Dr. Toshiyasu Taniguchi |
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Fred Hutchinson Cancer Research Center Human Biology Division Associate MemberAppointed: 2004 Howard Hughes Medical Institute HHMI Early Career ScientistAppointed: 2009 University of Washington School of Medicine Pathology Affiliate Assistant ProfessorAppointed: 2008 Fred Hutchinson Cancer Research Center Public Health Sciences Division Associate MemberAppointed: 2004 |  |
Mailing Address1100 Fairview Avenue N. C1-015 Seattle, Washington 98109-1024United States | Contact InformationPhone: (206) 667-7283 Fax: (206) 667-5815 ttaniguc@fhcrc.org http://bioeducation.com/research/ecs/taniguchi.html |
Qualifications
Ph.D., University of Tokyo, Medicine, 1999.
M.D., University of Tokyo, 1990.
Expertise and Research Interests
Major research interests of our laboratory are:
1. Fanconi anemia and cancer susceptibility
2. DNA repair and cell cycle checkpoints
3. Drug sensitivity and resistance in cancer chemotherapy
Studying rare genetic diseases with cancer susceptibility has been a productive way to get insights into pathogenesis of cancer in the general population. For example, mutations in p53, Rb, and ATM genes are responsible for the genetic diseases, Li-Fraumeni syndrome, familial retinoblastoma, and ataxia telangiectasia, respectively. Similarly, another rare cancer susceptibility syndrome called Fanconi anemia has more recently emerged in the DNA repair and signaling field. It has turned out that understanding this genetic disorder may greatly enhance our knowledge of the pathogenesis and progression of human cancers. Additionally, the Fanconi anemia pathway is an attractive model system for studying cancer, DNA repair and ubiquitin biology.
Genomic instability is a hallmark of most human cancers and is thought to be a main impetus behind premalignant cells transforming to a more malignant state through the acquisition of multiple somatic mutations. Defects of transforming the DNA damage response, such as activation of DNA repair and cell cycle checkpoints, can be a possible mechanism of genomic instability in cancer. It may also be responsible for the sensitivity of cancer cells to certain types of chemotherapeutic drugs and radiation. Thus, it is important to elucidate the cause of genomic instability and the mechanisms surrounding the DNA damage response pathway in order to achieve greater understanding of cancer and for developing new diagnostic and therapeutic strategies. The Fanconi anemia pathway plays a central role in preventing genomic instability.
Fanconi anemia (FA) is an autosomal recessive (or X-linked) cancer susceptibility syndrome characterized by chromosomal instability and cellular hypersensitivity to DNA crosslinking agents, such as cisplatin and mitomycin C. FA is comprised of at least 13 complementation groups (FA-A, B, C, D1, D2, E, F, G, I, J, L, M, and N) and all of the 13 FA genes (FANCA, B, C, D1(BRCA2), D2, E, F, G, I, J(BACH1/BRIP1), L, M and N(PALB2)) have been identified. The breast/ovarian cancer susceptibility gene products (BRCA1 and BRCA2 proteins) and all of the FA proteins cooperate in a common pathway required for the cellular resistance to DNA crosslinking agents, and this pathway is now called "the Fanconi anemia-BRCA pathway."
The key event in the FA-BRCA pathway is the monoubiquitination of one of the FA proteins, FANCD2. Monoubiquitination (conjugation of one ubiquitin molecule onto a protein) is a rather newly recognized type of posttranslational modification. Eight FA proteins (A, B, C, E, F, G, L and M) are components of a multi-subunit ubiquitin ligase complex (FA core complex) required for the monoubiquitination of FANCD2. FANCI and FANCD2 form another protein complex called the ID complex.
In response to DNA damage, this FA-BRCA pathway gets activated. After DNA damage, FANCD2 gets monoubiquitinated and targeted to BRCA1/BRCA2/RAD51-containing nuclear foci at the sites of DNA damage. FA core complex, BRCA1 and a DNA damage signaling kinase called ATR are required for this process. Monoubiquitinated FANCD2 controls the localization of BRCA2 and affects the efficiency of homologous recombination, which is a way of repairing damaged DNA. After ionizing radiation (IR) exposure, FANCD2 is directly phosphorylated by another DNA damage signaling kinase called ATM, and this phosphorylation is required for the establishment of IR-inducible S phase checkpoint. Thus, the FA-BRCA pathway is a DNA damage-activated signaling pathway which controls DNA repair and cell cycle checkpoint.
Interestingly, the FA-BRCA pathway is inactivated in a wide variety of human cancers (ovarian, breast, non-small cell lung, cervical, and head and neck squamous cell cancers) by methylation of one of the FA genes, FANCF. This inactivation causes cisplatin-sensitivity, suggesting a broad and important role of the pathway in human carcinogenesis.
The long-term objective of our research is to elucidate molecular mechanism of DNA damage response pathways, such as the FA-BRCA pathway, and their involvement in carcinogenesis and to utilize such information to refine diagnosis and therapy of patients with cancer or with FA. Currently, our lab is focusing on the following projects regarding the FA-BRCA pathway:
Basic science of FA.
1. Identification of novel genes involved in the FA-BRCA pathway
2. Elucidation of the function of the FA pathway in cell cycle checkpoints and in DNA repair
Clinical application of the basic science of FA.
1. The FA pathway in the pathogenesis of cancer
2. Identification of small molecules as FA pathway inhibitors and agonists
3. Cisplatin resistance and the FA pathway
Current lab members
Toshiyasu Taniguchi - PI
RaeLynn Endicott - Research Technician
Celine Jacquemont - Postdoctoral fellow
Kiranjit Dhillon - Postdoctoral fellow
Yemin Wang - Postdoctoral fellow
Maria Castella - Postdoctoral fellow
Jen-Wei Huang - MCB graduate student
Philamer Calses - MCB graduate student
1. Fanconi anemia and cancer susceptibility
2. DNA repair and cell cycle checkpoints
3. Drug sensitivity and resistance in cancer chemotherapy
Studying rare genetic diseases with cancer susceptibility has been a productive way to get insights into pathogenesis of cancer in the general population. For example, mutations in p53, Rb, and ATM genes are responsible for the genetic diseases, Li-Fraumeni syndrome, familial retinoblastoma, and ataxia telangiectasia, respectively. Similarly, another rare cancer susceptibility syndrome called Fanconi anemia has more recently emerged in the DNA repair and signaling field. It has turned out that understanding this genetic disorder may greatly enhance our knowledge of the pathogenesis and progression of human cancers. Additionally, the Fanconi anemia pathway is an attractive model system for studying cancer, DNA repair and ubiquitin biology.
Genomic instability is a hallmark of most human cancers and is thought to be a main impetus behind premalignant cells transforming to a more malignant state through the acquisition of multiple somatic mutations. Defects of transforming the DNA damage response, such as activation of DNA repair and cell cycle checkpoints, can be a possible mechanism of genomic instability in cancer. It may also be responsible for the sensitivity of cancer cells to certain types of chemotherapeutic drugs and radiation. Thus, it is important to elucidate the cause of genomic instability and the mechanisms surrounding the DNA damage response pathway in order to achieve greater understanding of cancer and for developing new diagnostic and therapeutic strategies. The Fanconi anemia pathway plays a central role in preventing genomic instability.
Fanconi anemia (FA) is an autosomal recessive (or X-linked) cancer susceptibility syndrome characterized by chromosomal instability and cellular hypersensitivity to DNA crosslinking agents, such as cisplatin and mitomycin C. FA is comprised of at least 13 complementation groups (FA-A, B, C, D1, D2, E, F, G, I, J, L, M, and N) and all of the 13 FA genes (FANCA, B, C, D1(BRCA2), D2, E, F, G, I, J(BACH1/BRIP1), L, M and N(PALB2)) have been identified. The breast/ovarian cancer susceptibility gene products (BRCA1 and BRCA2 proteins) and all of the FA proteins cooperate in a common pathway required for the cellular resistance to DNA crosslinking agents, and this pathway is now called "the Fanconi anemia-BRCA pathway."
The key event in the FA-BRCA pathway is the monoubiquitination of one of the FA proteins, FANCD2. Monoubiquitination (conjugation of one ubiquitin molecule onto a protein) is a rather newly recognized type of posttranslational modification. Eight FA proteins (A, B, C, E, F, G, L and M) are components of a multi-subunit ubiquitin ligase complex (FA core complex) required for the monoubiquitination of FANCD2. FANCI and FANCD2 form another protein complex called the ID complex.
In response to DNA damage, this FA-BRCA pathway gets activated. After DNA damage, FANCD2 gets monoubiquitinated and targeted to BRCA1/BRCA2/RAD51-containing nuclear foci at the sites of DNA damage. FA core complex, BRCA1 and a DNA damage signaling kinase called ATR are required for this process. Monoubiquitinated FANCD2 controls the localization of BRCA2 and affects the efficiency of homologous recombination, which is a way of repairing damaged DNA. After ionizing radiation (IR) exposure, FANCD2 is directly phosphorylated by another DNA damage signaling kinase called ATM, and this phosphorylation is required for the establishment of IR-inducible S phase checkpoint. Thus, the FA-BRCA pathway is a DNA damage-activated signaling pathway which controls DNA repair and cell cycle checkpoint.
Interestingly, the FA-BRCA pathway is inactivated in a wide variety of human cancers (ovarian, breast, non-small cell lung, cervical, and head and neck squamous cell cancers) by methylation of one of the FA genes, FANCF. This inactivation causes cisplatin-sensitivity, suggesting a broad and important role of the pathway in human carcinogenesis.
The long-term objective of our research is to elucidate molecular mechanism of DNA damage response pathways, such as the FA-BRCA pathway, and their involvement in carcinogenesis and to utilize such information to refine diagnosis and therapy of patients with cancer or with FA. Currently, our lab is focusing on the following projects regarding the FA-BRCA pathway:
Basic science of FA.
1. Identification of novel genes involved in the FA-BRCA pathway
2. Elucidation of the function of the FA pathway in cell cycle checkpoints and in DNA repair
Clinical application of the basic science of FA.
1. The FA pathway in the pathogenesis of cancer
2. Identification of small molecules as FA pathway inhibitors and agonists
3. Cisplatin resistance and the FA pathway
Current lab members
Toshiyasu Taniguchi - PI
RaeLynn Endicott - Research Technician
Celine Jacquemont - Postdoctoral fellow
Kiranjit Dhillon - Postdoctoral fellow
Yemin Wang - Postdoctoral fellow
Maria Castella - Postdoctoral fellow
Jen-Wei Huang - MCB graduate student
Philamer Calses - MCB graduate student
Keywords
COS Keywords:
Anemia, Cancer Or Carcinogenesis, Cell Cycle, DNA Repair, Drug Resistance, Genetic Diseases, Hematology, Oncology, Pediatrics, Public Health.Additional Terms:
DNA Repair and Cell Cycle Checkpoints, Drug Sensitivity and Resistance, Fanconi Anemia and Cancer Susceptibility.Languages
(Reading, Writing, Speaking)
English: (Fluent, Fluent, Fluent)
Japanese: (Fluent, Fluent, Fluent)
Memberships
American Association for Cancer Research
American Society of Hematology
Honors and Awards
2009-2015,
HHMI Early Career Scientist,
HHMI
2005-2008,
Searle Scholar Award,
Searle Funds,
Fred Hutchinson Cancer Research Center
2005-2007,
V Scholar Award,
V Foundation for Cancer Research,
Fred Hutchinson Cancer Research Center
2002-2004,
ASH Fellow Scholar Award - Basic Research,
American Society of Hematology,
Dana-Farber Cancer Institute
1999-2000,
Naito Foundation Fellowship for Research Abroad,
Naito Foundation,
Dana-Farber Cancer Institute
Previous Positions
2002-2004, Instructor,
Dana-Farber Cancer Institute,
Clinical and Basic Science Research,
Pediatric Oncology
1999-2002, Postdoctoral Fellow,
Dana-Farber Cancer Institute,
Clinical and Basic Science Research,
Pediatric Oncology
Funding Received
- National Institutes of Health (NIH): Project #4 in ovarian cancer SPORE P50 CA083636 , Clinical implication of the acquisition of BRCA1/2 function in BRCA1/2-deficient ovarian carcinoma, 2009 to 2014.
- HHMI: HHMI Early Career Scientist Award, 2009 to 2015.
- Fanconi Anemia Research Fund: , 2008 to 2009.
- FHCRC/UW Cancer Consortium: 2008 CCSG Pilot Grant, 2008 to 2008.
- Marsha Rivkin Center for Ovarian Cancer Research: Pilot Study Program Grant, 2008 to 2009.
- NIH/NHLBI, R21: ', 2008 to 2010.
- National Institutes of Health/National Cancer Institute, RO1: The Fanconi Anemia-BRCA Pathway and Chemosensitivity of Human Cancer, 2007 to 2012.
- Hartwell Innovation Fund: Significance of genetic reversion in acquired cisplatin resistance of BRCA1/2-mutated cancer, 2006 to 2007.
- Searle Scholars Program: Analysis of the Fanconi Anemia-BRCA Pathway in Cancer, 2005 to 2008.
- Mary Kay Ash Charitable Foundation: Sensitization of ovarian cancer cells to chemotherapy by modulating the Fanconi Anemia-BRCA Pathway, 2005 to 2007.
- The V Foundation for Cancer Research: Mechanism of BRCA2/FANCD1 protein inactivation/reactivation in ovarian cancer cells during cisplatin treatment, 2005 to 2007.
- AVON Breast Cancer Crusade Opportunity Fund (Pilot Project Fund for Innovative Breast Cancer Research): Analysis of the Fanconi Anemia Protein, FANCF, in Breast Cancer, 2005 to 2006.
- American Society of Hematology (ASH Fellow Scholar Award - Basic Research ): Functional Analysis of the Fanconi Anemia Proteins, 2002 to 2004.
Publications
- Toshiyasu Taniguchi (2009) The Fanconi anemia-BRCA pathway and cancer, The DNA Damage Response: Implications on Cancer Formation and Treatment, Springer, ISBN=9789048125609 (bookchapter)
- Wataru Sakai, Elizabeth M. Swisher, Céline Jacquemont, Kurapaty Venkatapoorna Chandramohan, Fergus J. Couch, Simon P. Langdon, Kaitlyn Wurz, Jake Higgins, Emily Villegas, Toshiyasu Taniguchi. (2009) Functional restoration of BRCA2 protein by secondary BRCA2 mutations in BRCA2-mutated ovarian carcinoma., Cancer Research, 69 (16), 6381-6
- Elizabeth M. Swisher, Rachel Gonzales-Hernandez, Toshiyasu Taniguchi, Rochelle L. Garcia, Tom Walsh, Boxin Zhang, Melissa Wollan, Julia Willner, Barbara A. Goff, Piri Welcsh. (2009) Methylation and protein expression of DNA repair genes: Association with chemotherapy exposure and survival in sporadic ovarian and peritoneal carcinomas., Molecular Cancer, 8 (1), 48
- Elizabeth M. Swisher, Wataru Sakai, Beth Y. Karlan, Kaitlyn Wurz, Nicole Urban, Toshiyasu Taniguchi (2008) Secondary BRCA1 mutations in BRCA1-mutated ovarian carcinomas with platinum resistance., Cancer Research, 68 (8), 2581-2586
- Wataru Sakai, Elizabeth M. Swisher, Beth Y. Karlan, Mukesh K. Agarwal, Jake Higgins, Cynthia Friedman, Emily Villegas, Céline Jacquemont, Daniel J. Farrugia, Fergus J. Couch, Nicole Urban & Toshiyasu Taniguchi (2008) Secondary mutations as a mechanism of cisplatin resistance in BRCA2-mutated cancers, Nature, 451 (7182), 1116-1120
- Céline Jacquemont, Toshiyasu Taniguchi (2007) Proteasome function is required for DNA damage response and Fanconi anemia pathway activation, Cancer Research, 67 (15), 7395-7405
- Toshiyasu Taniguchi, Fanconi Anemia, GeneReviews at GeneTests: Medical Genetics Information Resource [database online] Available at http://www.genetests.org, 2007
- Céline Jacquemont, Toshiyasu Taniguchi (2007) The Fanconi anemia pathway and ubiquitin. (review), BMC Biochemistry, 8 (Suppl 1), S10
- Clark C. Chen, Toshiyasu Taniguchi, Alan D'Andrea (2007) The Fanconi anemia (FA) pathway confers glioma resistance to DNA alkylating agents, Journal of Molecular Medicine, 85 (5), 497-509
- Céline Jacquemont, Toshiyasu Taniguchi (2006) Disruption of the Fanconi anemia pathway in human cancer in the general population. (Commentary), Cancer Biology & Therapy, 5 (12), 1637-9
- Gary P.H. Ho, Steven Margossian, Toshiyasu Taniguchi, Alan D. D'Andrea (2006) Phosphorylation of FANCD2 on Two Novel Sites is Required for MMC Resistance, Molecular and Cellular Biology, 26 (18), 7005-15
- Taniguchi T, D'Andrea AD (June 1, 2006) The Molecular Pathogenesis of Fanconi Anemia: Recent Progress (review), Blood, 107 (11), 4223-33
- Mankad A, Taniguchi T, Cox B, et al. (Apr 15, 2006) Natural gene therapy in monozygotic twins with Fanconi anemia, Blood, 107 (8), 3084-3090
- Chirnomas D, Taniguchi T, de la Vega M, Vaidya AP, Vasserman M, Hartman AR, Kennedy R, Foster R, Mahoney J, Seiden MV, D'Andrea AD. (April 1, 2006) Chemosensitization to cisplatin by inhibitors of the Fanconi anemia/BRCA pathway, Mol Cancer Ther, 5 (4), 952-61
- Toshiyasu Taniguchi (2006) Regulation of DNA repair by the ubiquitin system and its implication in cancer, AACR Education Book 2006, 166-170 pages (bookchapter)
- Travis LB, Rabkin CS, Brown LM, et al. (Jan 4, 2006) Cancer Survivorship - Genetic Susceptibility and Second Primary Cancers: Research Strategies and Recommendations (Commentary), Journal of the National Cancer Institute, 98 (1), 15-25
- Houghtaling S, Newell A, Akkari Y, Taniguchi T, Olson S, and Grompe M (Oct 15, 2005) Fancd2 Functions in a Double Strand Break Repair Pathway That Is Distinct From Non-homologous End Joining, Human Molecular Genetics, 14 (20), 3027-33
- Howlett NG, Taniguchi T, Durkin SG, D'Andrea AD, Glover TW (Mar 2005) The Fanconi anemia pathway is required for the DNA replication stress response and for the regulation of common fragile site stability., Human Molecular Genetics, 14 (5), 693-701
- Montes de Oca R, Andreassen PR, Margossian SP, Gregory RC, Taniguchi T, Wang X, Houghtaling S, Grompe M, D'Andrea AD (Feb 2005) Regulated interaction of the Fanconi anemia protein, FANCD2, with chromatin, Blood, 105 (3), 1003-9
- Nakanishi K, Yang YG, Pierce AJ, Taniguchi T, Digweed M, D'Andrea AD, Wang ZQ, Jasin M (Jan 2005) Human Fanconi anemia monoubiquitination pathway promotes homologous DNA repair, Proceedings of the National Academy of Sciences of the United States of America, 102 (4), 1110-5
- Andreassen PR, D'Andrea AD, Taniguchi T (Aug 2004) ATR couples FANCD2 monoubiquitination to the DNA-damage response, Genes & Development, 18 (16), 1958-63
- Tischkowitz M, Ameziane N, Waisfisz Q, De Winter JP, Harris R, Taniguchi T, D'Andrea A, Hodgson SV, Mathew CG, Joenje H (Nov 2003) Bi-allelic silencing of the Fanconi anaemia gene FANCF in acute myeloid leukaemia, British Journal of Haematology, 123 (3), 469-71
- Taniguchi T, Tischkowitz M, Ameziane N, Hodgson SV, Mathew CG, Joenje H, Mok SC, D'Andrea AD (May 2003) Disruption of the Fanconi anemia-BRCA pathway in cisplatin-sensitive ovarian tumors, Nature Medicine, 9 (5), 568-74
- Gregory RC, Taniguchi T, D'Andrea AD (Feb 2003) Regulation of the Fanconi anemia pathway by monoubiquitination (review), Seminars in Cancer Biology, 13 (1), 77-82
- Adachi D, Oda T, Yagasaki H, Nakasato K, Taniguchi T, D'Andrea AD, Asano S, Yamashita T (Dec 2002) Heterogeneous activation of the Fanconi anemia pathway by patient-derived FANCA mutants, Human Molecular Genetics, 11 (25), 3125-34
- Nakanishi K, Taniguchi T, Ranganathan V, New HV, Moreau LA, Stotsky M, Mathew CG, Kastan MB, Weaver DT, D'Andrea AD (Dec 2002) Interaction of FANCD2 and NBS1 in the DNA damage response, Nature Cell Biology, 4 (12), 913-20
- Taniguchi T, Garcia-Higuera I, Andreassen PR, Gregory RC, Grompe M, D'Andrea AD (Oct 2002) S-phase-specific interaction of the Fanconi anemia protein, FANCD2, with BRCA1 and RAD51, Blood, 100 (7), 2414-20
- Taniguchi T, D'Andrea AD (Oct 2002) The Fanconi anemia protein, FANCE, promotes the nuclear accumulation of FANCC, Blood, 100 (7), 2457-62
- Howlett NG, Taniguchi T, Olson S, Cox B, Waisfisz Q, De Die-Smulders C, Persky N, Grompe M, Joenje H, Pals G, Ikeda H, Fox EA, D'Andrea AD (Jul 2002) Biallelic inactivation of BRCA2 in Fanconi anemia, Science, 297 (5581), 606-9
- Taniguchi T, Garcia-Higuera I, Xu B, Andreassen PR, Gregory RC, Kim ST, Lane WS, Kastan MB, D'Andrea AD (May 2002) Convergence of the fanconi anemia and ataxia telangiectasia signaling pathways, Cell, 109 (4), 459-72
- Taniguchi T, Dandrea AD (Feb 2002) Molecular pathogenesis of fanconi anemia (review), International Journal of Hematology, 75 (2), 123-8
- Siddique MA, Nakanishi K, Taniguchi T, Grompe M, D'Andrea AD (Dec 2001) Function of the Fanconi anemia pathway in Fanconi anemia complementation group F and D1 cells, Experimental Hematology, 29 (12), 1448-55
- Garcia-Higuera I, Taniguchi T, Ganesan S, Meyn MS, Timmers C, Hejna J, Grompe M, D'Andrea AD (Feb 2001) Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway, Molecular Cell, 7 (2), 249-62
- Timmers C, Taniguchi T, Hejna J, Reifsteck C, Lucas L, Bruun D, Thayer M, Cox B, Olson S, D'Andrea AD, Moses R, Grompe M (Feb 2001) Positional cloning of a novel Fanconi anemia gene, FANCD2, Molecular Cell, 7 (2), 241-8
- Taniguchi T, Chikatsu N, Takahashi S, Fujita A, Uchimaru K, Asano S, Fujita T, Motokura T (Nov 1999) Expression of p16INK4A and p14ARF in hematological malignancies, Leukemia, 13 (11), 1760-9
- Ishida F, Kitano K, Ichikawa N, Ito T, Kohara Y, Taniguchi T, Motokura T, Kiyosawa K (Aug 1999) Hairy cell leukemia with translocation (11;20)(q13;q11) and overexpression of cyclin D1, Leukemia Research, 23 (8), 763-5
- Taniguchi T, Endo H, Chikatsu N, Uchimaru K, Asano S, Fujita T, Nakahata T, Motokura T (Jun 1999) Expression of p21(Cip1/Waf1/Sdi1) and p27(Kip1) cyclin-dependent kinase inhibitors during human hematopoiesis, Blood, 93 (12), 4167-78
- Yufu Y, Goto T, Choi I, Uike N, Kozuru M, Ohshima K, Taniguchi T, Motokura T, Yatabe Y, Nakamura S (Apr 1999) A new multiple myeloma cell line, MEF-1, possesses cyclin D1 overexpression and the p53 mutation, Cancer, 85 (8), 1750-7
- Uchimaru K, Taniguchi T, Yoshikawa M, Fujinuma H, Fujita T, Motokura T (May 1998) Growth arrest associated with 12-o-tetradecanoylphorbol-13-acetate-induced hematopoietic differentiation with a defective retinoblastoma tumor suppressor-mediated pathway, Leukemia Research, 22 (5), 413-20
- Taniguchi T, Fujita A, Takahashi S, Uchimaru K, Yoshikawa M, Asano S, Fujita T, Motokura T (Feb 1998) Cyclin D1 overexpression detected by a simple competitive reverse transcription-polymerase chain reaction assay for lymphoid malignancies, Japanese Journal of Cancer Research : Gann, 89 (2), 159-66
- Uchimaru K, Taniguchi T, Yoshikawa M, Asano S, Arnold A, Fujita T, Motokura T (Feb 1997) Detection of cyclin D1 (bcl-1, PRAD1) overexpression by a simple competitive reverse transcription-polymerase chain reaction assay in t(11;14)(q13;q32)-bearing B-cell malignancies and/or mantle cell lymphoma, Blood, 89 (3), 965-74
- Motokura T, Kobayashi Y, Fujita A, Nakamura Y, Taniguchi T, Uchimaru K, Asano S (Jan 1995) Clinical significance of serial measurement of the serum levels of soluble interleukin-2 receptor and soluble CD8 in malignant lymphoma, Leukemia & Lymphoma, 16 (3-4), 355-62
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