
Make sure your draft meets one of the criteria above before resubmitting. Learn about mistakes to avoid when addressing this issue. If the subject does not meet any of the criteria, it is not suitable for Wikipedia.