F
F. M. Marincola
Researcher at National Institutes of Health
Publications - 28
Citations - 1196
F. M. Marincola is an academic researcher from National Institutes of Health. The author has contributed to research in topics: T cell & CD8. The author has an hindex of 14, co-authored 28 publications receiving 1178 citations.
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Journal ArticleDOI
Consistent Cytotoxic-T-Lymphocyte Targeting of Immunodominant Regions in Human Immunodeficiency Virus across Multiple Ethnicities
Nicole Frahm,Bette T. Korber,Bette T. Korber,C. M. Adams,James J. Szinger,Rika Draenert,Marylyn M. Addo,Margaret E. Feeney,Karina Yusim,Kaori Sango,Nancy V. Brown,Devi SenGupta,Alicja Piechocka-Trocha,T. Simonis,F. M. Marincola,Alysse G. Wurcel,David Stone,Christopher J. Russell,P. Adolf,Daniel E. Cohen,Timothy Roach,A. StJohn,Ashok Khatri,K. Davis,James I. Mullins,Philip J. R. Goulder,Bruce D. Walker,Christian Brander +27 more
TL;DR: Factors that contribute to the immunogenicity of these highly targeted and relatively conserved sequences in HIV that may represent promising vaccine candidates for ethnically heterogeneous populations are identified.
Journal ArticleDOI
Sequential 5-Aza-2 deoxycytidine-depsipeptide FR901228 treatment induces apoptosis preferentially in cancer cells and facilitates their recognition by cytolytic T lymphocytes specific for NY-ESO-1.
Weiser Ts,Guo Zs,Galen A. Ohnmacht,Parkhurst Ml,Panida Tong-On,F. M. Marincola,Maria R. Fischette,Xiaodan Yu,G.A. Chen,Julie A. Hong,John H. Stewart,Dao M. Nguyen,Steven A. Rosenberg,David S. Schrump +13 more
TL;DR: Quantitative reverse-transcriptase polymerase chain reaction analysis revealed that, under exposure conditions potentially achievable in clinical settings, DAC dramatically induced NY-ESO-1 expression in cultured cancer lines, and sequential DAC–DP treatment may be a novel strategy to augment antitumor immunity in cancer patients.
Journal Article
Loss of HLA haplotype and B locus down-regulation in melanoma cell lines.
F. M. Marincola,P Shamamian,Richard B. Alexander,James R. Gnarra,R L Turetskaya,Sergei A. Nedospasov,Toni B. Simonis,Jeffery K. Taubenberger,John R. Yannelli,A. Mixon +9 more
TL;DR: Allele-specific PCR amplification demonstrated deletion of genes in linkage disequilibrium within the MHC class II, III, and I regions as well as loss of a genomic fragment in melanoma cells.
Journal ArticleDOI
Molecular Mechanisms Used by Tumors to Escape Immune Recognition: Immunogenetherapy and the Cell Biology of Major Histocompatibility Complex Class I
Nicholas P. Restifo,Yutaka Kawakami,F. M. Marincola,Peter Shamamian,Akash Taggarse,Fernando Esquivel,Steven A. Rosenberg +6 more
TL;DR: The hypothesis that tumor cells can escape recognition by CD8+ T cells via deficiencies in antigen processing and presentation is explored and mechanisms identified include down-regulation of antigen processing, loss of functional beta 2-microglobulin, and deletion of specific alpha-chain alleles.
Journal Article
Comparison of melanoma antigen recognized by T cells (MART-1) to HMB-45: additional evidence to support a common lineage for angiomyolipoma, lymphangiomyomatosis, and clear cell sugar tumor
TL;DR: Anti-MART-1 and HMB-45 share similar specificities for these nonmelanocytic tumors, but the former seems to be a less sensitive marker for these lesions, which lent additional support to previous studies that proposed a relationship between AML, LAM, and CCST.