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Andrei Thomas-Tikhonenko, Ph.D.
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Professor of Pathology and Laboratory Medicine
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Member, Abramson Cancer Center of the University of Pennsylvania
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Associate Professor of Pathology (with tenure), Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine
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Executive Committee Member , Cancer Biology Graduate Program, University of Pennsylvania
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Department: Pathology and Laboratory Medicine
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Graduate Group Affiliations
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- Cell and Molecular Biology 6a
- Pharmacology 5c
- Immunology e
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Contact information
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4056 Colket Translational Research Bldg
39 3501 Civic Center Blvd
Philadelphia, PA 19104
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39 3501 Civic Center Blvd
Philadelphia, PA 19104
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Office: 267-426-9699
32 Fax: 267-426-8125
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32 Fax: 267-426-8125
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Publications
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Links
c2 Search PubMed for articles
9a The Thomas-Tikhonenko lab at Children's Hospital of Philadelphia
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c2 Search PubMed for articles
9a The Thomas-Tikhonenko lab at Children's Hospital of Philadelphia
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Education:
21 8 BSc 22 (Biochemistry/Virology) c
30 Moscow State University, 1984.
21 8 PhD 1e (Oncology/Virology) c
3c Russian Academy of Medical Sciences, 1988.
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Permanent link21 8 BSc 22 (Biochemistry/Virology) c
30 Moscow State University, 1984.
21 8 PhD 1e (Oncology/Virology) c
3c Russian Academy of Medical Sciences, 1988.
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21 RESEARCH INTERESTS
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1fc Since its inception in 1997, the Thomas-Tikhonenko laboratory was broadly interested in the mechanisms of neoplastic transformation by the Myc family oncoproteins (including c- and N-Myc). The corresponding genes are altered via chromosomal translocation in B-cell lymphomas and are amplified or otherwise deregulated in many solid malignancies in adults and children alike. Yet their exact roles in promoting neoplastic growth in genetically complex human cancers remained only partially understood.
8
4b0 The major breakthrough in the field was the discovery of MYC-regulated microRNAs, in particular the miR-17~92 cluster, which is transcriptionally induced by both c- and N-Myc. Early on, we were able to demonstrate that in solid tumors, such as pediatric neuroblastoma and colon adenocarcinoma, deregulation of miR-17-92 leads to profound suppression of TGFβ signaling and sharply diminished production of many anti-angiogenic factors such as thrombospondin-1 and clusterin (Chayka et al, J Natl Cancer Inst 2009; Dews et al, Cancer Res 2010; Mestdagh et al, Mol Cell 2010, Sundaram et al, Cancer Res 2011, Fox et al, RNA 2013, Dews et al, J Natl Cancer Inst 2014). This brings about robust tumor neovascularization and enhanced neoplastic growth. In fact, our ‘06 discovery that miR-17~92 augments tumor angiogenesis (Dews et al, Nature Genet 2006) was the first example of the involvement of microRNAs in non-cell-autonomous tumor phenotypes and vascular biology. Subsequent studies also demonstrated that miR-17~92 participates in a cross-talk between TGFβ and WNT pathways, forming oncogenic feed-forward loops (Lanauze et al, Mol Cancer Res 2021; Sehgal et al, Mol Cancer Res 2021).
8
474 To determine the contribution of Myc to malignant growth in hematopoietic tissues, we developed several new mouse models for B-cell lymphoma based on infection of p53-deficient bone marrow progenitors by Myc-encoding retroviruses (Yu et al, Blood 2007; Cozma et al, J Clin Invest 2007; Amaravadi et al, J Clin Invest 2007). Unexpectedly, we discovered that the salient feature of Myc-induced lymphomagenesis was not only overexpression of the oncogenic miR-17-92 but also repression of several tumor suppressive microRNAs, such as miR-15/16 and miR-34 (Chang et al, Nature Genet 2008; Chang et al, Proc Natl Acad Sci 2009, Sotillo et al, Oncogene 2011). These microRNAs affect c-Myc expression levels and contribute to deregulation of multiple Myc target genes involved in therapeutic apoptosis and chemoresistance (Harrington et al, Leukemia 2019; Harrington et al, Trends Cancer 2021) and last but not least - B-cell receptor signaling. The role of BCR and its co-receptor CD19 in promoting lymphomagenesis was the focus of the two key papers published in early ‘10s (Chung et al, J Clin Invest 2012; Psathas et al, Blood 2013).
8
531 As CD19 became recognized as the major target for immunotherapy in general and chimeric antigen receptor-armed autologous T cells (CARTs) in particular, we dedicated major effort towards elucidating the mechanism of epitope loss in post-CART19 relapses of acute lymphoblastic leukemia. This work was aided by our participation in the multi-institutional Stand Up to Cancer-St. Baldrick's Pediatric Cancer Dream Team (2013-2022; 2021 AACR Team Science Award). Using whole exome and RNA sequencing, we identified two alternatively spliced CD19 mRNA species: one lacking exons 5-6 (Δex5-6), which encode the transmembrane domain, and another lacking exon 2 (Δex2). We further showed that skipping of exon 2 compromised surface localization of CD19 and yielded truncated CD19 protein variants, which fail to trigger killing by CART-19 (Sotillo et al, Cancer Discovery 2015; Bagashev et al, Mol Cell Biol 2018; Black et al, Nucl Acids Res 2018). Subsequent work identified additional aberrant splicing events (e.g., CD19 intron 2 retention) as major drivers of resistant to CD19-directed immunotherapy (Asnani et al, Leukemia 2020; Cortés-López et al, Nat Commun 2022) as well as similar splicing-based mechanisms of epitope loss affecting other targets (Zheng et al, Blood Cancer Discov 2022; Cai et al, Nat Commun 2022).
8
4a8 Since 2018, the Thomas-Tikhonenko lab has been an integral part of the Pediatric Immunotherapy Discovery and Development Network (PI-DDN) funded through Beau Biden Cancer Moonshot Initiative. Our most recent work informed the central hypothesis that non-canonical exon usage plays a dual role in leukemia and other pediatric cancers. On the one hand, it provides cancers with intrinsic mechanisms of epitope loss, which can render targeted immunotherapy ineffective. On the other hand, alternative splicing could be a source of cancer-specific epitopes and as such could aid immunotherapy. By simultaneously exploring the effects of alternative splicing on antigen loss and neo-epitope gain, we aspire to lay ground for the development of new immunotherapeutics that would target pediatric cancers with the specificity current modalities do not possess. In our latest paper we describe a splice variant of the neuronal cell adhesion molecule (NRCAM) expressed on a surface of high-glade glioma and glioblastoma cells, which when "painted" with a custom-made monoclonal antibody mediates killing by T cells expressing the Universal Immune Receptor (UIR) (Sehgal et al, Cell Rep 2025).
8
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20 ROTATION PROJECTS
98 1. To investigate the effects of aberrant splicing of cell surface antigens on cancer immunotherapy (CAR T cells, antibody-drug conjugates, etc)
80 2. To elucidate post-transcriptional mechanisms of cancer chemoresistance (aberrant splicing, protein degradation, etc.)
7b 3. To identify determinants of aberrant splicing in cancer, with focus on genetic variants and RNA-binding proteins
8
8
1c LAB PERSONNEL
30 Priyanka Sehgal, PhD, Research Scientist
2b Zhiwei Ang, PhD, Research Scientist
2f Jacinta Davis, PhD, Postdoctoral Fellow
33 Pamela Mishra, Bioinformatics Scientist III
2d Anette Castro, Research Technician IV
38 Grace Watterson, CAMB PhD Student (thesis-level)
49 Josie King, PGG PhD Student (thesis-level) | T32 GM008076 trainee
3b Anna Tangiyan, CAMB PhD Student (Fall '25 rotation)
49 Chistopher Kwok, Vagelos Life Sciences & Management (LSM) Student
40 Kathryn Wurges, MHA/MHE, Research Administrative Manager
2e Michele Haynes, Resource Coordinator V
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1c RECENT ALUMNI
59 Sisi Zheng, MD, Assistant Professor of Pediatrics, UT Southwestern Medical Center
43 Manuel Torres Diz, PhD, Bioinformatics Scientist, CHOP DBHi
59 Elena Sotillo-Piñeiro, PhD, Senior Research Scientist, Stanford Cancer Institute
45 Asen Bagashev, PhD, Principal Scientist, Carisma Therapeutics
4f Carolin Schmidt, Medical Student, Drexel University College of Medicine
59 Colleen Harrington, PhD, Researcher Scientist, Broad Institute of MIT and Harvard
37 Claudia Lanauze, PhD, Senior Associate, Clarion
4a Scarlett Yang, Senior Regulatory Affairs Associate, Gilead Sciences
6e
e 29
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Description of Research Expertise
1a7 My laboratory has a long-standing interest in pathobiology of solid and hematopoietic malignancies, in particular lymphomas and leukemias and other pediatric and adult cancers driven by MYC overexpression. The current research focuses on the role of non-coding RNAs (including microRNAs) and mRNA processing (splicing, polyadenylation, etc) in cancer pathogenesis and therapeutic resistance.8
8
21 RESEARCH INTERESTS
8
1fc Since its inception in 1997, the Thomas-Tikhonenko laboratory was broadly interested in the mechanisms of neoplastic transformation by the Myc family oncoproteins (including c- and N-Myc). The corresponding genes are altered via chromosomal translocation in B-cell lymphomas and are amplified or otherwise deregulated in many solid malignancies in adults and children alike. Yet their exact roles in promoting neoplastic growth in genetically complex human cancers remained only partially understood.
8
4b0 The major breakthrough in the field was the discovery of MYC-regulated microRNAs, in particular the miR-17~92 cluster, which is transcriptionally induced by both c- and N-Myc. Early on, we were able to demonstrate that in solid tumors, such as pediatric neuroblastoma and colon adenocarcinoma, deregulation of miR-17-92 leads to profound suppression of TGFβ signaling and sharply diminished production of many anti-angiogenic factors such as thrombospondin-1 and clusterin (Chayka et al, J Natl Cancer Inst 2009; Dews et al, Cancer Res 2010; Mestdagh et al, Mol Cell 2010, Sundaram et al, Cancer Res 2011, Fox et al, RNA 2013, Dews et al, J Natl Cancer Inst 2014). This brings about robust tumor neovascularization and enhanced neoplastic growth. In fact, our ‘06 discovery that miR-17~92 augments tumor angiogenesis (Dews et al, Nature Genet 2006) was the first example of the involvement of microRNAs in non-cell-autonomous tumor phenotypes and vascular biology. Subsequent studies also demonstrated that miR-17~92 participates in a cross-talk between TGFβ and WNT pathways, forming oncogenic feed-forward loops (Lanauze et al, Mol Cancer Res 2021; Sehgal et al, Mol Cancer Res 2021).
8
474 To determine the contribution of Myc to malignant growth in hematopoietic tissues, we developed several new mouse models for B-cell lymphoma based on infection of p53-deficient bone marrow progenitors by Myc-encoding retroviruses (Yu et al, Blood 2007; Cozma et al, J Clin Invest 2007; Amaravadi et al, J Clin Invest 2007). Unexpectedly, we discovered that the salient feature of Myc-induced lymphomagenesis was not only overexpression of the oncogenic miR-17-92 but also repression of several tumor suppressive microRNAs, such as miR-15/16 and miR-34 (Chang et al, Nature Genet 2008; Chang et al, Proc Natl Acad Sci 2009, Sotillo et al, Oncogene 2011). These microRNAs affect c-Myc expression levels and contribute to deregulation of multiple Myc target genes involved in therapeutic apoptosis and chemoresistance (Harrington et al, Leukemia 2019; Harrington et al, Trends Cancer 2021) and last but not least - B-cell receptor signaling. The role of BCR and its co-receptor CD19 in promoting lymphomagenesis was the focus of the two key papers published in early ‘10s (Chung et al, J Clin Invest 2012; Psathas et al, Blood 2013).
8
531 As CD19 became recognized as the major target for immunotherapy in general and chimeric antigen receptor-armed autologous T cells (CARTs) in particular, we dedicated major effort towards elucidating the mechanism of epitope loss in post-CART19 relapses of acute lymphoblastic leukemia. This work was aided by our participation in the multi-institutional Stand Up to Cancer-St. Baldrick's Pediatric Cancer Dream Team (2013-2022; 2021 AACR Team Science Award). Using whole exome and RNA sequencing, we identified two alternatively spliced CD19 mRNA species: one lacking exons 5-6 (Δex5-6), which encode the transmembrane domain, and another lacking exon 2 (Δex2). We further showed that skipping of exon 2 compromised surface localization of CD19 and yielded truncated CD19 protein variants, which fail to trigger killing by CART-19 (Sotillo et al, Cancer Discovery 2015; Bagashev et al, Mol Cell Biol 2018; Black et al, Nucl Acids Res 2018). Subsequent work identified additional aberrant splicing events (e.g., CD19 intron 2 retention) as major drivers of resistant to CD19-directed immunotherapy (Asnani et al, Leukemia 2020; Cortés-López et al, Nat Commun 2022) as well as similar splicing-based mechanisms of epitope loss affecting other targets (Zheng et al, Blood Cancer Discov 2022; Cai et al, Nat Commun 2022).
8
4a8 Since 2018, the Thomas-Tikhonenko lab has been an integral part of the Pediatric Immunotherapy Discovery and Development Network (PI-DDN) funded through Beau Biden Cancer Moonshot Initiative. Our most recent work informed the central hypothesis that non-canonical exon usage plays a dual role in leukemia and other pediatric cancers. On the one hand, it provides cancers with intrinsic mechanisms of epitope loss, which can render targeted immunotherapy ineffective. On the other hand, alternative splicing could be a source of cancer-specific epitopes and as such could aid immunotherapy. By simultaneously exploring the effects of alternative splicing on antigen loss and neo-epitope gain, we aspire to lay ground for the development of new immunotherapeutics that would target pediatric cancers with the specificity current modalities do not possess. In our latest paper we describe a splice variant of the neuronal cell adhesion molecule (NRCAM) expressed on a surface of high-glade glioma and glioblastoma cells, which when "painted" with a custom-made monoclonal antibody mediates killing by T cells expressing the Universal Immune Receptor (UIR) (Sehgal et al, Cell Rep 2025).
8
8
20 ROTATION PROJECTS
98 1. To investigate the effects of aberrant splicing of cell surface antigens on cancer immunotherapy (CAR T cells, antibody-drug conjugates, etc)
80 2. To elucidate post-transcriptional mechanisms of cancer chemoresistance (aberrant splicing, protein degradation, etc.)
7b 3. To identify determinants of aberrant splicing in cancer, with focus on genetic variants and RNA-binding proteins
8
8
1c LAB PERSONNEL
30 Priyanka Sehgal, PhD, Research Scientist
2b Zhiwei Ang, PhD, Research Scientist
2f Jacinta Davis, PhD, Postdoctoral Fellow
33 Pamela Mishra, Bioinformatics Scientist III
2d Anette Castro, Research Technician IV
38 Grace Watterson, CAMB PhD Student (thesis-level)
49 Josie King, PGG PhD Student (thesis-level) | T32 GM008076 trainee
3b Anna Tangiyan, CAMB PhD Student (Fall '25 rotation)
49 Chistopher Kwok, Vagelos Life Sciences & Management (LSM) Student
40 Kathryn Wurges, MHA/MHE, Research Administrative Manager
2e Michele Haynes, Resource Coordinator V
8
1c RECENT ALUMNI
59 Sisi Zheng, MD, Assistant Professor of Pediatrics, UT Southwestern Medical Center
43 Manuel Torres Diz, PhD, Bioinformatics Scientist, CHOP DBHi
59 Elena Sotillo-Piñeiro, PhD, Senior Research Scientist, Stanford Cancer Institute
45 Asen Bagashev, PhD, Principal Scientist, Carisma Therapeutics
4f Carolin Schmidt, Medical Student, Drexel University College of Medicine
59 Colleen Harrington, PhD, Researcher Scientist, Broad Institute of MIT and Harvard
37 Claudia Lanauze, PhD, Senior Associate, Clarion
4a Scarlett Yang, Senior Regulatory Affairs Associate, Gilead Sciences
6e
Description of Other Expertise
169 In 2008, I moved my lab across campus to The Children's Hospital of Philadelphia, where it became an integral part of the Center for Childhood Cancer Research. This integration allowed me to foster new collaborations with key physician-scientists and pursue multiple translational projects focused on (but not limited to) pediatric malignancies.e 29
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1a7 O.Anczukow, F.H.T.Allain, B.L.Angarola, D.L.Black, A.N.Brooks, C.Cheng, A.Conesa, E.I.Crosse, E.Eyras, E.Guccione, S.X.Lu, K.M.Neugebauer, P.Sehgal, X.Song, Z.Tothova, J.Valcárcel, K.M.Weeks, G.W.Yeo, and A.Thomas-Tikhonenko: Steering research on mRNA splicing in cancer towards clinical translation. Nat Rev Cancer 24(12): 887-905, Dec 2024.
6a M.Torres-Diz, C.Reglero, C.D.Falkenstein, A.Castro, K.E.Hayer, 13d C.M.Radens, M.Quesnel-Vallières, Z.Ang, P.Sehgal, M.M.Li, Y.Barash, S.K.Tasian, A.Ferrando, and A.Thomas-Tikhonenko: An Alternatively Spliced Gain-of-Function NT5C2 Isoform Contributes to Chemoresistance in Acute Lymphoblastic Leukemia. Cancer Res 84(20): 3327–3336, Oct 2024.
14a Z.Ang, L.Paruzzo, K.E.Hayer, C.Schmidt, M.Torres-Diz, S.Zheng, F.Xu, U.Zankharia, Y.Zhang, S.S.Soldan, S.Zheng, C.D.Falkenstein, J.P.Loftus, S.Y.Yang, M.Asnani, P.King Sainos, V.Pillai, E.Chong, M.M.Li, S.K.Tasian, Y.Barash, P.M.Lieberman, M.Ruella,S.J.Schuster, and A.Thomas-Tikhonenko 2 2 2 2 10 Vinodh Pillai, 12 Emeline R Chong, d Marilyn Li, 11 Sarah K Tasian, 10 Yoseph Barash, d8 : Alternative splicing of its 5’ untranslated region controls CD20 mRNA translation and enables resistance to CD20-directed immunotherapies. Blood 142(20): 1724-1739, Nov 2023.
171 S.Y.Yang, K.E.Hayer, H.Fazelinia, L.A.Spruce, M.Asnani, K.L.Black, A.S.Naqvi, V.Pillai, Y.Barash, K.S.J.Elenitoba-Johnson, and A.Thomas-Tikhonenko: FBXW7β isoform drives transcriptional activation of a proinflammatory TNF cluster in human pro-B cells. Blood Adv 7(7): 1077-1091, Apr 2023.
14d P.J.Krohl, J.Fine, H.Yang, D.VanDyke, Z.Ang, K.B.Kim, A.Thomas-Tikhonenko, and J.B.Spangler: Discovery of antibodies targeting multipass transmembrane proteins using a suspension cell-based evolutionary approach. Cell Rep Methods 3(3): 100429, Mar 2023.
11b D.Wang, M.Quesnel-Vallieres, P.Jewell, M.Elzubeir, K.W.Lynch, A.Thomas-Tikhonenko and Y.Barash: A Bayesian model for unsupervised detection of RNA splicing based subtypes in cancers. Nat Commun Jan 2023.
1f3 M.Cortés-López, L.Schulz, M.Enculescu, C.Paret, B.Spiekermann, M.Quesnel-Vallières, M.Torres-Diz, S.Unic, A.Busch, A.Orekhova, M Kuban, M.Mesitov, M.Mulorz, R.Shraim, F.Kielisch, J.Faber, Y.Barash, A.Thomas-Tikhonenko, K.Zarnack, S.Legewie, J.König: High-throughput mutagenesis identifies mutations and RNA-binding proteins controlling CD19 splicing and CART-19 therapy resistance. Nat Commun 13(1): 5570, Sep 2022.
222 S.Zheng, E.Gillespie, Ammar S. Naqvi, K.E.Hayer, Z.Ang, M.Torres-Diz, M.Quesnel-Vallières, D.A.Hottman, A.Bagashev, J.Chukinas, C.Schmidt, M.Asnani, R.Shraim, D.M.Taylor, S.R.Rheingold, M.M.O’Brien, N.Singh, K.W.Lynch, M.Ruella, Y.Barash, S.K.Tasian, and A.Thomas-Tikhonenko: Modulation of CD22 protein expression in childhood leukemia by pervasive splicing aberrations: implications for CD22-directed immunotherapy. Blood Cancer Discov 3(2): 103–115, Mar 2022.
181 L.Schulz, M.Torres-Diz, M.Cortés-López, K.E.Hayer, M.Asnani, S.K.Tasian, Y.Barash, E.Sotillo, K.Zarnack, J.König, and A.Thomas-Tikhonenko: Direct long-read RNA sequencing identifies a subset of questionable exitrons likely arising from reverse transcription artifacts. Genome Biol 22(1): 190, Jun 2021.
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Selected Publications
22c Sehgal P, Naqvi AS, Higgins M, Liu J, Harvey K, Jarroux J, Kim T, Mankaliye B, Mishra P, Watterson G, Fine J, Davis J, Hayer KE, Castro A, Mogbo A, Drummer C, Martinez D, Koptyra MP, Ang Z, Wang K, Farrel A, Quesnel-Vallieres M, Barash Y, Spangler JB, Rokita JL, Resnick AC, Tilgner HU, De Raedt T, Powell DJ, Thomas-Tikhonenko A.: NRCAM variant defined by microexon skipping is a targetable cell surface proteoform in high-grade gliomas. Cell Reports 44(8): 116099, Aug 2025.1a7 O.Anczukow, F.H.T.Allain, B.L.Angarola, D.L.Black, A.N.Brooks, C.Cheng, A.Conesa, E.I.Crosse, E.Eyras, E.Guccione, S.X.Lu, K.M.Neugebauer, P.Sehgal, X.Song, Z.Tothova, J.Valcárcel, K.M.Weeks, G.W.Yeo, and A.Thomas-Tikhonenko: Steering research on mRNA splicing in cancer towards clinical translation. Nat Rev Cancer 24(12): 887-905, Dec 2024.
6a M.Torres-Diz, C.Reglero, C.D.Falkenstein, A.Castro, K.E.Hayer, 13d C.M.Radens, M.Quesnel-Vallières, Z.Ang, P.Sehgal, M.M.Li, Y.Barash, S.K.Tasian, A.Ferrando, and A.Thomas-Tikhonenko: An Alternatively Spliced Gain-of-Function NT5C2 Isoform Contributes to Chemoresistance in Acute Lymphoblastic Leukemia. Cancer Res 84(20): 3327–3336, Oct 2024.
14a Z.Ang, L.Paruzzo, K.E.Hayer, C.Schmidt, M.Torres-Diz, S.Zheng, F.Xu, U.Zankharia, Y.Zhang, S.S.Soldan, S.Zheng, C.D.Falkenstein, J.P.Loftus, S.Y.Yang, M.Asnani, P.King Sainos, V.Pillai, E.Chong, M.M.Li, S.K.Tasian, Y.Barash, P.M.Lieberman, M.Ruella,S.J.Schuster, and A.Thomas-Tikhonenko 2 2 2 2 10 Vinodh Pillai, 12 Emeline R Chong, d Marilyn Li, 11 Sarah K Tasian, 10 Yoseph Barash, d8 : Alternative splicing of its 5’ untranslated region controls CD20 mRNA translation and enables resistance to CD20-directed immunotherapies. Blood 142(20): 1724-1739, Nov 2023.
171 S.Y.Yang, K.E.Hayer, H.Fazelinia, L.A.Spruce, M.Asnani, K.L.Black, A.S.Naqvi, V.Pillai, Y.Barash, K.S.J.Elenitoba-Johnson, and A.Thomas-Tikhonenko: FBXW7β isoform drives transcriptional activation of a proinflammatory TNF cluster in human pro-B cells. Blood Adv 7(7): 1077-1091, Apr 2023.
14d P.J.Krohl, J.Fine, H.Yang, D.VanDyke, Z.Ang, K.B.Kim, A.Thomas-Tikhonenko, and J.B.Spangler: Discovery of antibodies targeting multipass transmembrane proteins using a suspension cell-based evolutionary approach. Cell Rep Methods 3(3): 100429, Mar 2023.
11b D.Wang, M.Quesnel-Vallieres, P.Jewell, M.Elzubeir, K.W.Lynch, A.Thomas-Tikhonenko and Y.Barash: A Bayesian model for unsupervised detection of RNA splicing based subtypes in cancers. Nat Commun Jan 2023.
1f3 M.Cortés-López, L.Schulz, M.Enculescu, C.Paret, B.Spiekermann, M.Quesnel-Vallières, M.Torres-Diz, S.Unic, A.Busch, A.Orekhova, M Kuban, M.Mesitov, M.Mulorz, R.Shraim, F.Kielisch, J.Faber, Y.Barash, A.Thomas-Tikhonenko, K.Zarnack, S.Legewie, J.König: High-throughput mutagenesis identifies mutations and RNA-binding proteins controlling CD19 splicing and CART-19 therapy resistance. Nat Commun 13(1): 5570, Sep 2022.
222 S.Zheng, E.Gillespie, Ammar S. Naqvi, K.E.Hayer, Z.Ang, M.Torres-Diz, M.Quesnel-Vallières, D.A.Hottman, A.Bagashev, J.Chukinas, C.Schmidt, M.Asnani, R.Shraim, D.M.Taylor, S.R.Rheingold, M.M.O’Brien, N.Singh, K.W.Lynch, M.Ruella, Y.Barash, S.K.Tasian, and A.Thomas-Tikhonenko: Modulation of CD22 protein expression in childhood leukemia by pervasive splicing aberrations: implications for CD22-directed immunotherapy. Blood Cancer Discov 3(2): 103–115, Mar 2022.
181 L.Schulz, M.Torres-Diz, M.Cortés-López, K.E.Hayer, M.Asnani, S.K.Tasian, Y.Barash, E.Sotillo, K.Zarnack, J.König, and A.Thomas-Tikhonenko: Direct long-read RNA sequencing identifies a subset of questionable exitrons likely arising from reverse transcription artifacts. Genome Biol 22(1): 190, Jun 2021.
2c