168 results on '"Jhanwar, S C"'
Search Results
2. Persistence of expression of the TMPRSS2:ERG fusion gene after pre-surgery androgen ablation may be associated with early prostate specific antigen relapse of prostate cancer: Preliminary results
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Bonaccorsi, L., Nesi, G., Nuti, F., Paglierani, M., Krausz, C., Masieri, L., Serni, S., Proietti-Pannunzi, L., Fang, Y., Jhanwar, S. C., Orlando, C., Carini, M., Forti, G., Baldi, E., and Luzzatto, L.
- Published
- 2009
- Full Text
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3. Re-expression of the tumor suppressor NF2/merlin inhibits invasiveness in mesothelioma cells and negatively regulates FAK
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Poulikakos, P I, Xiao, G-H, Gallagher, R, Jablonski, S, Jhanwar, S C, and Testa, J R
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- 2006
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4. CD32B Expression Reflects Intraclonal Functional Heterogeity in Multiple Myeloma: B500
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Comenzo, R L, Jhanwar, S C, Nimer, S D, Zhou, P, Boruchov, A, Lu, P, Bonvini, E, and Hassoun, H
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- 2009
5. Will the new cytogenetics replace the old cytogenetics?
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Salman, M, Jhanwar, S C, and Ostrer, H
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- 2004
6. Activation of Cellular Onc (C-ONC) Genes: A Common Pathway for Oncogenesis
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Hayward, W. S., Neel, B. G., Jhanwar, S. C., Chaganti, R. S. K., Hollaender, Alexander, Probstein, Ronald F., Welch, Bruce L., Milman, Harry A., editor, and Sell, Stewart, editor
- Published
- 1983
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7. Abstracts of Selected Posters
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Albanese, R., Antoine, J. L., Dutrillaux, B., Ashley, T., Avivi, L., Kariv, I., Barigozzi, C., Baratelli, L., Profeta, S., Bartram, C. R., de Klein, A., Hagemeijer, A., Grosveld, G., Bootsma, D., Bennett, Michael D., Smith, J. B., Ward, J. P., Heslop-Harrison, J. S., Blin, N., Kopun, M., Buys, C. H. C. M., Koerts, T., van der Veen, A. Y., de Leij, L., Civitelli, M. V., Capanna, E., Couturier, J., Arnason, U., Mandahl, N., Créau-Goldberg, N., Turleau, C., Cochet, C., de Grouchy, J., Dietrich, A. J. J., Delhanty, J. D. A., Mazzullo, H. A., Cooke, H. M. G., Dotan, A., Dresser, M. E., Moses, M. J., Evans, E. P., Burgoyne, P. B., Ferraro, M., Lavia, P., Fonatsch, C., Kirchner, H. H., Pajunk, A., Schaadt, M., Burrichter, H., Diehl, V., Ford, J. H., Roberts, C. G., Friebe, B., Vogel, R., Friedländer, M., Gamperl, R., Amtmann, E., Pfister, H., Gebhart, E., Wagner, H., Goetz, P., Chandley, A. C., Speed, R. M., Goyanes, V. J., Schvartzman, J. B., Graeven, U., Weh, H. J., Hossfeld, D. K., Greenblatt, I. M., Gripenberg, U., Söderlund, V., Wahlberg, C., Blomqvist, L., Guichaoua, M. R., Delafontaine, D., Taillemite, J. L., Luciani, J. M., Naaf, T., Grunert, D., Schmid, M., Hameister, H., Sperling, K., Hamers, A., Jongbloet, P., Peeters, G., Geraedts, J., Hartley-Asp, B., Heneen, W. K., Hens, L., Kirsch-Volders, M., Susanne, C., Herbst, E. W., Winking, H., Claussen, C. P., Putz, B., Sellin, D., Kolbus, U., Gropp, A., Bennett, M. D., Heyting, C., Koperdraad, F., Redeker, E. J. W., Holmquist, G., Goldman, M., Jaworska, Halina, Johannisson, R., Kerem, B., Goitein, R., Richier, C., Marcus, M., Cedar, H., Koch, H., Hoehn, H., Kubbies, Manfred, Rabinovitch, Peter S., Kunz, W., Franz, G., Lacadena, J. R., Cermeno, M. C., Orellana, J., Santos, J. L., Lemeunier, F., Derbin, C., Lin, C. C., Hoar, D. I., Hoo, J. J., Macgregor, H. C., Sims, S., Horner, H. A., Pellatt, P., Mackay, J. M., Fox, D. P., Brunt, P. W., Johnston, A. W., Magenis, R. E., Chamberlin, J., Allen, L., Tomar, D., Olson, S., Donlon, T., Marlekaj, P., Balcini, A., Fantoni, A., de Capoa, A., Martinsson, T., Dahllöf, B., Levan, G., Matsukuma, S., Utakoji, T., del Mazo, J., Avila, J., Miller, D. A., Feinstein, S. I., Miller, O. J., Morita, T., Delarbre, C., Gachelin, G., Kourilsky, P., Moritz, K., Moriwaki, K., Miyashita, N., Imai, H. T., Wang, C. H., Bonhomme, F., Murer-Orlando, M., Peterson, A. C., Neitzel, H., Bogenberger, J., Fittler, F., Gaenge, M., Schulze, C., Nietzel, H., Nürnberger, F., Höhn, H., van Ommen, G. J. B., Baas, F., Arnberg, A. C., Pearson, P. L., De Vijilder, J. J. M., Bakker, E., Hofker, M., Wapenaar, M. C., Parrington, J. M., West, L. F., Povey, S., Pasquali, F., Casalone, R., Bernasconi, P., Paul, J., Froster-Iskenius, U., Schwinger, E., Moje, W., Pearson, P. O., Beverstock, G. C., Veenema, H., v.d Kamp, J. J., Petitpierre, E., Philip, J., Lundsteen, C., van der Ploeg, M., van Prooijen-Knegt, A. C., Bauman, J. G. J., van Duijn, P., Puertas, M. J., de la Pena, A., Estades, B., Merino, F., Rao, S. R. V., Vasantha, K., Thelma, B. K., Juyal, R. C., Jhanwar, S. C., Ratomponirina, Ch, Hamilton, A., Rumpler, Y., Moses, M., Raveh, D., Ben-Zeoev, A., Redi, C. A., Garagna, S., Italy, C. N. R., Robert-Nicoud, M., Streichhan, I., Möhr, E., Westermann, R., Grossbach, U., Sandberg, P., Levan, A., Schäfer, Mireille, Schempp, W., Scheres, J. M. J. C., Hustinx, T. W. J., Holdrinet, R. S. G., Tice, R. R., Schwarzacher, T., Finch, R. A., Searle, J. B., Sharma, T., Sen, S., Cheong, N., Siebert, E., Loidl, J., Slater, R. M., de Kraker, J., Voute, P. A., Delemarre, J. F. M., Smeets, D. F. C. M., Smits, A. P. T., Solleder, E., Inglin, B., Geile, B., Somssich, I., Schwarz, E., Speit, G., Mehnert, K., Vogel, W., Stahl, A., Hartung, M., Devictor, M., Guichaoua, M., Stoll, C., Roth, M.-P., Dott, B., Tabor, A., Madsen, M., Tommerup, N., Traut, W., Chavin-Colin, F., Junien, C., Vekemans, M., Esseltine, D., Venegas, W., Lasne, Cl, Chouroulinkov, I., Vidal, F., Navarro, J., Templado, C., Egozcue, J., Viegas-Péquignot, E., Malfoy, B., Taillandier, E., Leng, M., Viinikka, Y., Spielmann, H., Boldin, S., Volobouev, V. T., Webb, G. C., Krumins, E., Wegner, R.-D., Lüdtke, E.-L., Weith, A., Westerman, M., Thomson, R., Sinclair, A., Yacobi, Y. Z., Feldman, M., Yoon, J. S., Bennett, M. D., editor, Gropp, A., editor, and Wolf, U., editor
- Published
- 1984
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8. Definitive chromosomal location of the H-2 complex by in situ hybridization to pachytene chromosomes
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Lader, Eric, Clark, Brian T., Jhanwar, S. C., Chaganti, R. S. K., and Bennett, Dorothea
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- 1985
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9. Recursive partitioning analysis of prognostic variables in newly diagnosed anaplastic oligodendroglial tumors
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Panageas, K. S., primary, Reiner, A. S., additional, Iwamoto, F. M., additional, Cloughesy, T. F., additional, Aldape, K. D., additional, Rivera, A. L., additional, Eichler, A. F., additional, Louis, D. N., additional, Paleologos, N. A., additional, Fisher, B. J., additional, Ashby, L. S., additional, Cairncross, J. G., additional, Roldan Urgoiti, G. B., additional, Wen, P. Y., additional, Ligon, K. L., additional, Schiff, D., additional, Robins, H. I., additional, Rocque, B. G., additional, Chamberlain, M. C., additional, Mason, W. P., additional, Weaver, S. A., additional, Green, R. M., additional, Kamar, F. G., additional, Abrey, L. E., additional, DeAngelis, L. M., additional, Jhanwar, S. C., additional, Rosenblum, M. K., additional, and Lassman, A. B., additional
- Published
- 2014
- Full Text
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10. Response to Weltman and Fleury Malheiros, re Lassman et al.
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Lassman, A. B., primary, Iwamoto, F. M., additional, Cloughesy, T. F., additional, Aldape, K. D., additional, Rivera, A. L., additional, Eichler, A. F., additional, Louis, D. N., additional, Paleologos, N. A., additional, Fisher, B. J., additional, Ashby, L. S., additional, Cairncross, J. G., additional, Roldan Urgoiti, G. B., additional, Wen, P. Y., additional, Ligon, K. L., additional, Schiff, D., additional, Robins, H. I., additional, Rocque, B. G., additional, Chamberlain, M. C., additional, Mason, W. P., additional, Weaver, S. A., additional, Green, R. M., additional, Kamar, F. G., additional, Abrey, L. E., additional, DeAngelis, L. M., additional, Jhanwar, S. C., additional, Rosenblum, M. K., additional, and Panageas, K. S., additional
- Published
- 2012
- Full Text
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11. Initial treatment patterns over time for anaplastic oligodendroglial tumors
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Panageas, K. S., primary, Iwamoto, F. M., additional, Cloughesy, T. F., additional, Aldape, K. D., additional, Rivera, A. L., additional, Eichler, A. F., additional, Louis, D. N., additional, Paleologos, N. A., additional, Fisher, B. J., additional, Ashby, L. S., additional, Cairncross, J. G., additional, Roldan Urgoiti, G. B., additional, Wen, P. Y., additional, Ligon, K. L., additional, Schiff, D., additional, Robins, H. I., additional, Rocque, B. G., additional, Chamberlain, M. C., additional, Mason, W. P., additional, Weaver, S. A., additional, Green, R. M., additional, Kamar, F. G., additional, Abrey, L. E., additional, DeAngelis, L. M., additional, Jhanwar, S. C., additional, Rosenblum, M. K., additional, and Lassman, A. B., additional
- Published
- 2012
- Full Text
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12. Molecular diagnosis of synovial sarcoma and characterization of a variant SYT-SSX2 fusion transcript
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Fligman, I., Lonardo, F., Jhanwar, S. C., Gerald, W. L., Woodruff, J., and Ladanyi, M.
- Subjects
Adult ,Male ,Neoplasms, Connective Tissue ,Adolescent ,Base Sequence ,Transcription, Genetic ,Recombinant Fusion Proteins ,Molecular Sequence Data ,Proteins ,Middle Aged ,Polymerase Chain Reaction ,Translocation, Genetic ,Neoplasm Proteins ,Repressor Proteins ,Sarcoma, Synovial ,Proto-Oncogene Proteins ,Humans ,Female ,Amino Acid Sequence ,RNA, Neoplasm ,Research Article ,Aged - Abstract
The translocation t(X;18)(p11;q11) is seen in > 80% of synovial sarcomas (SS) with informative karyotypes. The breakpoints of the t(X;18) have been cloned and shown to involve two novel genes, SSX (at Xp11) and SYT (at 18q11), which produce a chimeric SYT-SSX transcript as a result of the translocation. Recently, SSX has been shown to be duplicated, with both copies, SSX1 and SSX2, located within distinct subregions of Xp11. We performed a reverse transcriptase polymerase chain reaction (RT-PCR) assay for both chimeric SYT-SSX transcripts in a series of 35 SS (29 monophasic, 6 biphasic) to assess its usefulness in molecular diagnosis and to evaluate the incidence of molecular variants. Of the 35 cases, 29 (83%) showed a specific SYT-SSX RT-PCR product, using a consensus primer for SSX1 and SSX2 Upon excluding three negative cases that had poor quality RNA, the proportion of positives rose to 91% (29/32). The 29 positive cases were further studied using primers specific for either SSX1 or SSX2; 19 cases were positive for SYT-SSX1 and 10 for SYT-SSX2. The relationship of histological subtype (monophasic versus biphasic) to SSX1 or SSX2 involvement was not statistically significant. In a single histologically unremarkable monophasic SS, a slightly larger SYT-SSX2 RT-PCR product was observed. Sequencing of this novel variant showed a 129-bp segment inserted between the usual SYT and SSX2 fusion points, of which 126 bp were derived from a more proximal (5') portion of SSX2 The 3 bp immediately 5' to the fusion point could not be assigned to either SYT or SSX2 and may represent an insertion-deletion or a cryptic splicing event. This fragment maintains the reading frame of the chimeric product and encodes a predicted protein larger by 43 amino acids, which nevertheless replaces the region homologous to the transcriptional repression domain Kruppel-associated box, recently recognized in the 5' portion of the SSX genes, with all but the 3' end of the SYT transcript. Thus, a diagnosis of SS may be confirmed in > 90% of cases using RT-PCR detection of the chimeric transcript resulting from the t(X;18), and the incidence of molecular variants appears low.
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- 1995
13. MEDICAL AND NEURO-ONCOLOGY
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Prithviraj, G. K., primary, Sommers, S. R., additional, Jump, R. L., additional, Halmos, B., additional, Chambless, L. B., additional, Parker, S. L., additional, Hassam-Malani, L., additional, McGirt, M. J., additional, Thompson, R. C., additional, Hunter, K., additional, Chamberlain, M. C., additional, Le, E. M., additional, Lee, E. L. T., additional, Sadighi, Z. S., additional, Pearlman, M. L., additional, Slopis, J. M., additional, Vats, T. S., additional, Khatua, S., additional, DeVito, N. C., additional, Yu, M., additional, Chen, R., additional, Pan, E., additional, Cloughesy, T., additional, Raizer, J., additional, Drappatz, J., additional, Gerena-Lewis, M., additional, Rogerio, J., additional, Yacoub, S., additional, Desjardin, A., additional, Groves, M. D., additional, DeGroot, J., additional, Loghin, M., additional, Conrad, C. A., additional, Hess, K., additional, Ni, J., additional, Ictech, S., additional, Yung, W. A., additional, Porter, A. B., additional, Dueck, A. C., additional, Karlin, N. J., additional, Olson, J., additional, Silber, J., additional, Reiner, A. S., additional, Panageas, K. S., additional, Iwamoto, F. M., additional, Cloughesy, T. F., additional, Aldape, K. D., additional, Rivera, A. L., additional, Eichler, A. F., additional, Louis, D. N., additional, Paleologos, N. A., additional, Fisher, B. J., additional, Ashby, L. S., additional, Cairncross, J. G., additional, Roldan, G. B., additional, Wen, P. Y., additional, Ligon, K. L., additional, Shiff, D., additional, Robins, H. I., additional, Rocque, B. G., additional, Mason, W. P., additional, Weaver, S. A., additional, Green, R. M., additional, Kamar, F. G., additional, Abrey, L. E., additional, DeAngelis, L. M., additional, Jhanwar, S. C., additional, Rosenblum, M. K., additional, Lassman, A. B., additional, Cachia, D., additional, Alderson, L., additional, Moser, R., additional, Smith, T., additional, Yunus, S., additional, Saito, K., additional, Mukasa, A., additional, Narita, Y., additional, Tabei, Y., additional, Shinoura, N., additional, Shibui, S., additional, Saito, N., additional, Flechl, B., additional, Ackerl, M., additional, Sax, C., additional, Dieckmann, K., additional, Crevenna, R., additional, Widhalm, G., additional, Preusser, M., additional, Marosi, C., additional, Ay, C., additional, Dunkler, D., additional, Pabinger, I., additional, Zielinski, C., additional, Belongia, M., additional, Jogal, S., additional, Schlingensiepen, K.-H., additional, Bogdahn, U., additional, Stockhammer, G., additional, Mahapatra, A. K., additional, Venkataramana, N. K., additional, Oliushine, V., additional, Parfenov, V., additional, Poverennova, I., additional, Hau, P., additional, Jachimczak, P., additional, Heinrichs, H., additional, Mammoser, A. G., additional, Shonka, N. A., additional, de Groot, J. F., additional, Shibahara, I., additional, Sonoda, Y., additional, Kumabe, T., additional, Saito, R., additional, Kanamori, M., additional, Yamashita, Y., additional, Watanabe, M., additional, Ishioka, C., additional, Tominaga, T., additional, Silvani, A., additional, Gaviani, P., additional, Lamperti, E., additional, Botturi, A., additional, DiMeco, F., additional, Broggi, G., additional, Fariselli, L., additional, Solero, C. L., additional, Salmaggi, A., additional, Woyshner, E. A., additional, Shu, F., additional, Oh, Y. S., additional, Iganej, S., additional, Singh, G., additional, Vemuri, S. L., additional, Theeler, B. J., additional, Ellezam, B., additional, Gilbert, M. R., additional, Aoki, T., additional, Kobayashi, H., additional, Takano, S., additional, Nishikawa, R., additional, Nagane, M., additional, Muragaki, Y., additional, Sugiyama, K., additional, Kuratsu, J., additional, Matsutani, M., additional, Langford, L. A., additional, Puduvalli, V. K., additional, Shen, D., additional, Chen, Z.-p., additional, Zhang, J.-p., additional, Bedekar, D., additional, Rand, S., additional, Connelly, J., additional, Malkin, M., additional, Paulson, E., additional, Mueller, W., additional, Schmainda, K., additional, Gallego, O., additional, Benavides, M., additional, Segura, P. P., additional, Balana, C., additional, Gil, M., additional, Berrocal, A., additional, Reynes, G., additional, Garcia, J. L., additional, Murata, P., additional, Bague, S., additional, Quintana, M. J., additional, Vasishta, V. G., additional, Kobayashi, K., additional, Tanaka, M., additional, Tsuchiya, K., additional, Shiokawa, Y., additional, Bavle, A. A., additional, Ayyanar, K., additional, Prado, M. P., additional, Hess, K. R., additional, Liu, V., additional, de Groot, J., additional, Loghin, M. E., additional, Colman, H., additional, Levin, V. A., additional, Alfred Yung, W. K., additional, Hackney, J. R., additional, Palmer, C. A., additional, Markert, J. M., additional, Cure, J., additional, Riley, K. O., additional, Fathallah-Shaykh, H., additional, Nabors, L. B., additional, Saria, M. G., additional, Corle, C., additional, Hu, J., additional, Rudnick, J., additional, Phuphanich, S., additional, Mrugala, M. M., additional, Lee, L. K., additional, Fu, B. D., additional, Bota, D. A., additional, Kim, R. Y., additional, Brown, T., additional, Feely, H., additional, Hu, A., additional, Lee, J. W., additional, Carter, B., additional, Kesari, S., additional, Kong, X.-T., additional, Sparagana, S., additional, Belousova, E., additional, Jozwiak, S., additional, Korf, B., additional, Frost, M., additional, Kuperman, R., additional, Kohrman, M., additional, Witt, O., additional, Wu, J., additional, Flamini, R., additional, Jansen, A., additional, Curtalolo, P., additional, Thiele, E., additional, Whittemore, V., additional, De Vries, P., additional, Ford, J., additional, Shah, G., additional, Cauwel, H., additional, Edrich, P., additional, Sahmoud, T., additional, Franz, D., additional, Khasraw, M., additional, Brown, C., additional, Ashley, D. M., additional, Rosenthal, M. A., additional, Jiang, X., additional, Mou, Y. g., additional, Chen, Z. p., additional, Oh, M., additional, kim, E., additional, Chang, J., additional, Juratli, T. A., additional, Kirsch, M., additional, Schackert, G., additional, Krex, D., additional, Wang, M., additional, Stupp, R., additional, Hegi, M., additional, Jaeckle, K. A., additional, Armstrong, T. S., additional, Wefel, J. S., additional, Won, M., additional, Blumenthal, D. T., additional, Mahajan, A., additional, Schultz, C. J., additional, Erridge, S. C., additional, Brown, P. D., additional, Chakravarti, A., additional, Curran, W. J., additional, Mehta, M. P., additional, Hofland, K. F., additional, Hansen, S., additional, Sorensen, M., additional, Schultz, H., additional, Muhic, A., additional, Engelholm, S., additional, Ask, A., additional, Kristiansen, C., additional, Thomsen, C., additional, Poulsen, H. S., additional, Lassen, U. N., additional, Zalatimo, O., additional, Weston, C., additional, Zoccoli, C., additional, Glantz, M., additional, Rahmanuddin, S., additional, Shiroishi, M. S., additional, Cen, S. Y., additional, Jones, J., additional, Chen, T., additional, Pagnini, P., additional, Go, J., additional, Lerner, A., additional, Gomez, J., additional, Law, M., additional, Ram, Z., additional, Wong, E. T., additional, Gutin, P. H., additional, Bobola, M. S., additional, Alnoor, M., additional, Silbergeld, D. L., additional, Rostomily, R. C., additional, Silber, J. R., additional, Martha, N., additional, Jacqueline, S., additional, Thaddaus, G., additional, Daniel, P., additional, Hans, M., additional, Armin, M., additional, Eugen, T., additional, Gunther, S., additional, Hutterer, M., additional, Tseng, H.-M., additional, Zoccoli, C. M., additional, Patel, A., additional, Rizzo, K., additional, Sheehan, J. M., additional, Sumrall, A. L., additional, Vredenburgh, J. J., additional, Desjardins, A., additional, Reardon, D. A., additional, Friiedman, H. S., additional, Peters, K. B., additional, Taylor, L. P., additional, Stewart, M., additional, Blondin, N. A., additional, Baehring, J. M., additional, Foote, T., additional, Laack, N., additional, Call, J., additional, Hamilton, M. G., additional, Walling, S., additional, Eliasziw, M., additional, Easaw, J., additional, Shirsat, N. V., additional, Kundar, R., additional, Gokhale, A., additional, Goel, A., additional, Moiyadi, A. A., additional, Wang, J., additional, Mutlu, E., additional, Oyan, A., additional, Yan, T., additional, Tsinkalovsky, O., additional, Jacobsen, H. K., additional, Talasila, K. M., additional, Sleire, L., additional, Pettersen, K., additional, Miletic, H., additional, Andersen, S., additional, Mitra, S., additional, Weissman, I., additional, Li, X., additional, Kalland, K.-H., additional, Enger, P. O., additional, Sepulveda, J., additional, Belda, C., additional, Sitt, R., additional, Phishniak, L., additional, Bokstein, F., additional, Philippe, M., additional, Carole, C., additional, Andre, M. d. P., additional, Marylin, B., additional, Olivier, C., additional, L'Houcine, O., additional, Dominique, F.-B., additional, Isabelle, N.-M., additional, Frederic, F., additional, Stephane, F., additional, Henry, D., additional, Errico, M. A., additional, Kunschner, L. J., additional, Soffietti, R., additional, Trevisan, E., additional, Ruda, R., additional, Bertero, L., additional, Bosa, C., additional, Fabrini, M. G., additional, Lolli, I., additional, Jalali, R., additional, Julka, P. K., additional, Anand, A. K., additional, Bhavsar, D., additional, Singhal, N., additional, Naik, R., additional, John, S., additional, Mathew, B. S., additional, Thaipisuttikul, I., additional, Graber, J., additional, Shirinian, M., additional, Fontebasso, A. M., additional, Jacob, K., additional, Gerges, N., additional, Montpetit, A., additional, Nantel, A., additional, Albrecht, S., additional, Jabado, N., additional, Shah, K., additional, Di, K., additional, Linskey, M., additional, Thon, N., additional, Eigenbrod, S., additional, Kreth, S., additional, Lutz, J., additional, Tonn, J.-C., additional, Kretzschmar, H., additional, Peraud, A., additional, Kreth, F.-W., additional, Muggeri, A. D., additional, Alderuccio, J. P., additional, Diez, B. D., additional, Jiang, P., additional, Chao, Y., additional, Gallagher, M., additional, Kim, R., additional, Pastorino, S., additional, Fogal, V., additional, Rudnick, J. D., additional, Bresee, C., additional, Rogatko, A., additional, Sakowsky, S., additional, Franco, M., additional, Lim, S., additional, Lopez, A., additional, Yu, L., additional, Ryback, K., additional, Tsang, V., additional, Lill, M., additional, Steinberg, A., additional, Sheth, R., additional, Grimm, S., additional, Helenowski, I., additional, Rademaker, A., additional, Nunes, F. P., additional, Merker, V., additional, Jennings, D., additional, Caruso, P., additional, Muzikansky, A., additional, Stemmer-Rachamimov, A., additional, Plotkin, S., additional, Spalding, A. C., additional, Vitaz, T. W., additional, Sun, D. A., additional, Parsons, S., additional, Welch, M. R., additional, Omuro, A., additional, Beal, K., additional, Correa, D., additional, Chan, T., additional, DeAngelis, L., additional, Gavrilovic, I., additional, Nolan, C., additional, Hormigo, A., additional, Kaley, T., additional, Mellinghoff, I., additional, Grommes, C., additional, Panageas, K., additional, Reiner, A., additional, Barradas, R., additional, Abrey, L., additional, Gutin, P., additional, Lee, S. Y., additional, Slagle-Webb, B., additional, Glantz, M. J., additional, Connor, J. R., additional, Schlimper, C. A., additional, Schlag, H., additional, Stoffels, G., additional, Weber, F., additional, Krueger, D. A., additional, Care, M. M., additional, Holland, K., additional, Agricola, K., additional, Tudor, C., additional, Byars, A., additional, Franz, D. N., additional, Rice, L., additional, Chandler, J., additional, Levy, R., additional, Muro, K., additional, Nayak, L., additional, Norden, A. D., additional, Kaley, T. J., additional, Thomas, A. A., additional, Fadul, C. E., additional, Meyer, L. P., additional, Lallana, E. C., additional, Gilbert, M., additional, Aldape, K., additional, De Groot, J., additional, Conrad, C., additional, Levin, V., additional, Groves, M., additional, Chris, P., additional, Puduvalli, V., additional, Nagpal, S., additional, Feroze, A., additional, Recht, L., additional, Rangarajan, H. G., additional, Kieran, M. W., additional, Scott, R. M., additional, Lew, S. M., additional, Firat, S. Y., additional, Segura, A. D., additional, Jogal, S. A., additional, Kumthekar, P. U., additional, Grimm, S. A., additional, Avram, M., additional, Patel, J., additional, Kaklamani, V., additional, McCarthy, K., additional, Cianfrocca, M., additional, Gradishar, W., additional, Mulcahy, M., additional, Von Roenn, J., additional, Galanis, E., additional, Anderson, S. K., additional, Lafky, J. M., additional, Kaufmann, T. J., additional, Uhm, J. H., additional, Giannini, C., additional, Kumar, S. K., additional, Northfelt, D. W., additional, Flynn, P. J., additional, Buckner, J. C., additional, Omar, A. I., additional, Schiff, D., additional, Delios, A., additional, Jakubowski, A., additional, Melguizo-Gavilanes, I., additional, Qiao, W., additional, Wang, X., additional, Hashemi-Sadraei, N., additional, Bawa, H., additional, Rahmathulla, G., additional, Patel, M., additional, Elson, P., additional, Stevens, G., additional, Peereboom, D., additional, Vogelbaum, M., additional, Weil, R., additional, Barnett, G., additional, Ahluwalia, M. S., additional, Alvord, E. C., additional, Rockne, R. C., additional, Rockhill, J. K., additional, Rostomily, R., additional, Lai, A., additional, Wardlaw, J., additional, Spence, A. M., additional, Swanson, K. R., additional, Zadeh, G., additional, Alahmadi, H., additional, Wilson, J., additional, Gentili, F., additional, Beumer, J. J., additional, Wright, J., additional, Takebe, N., additional, Gaur, R., additional, Werner-Wasik, M., additional, Gupta, A. J., additional, Campos-Gines, A., additional, Le, K., additional, Arango, C., additional, Richards, M., additional, Landeros, M., additional, Juan, H., additional, Chang, J. H., additional, Kim, J. S., additional, Cho, J. H., additional, Seo, C. O., additional, Baldock, A. L., additional, Rockne, R., additional, Canoll, P., additional, Born, D., additional, Yagle, K., additional, Alexandru, D., additional, Bota, D., additional, Linskey, M. E., additional, Nabeel, S., additional, Raval, S. N., additional, Rosenow, J., additional, Bredel, M., additional, New, P. Z., additional, Plotkin, S. R., additional, Supko, J. G., additional, Curry, W. T., additional, Chi, A. S., additional, Gerstner, E. R., additional, Batchelor, T. T., additional, Hashemi, N., additional, Chao, S. T., additional, Weil, R. J., additional, Suh, J. H., additional, Vogelbaum, M. A., additional, Stevens, G. H., additional, Barnett, G. H., additional, Corwin, D., additional, Holdsworth, C., additional, Stewart, R., additional, Swanson, K., additional, Graber, J. J., additional, Anderson, A. R., additional, Jeyapalan, S., additional, Goldman, M., additional, Boxerman, J., additional, Donahue, J., additional, Elinzano, H., additional, Evans, D., additional, O'Connor, B., additional, Puthawala, M. Y., additional, Oyelese, A., additional, Cielo, D., additional, Blitstein, M., additional, Dargush, M., additional, Santaniello, A., additional, Constantinou, M., additional, DiPetrillo, T., additional, Safran, H., additional, Halpin, C., additional, Barker, F. G., additional, Maher, E. A., additional, Ganji, S., additional, DeBerardinis, R., additional, Hatanpaa, K., additional, Rakheja, D., additional, Yang, X.-L., additional, Mashimo, T., additional, Raisanen, J., additional, Madden, C., additional, Mickey, B., additional, Malloy, C., additional, Bachoo, R., additional, Choi, C., additional, Ranjan, T., additional, Yono, N., additional, Han, S. J., additional, Sun, M., additional, Berger, M. S., additional, Aghi, M., additional, Gupta, N., additional, and Parsa, A. T., additional
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- 2011
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14. International retrospective study of over 1000 adults with anaplastic oligodendroglial tumors
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Lassman, A. B., primary, Iwamoto, F. M., additional, Cloughesy, T. F., additional, Aldape, K. D., additional, Rivera, A. L., additional, Eichler, A. F., additional, Louis, D. N., additional, Paleologos, N. A., additional, Fisher, B. J., additional, Ashby, L. S., additional, Cairncross, J. G., additional, Roldan, G. B., additional, Wen, P. Y., additional, Ligon, K. L., additional, Schiff, D., additional, Robins, H. I., additional, Rocque, B. G., additional, Chamberlain, M. C., additional, Mason, W. P., additional, Weaver, S. A., additional, Green, R. M., additional, Kamar, F. G., additional, Abrey, L. E., additional, DeAngelis, L. M., additional, Jhanwar, S. C., additional, Rosenblum, M. K., additional, and Panageas, K. S., additional
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- 2011
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15. ETV6-ABL1-positive "chronic myeloid leukemia": clinical and molecular response to tyrosine kinase inhibition
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Perna, F., primary, Abdel-Wahab, O., additional, Levine, R. L., additional, Jhanwar, S. C., additional, Imada, K., additional, and Nimer, S. D., additional
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- 2010
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16. The promyelocytic leukemia zinc-finger gene, PLZF, is frequently downregulated in malignant mesothelioma cells and contributes to cell survival
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Cheung, M, primary, Pei, J, additional, Pei, Y, additional, Jhanwar, S C, additional, Pass, H I, additional, and Testa, J R, additional
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- 2009
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17. Neuroblastoma and treatment-related myelodysplasia/leukemia: the Memorial Sloan-Kettering experience and a literature review.
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Kushner, B H, primary, Cheung, N K, additional, Kramer, K, additional, Heller, G, additional, and Jhanwar, S C, additional
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- 1998
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18. EWS-FLI1 fusion transcript structure is an independent determinant of prognosis in Ewing's sarcoma.
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de Alava, E, primary, Kawai, A, additional, Healey, J H, additional, Fligman, I, additional, Meyers, P A, additional, Huvos, A G, additional, Gerald, W L, additional, Jhanwar, S C, additional, Argani, P, additional, Antonescu, C R, additional, Pardo-Mindan, F J, additional, Ginsberg, J, additional, Womer, R, additional, Lawlor, E R, additional, Wunder, J, additional, Andrulis, I, additional, Sorensen, P H, additional, Barr, F G, additional, and Ladanyi, M, additional
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- 1998
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19. High frequency of inactivating mutations in the neurofibromatosis type 2 gene (NF2) in primary malignant mesotheliomas.
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Bianchi, A B, primary, Mitsunaga, S I, additional, Cheng, J Q, additional, Klein, W M, additional, Jhanwar, S C, additional, Seizinger, B, additional, Kley, N, additional, Klein-Szanto, A J, additional, and Testa, J R, additional
- Published
- 1995
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20. Molecular cytogenetic analysis of follicular lymphoma (FL) provides detailed characterization of chromosomal instability associated with the t(14;18)(q32;q21) positive and negative subsets and histologic progression.
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Nanjangud, G., Rao, P. H., Teruya-Feldstein, J., Donnelly, G., Qin, J., Mehra, S., Jhanwar, S. C., Zelenetz, A. D., and Chaganti, R. S. K.
- Subjects
CYTOGENETICS ,LYMPHOMAS ,KARYOTYPES ,HODGKIN'S disease ,CYTOLOGY - Abstract
We analyzed a cohort of 61 follicular lymphomas (FL) with an abnormal G-banded karyotype by spectral karyotyping (SKY) to better define the chromosome instability associated with the t(14;18)(q32;q21) positive and negative subsets of FL and histologic grade. In more than 70% of the patients, SKY provided additional cytogenetic information and up to 40% of the structural abnormalities were revised. The six most frequent breakpoints in both SKY and G-banding analyses were 14q32, 18q21, 3q27, 1q11–q21, 6q11–q15 and 1p36 (15–77%). SKY detected nine additional sites (1p11–p13, 2p11–p13, 6q21, 8q24, 6q21, 9p13, 10q22–q24, 12q11–q13 and 17q11–q21) at an incidence of >10%. In addition to the known recurring translocations, t(14;18)(q32;q21) [70%], t(3;14)(q27;q32) [10%], t(1;14)(q21;q32) [5%] and t(8;14)(q24;q32) [2%] and their variants, 125 non-IG gene translocations were identified of which four were recurrent within this series. In contrast to G-banding analysis, SKY revealed a greater degree of karyotypic instability in the t(14;18) (q32;q21) negative subset compared to the t(14;18)(q32;q21) positive subset. Translocations of 3q27 and gains of chromosome 1 were significantly more frequent in the former subset. SKY also allowed a better definition of chromosomal imbalances, thus 37% of the deletions detected by G-banding were shown to be unbalanced translocations leading to gain of genetic material. The majority of recurring (>10%) imbalances were detected at a greater (2–3 fold) incidence by SKY and several regions were narrowed down, notably at gain 2p13–p21, 2q11–q21, 2q31–q37, 12q12–q15, 17q21–q25 and 18q21. Chromosomal abnormalities among the different histologic grades were consistent with an evolution from low to high grade disease and breaks at 6q11–q15 and 8q24 and gain of 7/7q and 8/8q associated significantly with histologic progression. This study also indicates that in addition to gains and losses, non-IG gene translocations involving 1p11–p13, 1p36, 1q11–q21, 8q24, 9p13, and 17q11–q21 play an important role in the histologic progression of FL with t(14;18)(q32;q21) and t(3q27). Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]
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- 2007
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21. Cytogenetic and Immunohistochemical Evidence for the Germ Cell Origin of a Subset of Acute Leukemias Associated With Mediastinal Germ Cell Tumors
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Ladanyi, M., primary, Samaniego, F., additional, Reuter, V. E., additional, Motzer, R. J., additional, Jhanwar, S. C., additional, Bosl, G. J., additional, and Chaganti, R. S. K., additional
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- 1990
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22. Engraftment and growth of patient-derived retinoblastoma tumour in severe combined immunodeficiency mice
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Yan, Y., Dunkel, I. J., Guan, X., Abramson, D. H., Jhanwar, S. C., and O'Reilly, R. J.
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- 2000
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23. Interferon-inducible gene maps to a chromosomal band associated with a (4;11) translocation in acute leukemia cells.
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Luster, A D, Jhanwar, S C, Chaganti, R S, Kersey, J H, and Ravetch, J V
- Abstract
An interferon-inducible cytokine, IP-10, containing homology to a family of proteins having chemotactic (platelet factor 4, beta-thromboglobulin) and mitogenic (connective tissue-activating peptide III) activities has been mapped to chromosome 4 at band q21, a locus associated with an acute monocytic/B-lymphocyte lineage leukemia that exhibits the nonrandom translocation t(4;11)(q21;q23). In situ hybridization of t(4;11)(q21;q23)-carrying leukemic cells revealed that the IP-10 gene is proximal to the breakpoint of this translocation. No DNA rearrangement was evident when the IP-10 gene was hybridized to genomic DNA isolated from two patients' leukemic cells that contain t(4;11)(q21;q23). However, restriction fragment length polymorphism in the 5' region of the IP-10 gene was detected. The ETS1 protooncogene is located at 11q23 and is known to translocate to chromosome 4 in t(4;11) (q21;q23) and into the interferon gene cluster in (9;11) (p22;q23). Both translocations are associated with acute monocytic leukemia. These results suggest a model in which juxtaposition of genetic loci regulated by antiproliferative signals, such as interferon, next to an oncogene, like ETS1, could effectively short circuit homeostatic control circuits and contribute to the neoplastic state.
- Published
- 1987
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24. Two human c-onc genes are located on the long arm of chromosome 8.
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Neel, B G, Jhanwar, S C, Chaganti, R S, and Hayward, W S
- Abstract
We have used in situ chromosome hybridization techniques to map the human cellular counterparts (c-onc genes) of the transforming genes of two RNA tumor viruses on human meiotic pachytene and somatic metaphase chromosomes. We find that the human c-mos gene is located on chromosome 8 at a position corresponding to band 8q22 on the somatic map. The human c-myc gene is found on chromosome 8 at position 8q24. These regions on the long arm of chromosome 8 have been previously reported to be involved in specific translocations found in the M-2 subset of acute nonlymphoblastic leukemias. Burkitt lymphoma, and other forms of non-Hodgkin lymphoma, and a familial abnormality that predisposes to renal cell carcinoma. These results suggest that translocations of the human c-mos or c-myc genes may be causally related to neoplastic transformation.
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- 1982
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25. Hormonal regulation of the p53 tumor suppressor protein in T47D human breast carcinoma cell line.
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Hurd, C, Khattree, N, Alban, P, Nag, K, Jhanwar, S C, Dinda, S, and Moudgil, V K
- Abstract
Under normal culturing conditions, the T47D human breast cancer cell line expresses progesterone receptor constitutively and is responsive to estrogen. Because the tumor suppressor protein p53 plays a central role in determining genetic stability and cell proliferation, we have examined the effects of 17 beta-estradiol, the synthetic progestin R5020, and the antiprogestin RU486 on the levels of this protein in T47D cells. Western blot analysis of cellular extracts, performed with a monoclonal antibody capable of quantitatively supershifting a specific p53-p53 response element complex in a gel mobility shift assay, detected a single immunoreactive band representing p53. When cells were grown for 4-5 days in culture medium containing charcoal-treated fetal calf serum, p53 levels declined to 10% of the level seen in the control (no charcoal treatment) group. Supplementation of culture medium containing charcoal-treated calf serum with 0.1-1 nM 17 beta-estradiol restored p53 to its normal levels. A 4-day treatment of cells with R5020 or RU486 lowered the p53 levels in cells grown in normal culturing conditions to 15 and 30% of control levels, respectively. R5020 and RU486 treatments also caused down-regulation and/or hyperphosphorylation of the progesterone receptor, which correlated with the down-regulation of p53. These observations by estradiol while R5020 down-regulates this protein. Since estradiol is known to promote cell proliferation, the induction of p53 observed in this study leads us to propose that estradiol stimulates p53 to regulate proliferation of T47D cells in culture.
- Published
- 1995
26. Localization of c-ras oncogene family on human germ-line chromosomes.
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Jhanwar, S C, Neel, B G, Hayward, W S, and Chaganti, R S
- Abstract
The c-ras family is a set of c-onc genes that are highly conserved in vertebrates. The genes in this family are homologous to the transforming genes of Harvey and Kirsten murine sarcoma viruses (v-Ha-ras and v-Ki-ras, respectively). Using an in situ molecular hybridization method, we detected three sites on the human pachytene chromosomes that exhibited significant hybridization to v-Ki-ras and v-Ha-ras probes. These were chromomere positions that corresponded to bands 11p14.1, 12p12.1, and 12q24.2 of somatic chromosomes. The relationship between these chromosomal sites and previously defined members of the human c-ras gene family is discussed. These chromosomal sites are known to be involved in specific chromosome changes in a variety of tumors and in several congenital disorders that predispose to neoplastic disease.
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- 1983
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27. A FISH assay for detection of excess chromosome 12p material to distinguish germ cell tumors from somatic carcinoma
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Elliott, R. M., Rao, M. K., Wang, K., Hikmat Al-Ahmadie, Chen, Y., Fine, S. W., Gopalan, A., Tickoo, S. K., Jhanwar, S. C., and Reuter, V. E.
28. MDM2 GENE AMPLIFICATION IN METASTATIC OSTEOSARCOMA
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Ladanyi, M., Cha, C., Lewis, R., Jhanwar, S. C., Huvos, A. G., and John Healey
29. Monoclonality of multifocal myxoid liposarcoma: Confirmation by analysis of TLS-CHOP or EWS-CHOP rearrangements
- Author
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Antonescu, C. R., Elahi, A., Healey, J. H., Murray Brennan, Lui, M. Y., Lewis, J., Jhanwar, S. C., Woodruff, J. M., and Ladanyi, M.
30. 13-cis-Retinoic acid does not increase the true remission rate and the duration of true remission (induced by cytotoxic chemotherapy) in patients with chronic phase chronic myelogenous leukemia.
- Author
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Arlin, Z A, primary, Mertelsmann, R, additional, Berman, E, additional, Gee, T, additional, Kurland, E, additional, Chaganti, R S, additional, Jhanwar, S C, additional, Moore, M A, additional, and Clarkson, B D, additional
- Published
- 1985
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31. Marrow cytogenetic and cell-culture analyses of the myelodysplastic syndromes: insights to pathophysiology and prognosis.
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Gold, E J, primary, Conjalka, M, additional, Pelus, L M, additional, Jhanwar, S C, additional, Broxmeyer, H, additional, Middleton, A B, additional, Clarkson, B D, additional, and Moore, M A, additional
- Published
- 1983
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32. Loss of Heterozygosity and Homozygous Deletion of the tpr Locus in Human Gastric Cancer
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Cunningham, J. D., Schwartz, G. K., Karpeh, M., Blundell, M., Kelson, D. P., Jhanwar, S. C., and Albino, A. P.
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- 1997
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33. Cytogenetic Analysis of Soft Tissue Sarcomas: Recurrent Chromosome Abnormalities in Malignant Peripheral Nerve Sheath Tumors (MPNST)
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Jhanwar, S. C., Chen, Q., Li, F. P., and Brennan, M. F.
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- 1994
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34. Characterization of 9q;15q Whole-Arm Translocation Derivatives in Non-Small Cell Lung Carcinomas by Fluorescence In Situ Hybridization
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Zhou, J.-Y., Taguchi, T., Siegfried, J. M., and Jhanwar, S. C.
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- 1993
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35. Deregulation of FCGR2B expression by 1q21 rearrangements in follicular lymphomas.
- Author
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Chen W, Palanisamy N, Schmidt H, Teruya-Feldstein J, Jhanwar SC, Zelenetz AD, Houldsworth J, and Chaganti RS
- Subjects
- Adult, Blotting, Southern methods, Chromosome Aberrations, Cloning, Molecular, Female, Gene Rearrangement, Humans, In Situ Hybridization, Fluorescence methods, Lymphoma, Non-Hodgkin genetics, Mutagenesis, Insertional, Proto-Oncogene Proteins c-bcl-2 genetics, Antigens, CD genetics, Chromosomes, Human, Pair 1, Chromosomes, Human, Pair 14, Gene Expression Regulation, Lymphoma, Follicular genetics, Receptors, IgG genetics, Translocation, Genetic
- Abstract
We report here the molecular cloning and characterization of a t(1;14)(q21;q32) in a follicular lymphoma (FL) with an unusual BCL2 aberration. Fluorescence in situ hybridization (FISH) and Southern blot analysis of tumor cells identified the translocation breakpoint within the 5' switch region of IGHG (Sgamma). We cloned the chimeric breakpoint region approximately 1.5 kbp downstream from the HindIII site of 5'Sgamma2 on chromosome 14q32 and identified a 360-bp novel segment with homology to the CpG island clone 11h8. Two BAC clones containing this sequence were isolated and mapped to 1q21 by FISH. BAC 342/P13 contained sequences homologous to Fcgamma receptors 2A, 3A, 2B, 3B, and a heat shock protein gene HSP70B. The translocation brought the Sgamma2 region of a productive IGH allele 20 approximately 30 kbp upstream of FCGR2B. As a result of the translocation, the b2 isoform of FCGR2B was overexpressed in the tumor. Screening of a panel of 76 B-cell lymphomas with 1q21-23 cytogenetic aberrations by Southern blot analysis using breakpoint probes identified an additional FL with a t(14;18)(q32;q21) and a breakpoint in the FCGR2B region. These results suggest that FCGR2B may be deregulated by 1q21 aberration in BCL2 rearranged FLs and possibly play a role in their progression.
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- 2001
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36. Frequent gain of chromosome 19 in megakaryoblastic leukemias detected by comparative genomic hybridization.
- Author
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Alvarez S, MacGrogan D, Calasanz MJ, Nimer SD, and Jhanwar SC
- Subjects
- Adult, Aged, Child, Preschool, Chromosome Aberrations, Chromosome Painting, Female, Humans, Male, Middle Aged, Nucleic Acid Hybridization, Chromosomes, Human, Pair 19 genetics, Gene Amplification genetics, Leukemia, Megakaryoblastic, Acute genetics
- Abstract
Acute megakaryocytic leukemia is a rare subtype of AML that is often difficult to diagnose; it is most commonly associated with Down syndrome in children. To identify chromosomal imbalances and rearrangements associated with acute megakaryocytic leukemia, we used G-banding, comparative genomic hybridization (CGH), and whole chromosome painting (WCP) on a variety of primary patients' samples and leukemia cell lines. The most common abnormality was gain of chromosome 19 or arm 19q, which was detected by CGH in four of 12 (33.3%) primary samples and nine of 11 (81.8%) cell lines. In none of the primary samples was this abnormality detected by G-banding analysis. WCP was used to define further the nature of the chromosome 19 gain in the cell lines, which was found to be due to the presence of additional 19q material on marker chromosomes or to cryptic translocations involving 19q. The most common chromosomal loss--detected only in the cell lines--was deletion of chromosomal band 13q14, which was seen in six of 11 (54.5%) cell lines. Other recurrent changes included gains of 1p, 6p, 8q, 11q, 15q, 17q, and 21q and losses of 2, 4q, 5q, 7q, 9p, and 11p. Combining conventional and molecular cytogenetic analyses defined recurrent clonal chromosomal abnormalities, which will aid in the identification of critical genes that are abnormal in acute megakaryocytic leukemia cells., (Copyright 2001 Wiley-Liss, Inc.)
- Published
- 2001
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37. Loss of heterozygosity analysis defines a 3-cM region of 15q commonly deleted in human malignant mesothelioma.
- Author
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De Rienzo A, Balsara BR, Apostolou S, Jhanwar SC, and Testa JR
- Subjects
- Alleles, Chromosome Mapping, Chromosomes, Artificial, Yeast, Heterozygote, Humans, In Situ Hybridization, Fluorescence, Microsatellite Repeats, Models, Genetic, Polymorphism, Genetic, Tumor Cells, Cultured, Chromosome Deletion, Chromosomes, Human, Pair 15, Loss of Heterozygosity, Mesothelioma genetics
- Abstract
Previous comparative genomic hybridization and allelic loss analyses demonstrated frequent deletions from 15q11.1-15 in malignant mesothelioma. Recurrent losses of 15q11-22 have also been reported in several other tumor types such as breast and colorectal cancers. To more precisely map the commonly deleted region, we have performed a high density loss of heterozygosity analysis of 46 malignant mesotheliomas, using 26 polymorphic microsatellite markers spanning the entire long arm of chromosome 15. Allelic loss from 15q was observed in 22 of 46 (48%) cases. These analyses have defined a minimally deleted region of approximately 3-cM, which was confirmed to reside at 15q15 by fluorescence in situ hybridization analysis with yeast artificial chromosome probes. No tumor suppressor genes have been reported to map to this site. The minimally deleted region identified in this investigation overlaps those observed in other kinds of cancer, and is the smallest site of recurrent 15q loss identified to date in human tumors. The identification of this commonly deleted site implicates a putative tumor suppressor gene(s) at 15q15 involved in diverse forms of human neoplasia.
- Published
- 2001
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38. Identification of candidate genes on chromosome band 20q12 by physical mapping of translocation breakpoints found in myeloid leukemia cell lines.
- Author
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MacGrogan D, Alvarez S, DeBlasio T, Jhanwar SC, and Nimer SD
- Subjects
- Base Sequence, Blotting, Southern, Chromosomes, Artificial, Yeast, DNA Primers, Gene Expression, Humans, In Situ Hybridization, Fluorescence, Leukemia, Myeloid pathology, Loss of Heterozygosity, Microsatellite Repeats genetics, Reverse Transcriptase Polymerase Chain Reaction, Tumor Cells, Cultured, Chromosome Fragility, Chromosomes, Human, Pair 20, Leukemia, Myeloid genetics, Translocation, Genetic
- Abstract
Deletions of the long arm of chromosome 20 have been reported in a wide range of myeloid disorders and may reflect loss of critical tumor suppressor gene(s). To identify such candidate genes, 65 human myeloid cell line DNAs were screened by polymerase chain reaction (PCR) for evidence of allelic loss at 39 highly polymorphic loci on the long arm of chromosome 20. A mono-allelic pattern was present in eight cell lines at multiple adjacent loci spanning the common deleted regions (CDRs) previously defined in primary hematological samples, suggesting loss of heterozygosity (LOH) at 20q. Fluorescence in situ hybridization (FISH) was then performed using a series of yeast artificial chromosomes (YACs) ordered in the CDR, and in five of eight cell lines, the deletions resulted from cytogenetically detectable whole chromosomal loss or large interstitial deletion, whereas in another cell line deletion was associated with an unbalanced translocation. LOH in the CMK megakaryocytic cell line, which has a hypotetraploid karyotype, was associated with a der(20)t(1;20)(q32;q12)x2 leading to complete deletion of the CDR. Three additional unbalanced translocations were found within the CDR and all three breakpoints mapped to a single YAC. We then used a series of P1 artificial chromosomes (PACs) spanning this YAC clone, and two PACs produced 'split' signals suggesting that they each span one of these breakpoints. Exon trapping using PACs that overlap the breakpoint regions yielded portions of six genes and evaluation of these genes as candidate tumor suppressor genes is underway. The limited information available about these genes suggests that the h-l(3)mbt gene is the most attractive candidate.
- Published
- 2001
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39. Rearrangement in the coding region of the MYCN gene in a subset of amplicons in a case of neuroblastoma with MYCN amplification.
- Author
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Chen B, Jhanwar SC, and Ladanyi M
- Subjects
- Abdominal Neoplasms pathology, Abdominal Neoplasms therapy, Base Sequence, Blotting, Southern, Child, Preschool, Chromosome Fragility, Combined Modality Therapy, DNA, Neoplasm analysis, Fatal Outcome, Gene Amplification, Humans, In Situ Hybridization, Fluorescence, Male, Molecular Sequence Data, Neuroblastoma secondary, Neuroblastoma therapy, Polymerase Chain Reaction, Abdominal Neoplasms genetics, Gene Rearrangement, Genes, myc genetics, Neuroblastoma genetics
- Abstract
The MYCN gene is often amplified but rarely rearranged in neuroblastoma. We report, for the first time, a rearrangement within the MYCN coding region in a metastatic neuroblastoma in a 3-year-old boy with MYCN amplification in his primary tumor. The rearrangement occurred 46 nucleotides downstream from the ATG codon in exon 2 of MYCN. The amplification level of the rearranged copies of the MYCN gene was lower than that of the unrearranged copies of MYCN. These results indicate that the rearrangement occurred after initial MYCN gene amplification. Monochromosomal somatic cell hybrid mapping of the novel region fused to exon 2 of MYCN localized it to chromosome 2, suggesting that this rearrangement resulted from an interstitial deletion, presumably within the MYCN amplicon itself.
- Published
- 2001
- Full Text
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40. Absence of post-transcriptional RNA modifications of BCL10 in human malignant mesothelioma and colorectal cancer.
- Author
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Apostolou S, Murthy SS, Kolachana P, Jhanwar SC, and Testa JR
- Subjects
- B-Cell CLL-Lymphoma 10 Protein, Chromosome Aberrations genetics, Chromosome Disorders, DNA Mutational Analysis, Humans, Point Mutation, Polymorphism, Single-Stranded Conformational, RNA, Neoplasm genetics, Sequence Deletion, Tumor Cells, Cultured, Adaptor Proteins, Signal Transducing, Colorectal Neoplasms genetics, Mesothelioma genetics, Mutation, Neoplasm Proteins genetics, RNA Processing, Post-Transcriptional genetics
- Abstract
The BCL10 gene, located at 1p22, has been implicated in a number of human malignancies, including malignant mesotheliomas (MMs) and colorectal carcinomas. Subsequent reports, however, have revealed an absence of BCL10 mutations in genomic DNA from such tumors. It has been proposed that some abnormalities of this gene may be found only in RNA and not in genomic DNA, suggesting that BCL10 may be mutated post-transcriptionally, rather than at the genomic level. To explore this possibility, we performed SSCP mutation analysis and direct sequencing of cDNA from 17 MM cell lines displaying LOH in 1p22, 12 MM tumor specimens, and 11 colon carcinoma cell lines. SSCP revealed several different band shifts in these samples. The nucleotide changes observed in the cDNA samples were also seen in matched genomic DNA and corresponded to known polymorphisms in the general population. Thus, we conclude the BCL10 mutations are absent at the cDNA level, and that this gene does not undergo "molecular misreading." Since BCL10 also does not possess mutations at the genomic DNA level, it can be ruled out as a gene involved in the pathogenesis of MM and colorectal cancer.
- Published
- 2001
- Full Text
- View/download PDF
41. Characterization and drug sensitivity of four newly established colon adenocarcinoma cell lines to antifolate inhibitors of thymidylate synthase.
- Author
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Longo GS, Izzo J, Gorlick R, Banerjee D, Jhanwar SC, and Bertino JR
- Subjects
- Adenocarcinoma enzymology, Adenocarcinoma genetics, Adenocarcinoma pathology, Aneuploidy, Animals, Antimetabolites, Antineoplastic metabolism, Blotting, Western, Cell Division drug effects, Chromosome Banding, Colonic Neoplasms enzymology, Colonic Neoplasms genetics, Colonic Neoplasms pathology, Drug Resistance, Neoplasm, Folic Acid Antagonists metabolism, Humans, Immunohistochemistry, Karyotyping, Kinetics, Mice, Mice, Nude, Thymidylate Synthase genetics, Thymidylate Synthase metabolism, Tumor Stem Cell Assay, Tumor Suppressor Protein p53 analysis, Tumor Suppressor Protein p53 immunology, Xenograft Model Antitumor Assays, Adenocarcinoma drug therapy, Antimetabolites, Antineoplastic pharmacology, Colonic Neoplasms drug therapy, Folic Acid Antagonists pharmacology, Thymidylate Synthase antagonists & inhibitors, Tumor Cells, Cultured
- Abstract
Four new cell lines were established from the primary tumors of patients with untreated colorectal adenocarcinoma. Drug sensitivity and characterization of these cell lines was performed. Three of the four cell lines formed colonies in soft agar and all were tumorigenic in nude mice. The cell lines were morphologically similar but had differences in growth characteristics. Two of the cell lines, C18 (CCCL-4) and C29 (CCCL-6), had a longer doubling time compared with C85 (CCCL-1) and C86 (CCCL-2). The C18 and C29 cell lines had chromosome 17 abnormalities and evidence by immunohistochemistry of a mutant p53 and had decreased levels of thymidylate synthase and dihydrofolate reductase proteins, associated with decreased thymidylate synthase catalytic activity in C18 and no detectable activity in C29. Raltitrexed and GW1843U89 showed potent cytotoxic activity and all four cell lines displayed similar cytotoxicity to these folate thymidylate synthase inhibitors. The C18 and C29 cell lines were in general resistant to the other agents tested (methotrexate, 5-fluorouracil, nolatrexed) when compared with the C85 and C86 cell lines. These new cell lines may be useful for the study of colorectal adenocarcinoma and for evaluating new drugs or treatment schedules.
- Published
- 2001
- Full Text
- View/download PDF
42. Establishment of a human cell line (SKI-DLCL-1) with a t(1;14)(q21;q32) translocation from the ascites of a patient with diffuse large cell lymphoma.
- Author
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Goy A, Gilles F, Remache Y, Filippa D, Portlock CS, Jhanwar SC, and Zelenetz AD
- Subjects
- Aged, Ascites genetics, Ascites pathology, Cytogenetic Analysis, Humans, Lymphoma, B-Cell genetics, Lymphoma, B-Cell pathology, Male, Tumor Cells, Cultured metabolism, Chromosomes, Human, Pair 1, Chromosomes, Human, Pair 14, Lymphoma, Large B-Cell, Diffuse genetics, Lymphoma, Large B-Cell, Diffuse pathology, Translocation, Genetic genetics, Tumor Cells, Cultured cytology
- Abstract
Cytogenetic abnormalities at chromosome 1q21 are among the most common second genetic events observed in Non-Hodgkin's Lymphomas and have prognostic significance. Recently, BCL9 has been cloned from a pre-B-cell lymphoblastic leukemia cell line, which carried a t(1:14)(q21;q32). However, among a panel of 39 B-cell malignancies with 1q21 translocation, only two cases showed rearrangement for the BCL9 gene. We report the establishment of a new lymphoma cell line from a patient with relapsed diffuse large cell lymphoma. This cell line SKI-DLCL-1 showed cell surface antigens identical to the original tumor and demonstrated the profile of a mature B-cell phenotype: CD19 and CD20 positive, CD5 and C10 negative. It carried a t(1;14)(q21;q32) translocation identical to the original tumor. Although the clinical presentation was an isolated effusion lymphoma, studies for HIV-1, HHV8 and EBV were all negative. Southern blot analysis demonstrated that BCL9 was not rearranged in the SKI-DLCL-1 cell line. In addition, the BCL9 gene was not over-expressed in SKI-DLCL-1 cell line. The identification of a new locus at 1q21 will help clarify the pathogenesis of B-cell malignancies with a translocation involving this locus.
- Published
- 2001
- Full Text
- View/download PDF
43. Comparison of a multiplex reverse transcriptase-polymerase chain reaction for BCR-ABL to fluorescence in situ hybridization, Southern blotting, and conventional cytogenetics in the monitoring of patients with Ph1-positive leukemias.
- Author
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Colleoni GW, Jhanwar SC, Ladanyi M, and Chen B
- Subjects
- Adolescent, Adult, Child, Female, Humans, K562 Cells, Male, Middle Aged, Tumor Cells, Cultured, Blotting, Southern, Cytogenetic Analysis, Genes, abl genetics, In Situ Hybridization, Fluorescence, Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics, Reverse Transcriptase Polymerase Chain Reaction
- Abstract
A multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) assay for both major forms of BCR-ABL was compared with fluorescence in situ hybridization (FISH), karyotyping, and Southern blotting for disease monitoring in 37 follow-up bone marrow samples from 32 patients with Ph1-positive leukemia. Of these 37 samples, 33 were from patients with chronic myeloid leukemia (CML) (26 post allogeneic bone marrow transplantation [AlloBMT] and seven during interferon-alpha therapy) and 4 from Ph1-positive acute lymphoblastic leukemia (ALL) patients (1 post AlloBMT and 3 post high dose chemotherapy). For the 27 samples studied after AlloBMT (26 CML and 1 Ph1-positive ALL) the time after transplantation ranged from 1 to 107 months (median 47.5 months). In 8 (22%) of the 37 samples there were discrepant results among methods. The discrepancy rates relative to other techniques were: karyotyping 17% (5 of 29), Southern blotting 18% (6 of 33), multiplex RT-PCR 8% (3 of 37), and FISH 8% (3 of 37). Therefore, the relative accuracy of each method for disease monitoring in Ph1-positive leukemia was: 83% (24 of 29) for karyotyping, 82% (27 of 33) for Southern blotting, 92% (34 of 37) for FISH, and 92% (34 of 37) for multiplex RT-PCR. This multiplex RT-PCR assay appears equivalent to FISH in terms of accuracy, simplicity, and turnaround time and both are superior to Southern blot and conventional cytogenetics in the laboratory monitoring of Ph1-positive leukemias.
- Published
- 2000
- Full Text
- View/download PDF
44. Specificity of TLS-CHOP rearrangement for classic myxoid/round cell liposarcoma: absence in predominantly myxoid well-differentiated liposarcomas.
- Author
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Antonescu CR, Elahi A, Humphrey M, Lui MY, Healey JH, Brennan MF, Woodruff JM, Jhanwar SC, and Ladanyi M
- Subjects
- Blotting, Southern, Carcinoma, Small Cell classification, Chromosome Breakage genetics, Chromosome Mapping, Fibroma genetics, Heterogeneous-Nuclear Ribonucleoproteins, Histocytochemistry, Humans, Liposarcoma, Myxoid classification, RNA-Binding Protein EWS, RNA-Binding Protein FUS, Ribonucleoproteins genetics, Transcription Factor CHOP, Translocation, Genetic genetics, CCAAT-Enhancer-Binding Proteins genetics, Carcinoma, Small Cell diagnosis, Carcinoma, Small Cell genetics, Liposarcoma, Myxoid diagnosis, Liposarcoma, Myxoid genetics, Oncogene Proteins, Fusion genetics
- Abstract
Myxoid liposarcoma (LS), the most common subtype of LS, is known to be characterized by the specific t(12;16) resulting in a TLS-CHOP fusion in almost all cases. We wished to address the following questions: (i) Is this genetic hallmark also present in other types of LS with predominant myxoid change? (ii) What is the proportion of cases with the variant EWS-CHOP fusion? (iii) What is the optimal approach for Southern blot detection of TLS breakpoints? We identified 59 LS characterized histologically by >90% myxoid component, in which frozen tissue tumor was available for DNA extraction. These 59 LS with myxoid features were divided into 2 groups: 42 LS with classic myxoid/round cell appearance (myxoid LS) and 17 well-differentiated LS (WDLS) with a predominant (>90%) myxoid component. Within the myxoid LS group, 29 tumors were low grade and 13 high grade (>20% round cell component). Among the 17 predominantly myxoid WDLS, there were 15 low grade and 2 focally high grade tumors. In addition, we selected as control group, 20 LS of other histological types with minimal or no myxoid change (17 WDLS and 3 pleomorphic LS) and 13 myxofibrosarcomas. Southern blot analysis was performed in all cases using a CHOP cDNA probe, and in all CHOP rearranged cases using a TLS cDNA probe. Probe/enzyme combinations for Southern blot analysis were CHOP exon 3-4 cDNA probe with BamHI or SacI, TLS exon 3-6 cDNA probe with BclI. All 42 cases of myxoid LS showed a CHOP rearrangement and 38 of them also had a TLS rearrangement. Among the 4 myxoid LS without Southern blot evidence of TLS rearrangement, 1 showed an EWS-CHOP fusion by Southern blotting and reverse transcriptase-polymerase chain reaction and in another case, reverse transcriptase-polymerase chain reaction detected a TLS-CHOP fusion transcript. None of the predominantly myxoid WDLS and none of the tumors included in the control group showed rearranegements with CHOP probe. In addition, 12 predominantly myxoid WDLS, 10 other LS, and 5 myxofibrosarcoma from the control group were also tested for TLS rearrangement; all were negative. The TLS-CHOP fusion is highly sensitive and specific for the entity of classic myxoid/round cell LS. Other types of LS, even with a predominant myxoid component, lack the TLS-CHOP rearrangement, confirming that they represent a genetically distinct group of LS. The prevalence of the EWS-CHOP variant fusion was approximately 2% in this series. The optimal enzyme for TLS genomic breakpoint detection is BclI.
- Published
- 2000
- Full Text
- View/download PDF
45. Loss of heterozygosity analysis of 13q and 14q in human malignant mesothelioma.
- Author
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De Rienzo A, Jhanwar SC, and Testa JR
- Subjects
- Alleles, Humans, Karyotyping, Mesothelioma epidemiology, Pleural Neoplasms epidemiology, Tumor Cells, Cultured, Chromosomes, Human, Pair 13 genetics, Chromosomes, Human, Pair 14 genetics, Loss of Heterozygosity genetics, Mesothelioma genetics, Pleural Neoplasms genetics
- Abstract
Cytogenetic investigations of malignant mesothelioma (MM) have revealed frequent losses in chromosomes 13 and 14, suggesting that inactivation of tumor suppressor genes (TSGs) residing in these chromosomes may contribute to mesothelial cell tumorigenesis. To define the shortest region of overlap (SRO) of deletions from these chromosomes, we performed loss of heterozygosity (LOH) analyses on 30 MMs using 25 microsatellite markers in 13q and 21 markers in 14q. Twenty of the 30 MMs (67%) showed allelic loss of at least one marker in 13q. The SRO of deletions was delineated as an approximately 7 centiMorgan region, flanked by markers D13S1253 and D13S291, located at 13q13.3-14.2. Thirteen of the 30 MMs (43%) displayed allelic losses from 14q, with at least three distinct regions of LOH located at segments q11.2-13.2, q22.3-24.3, and q32. 12. These data highlight a single region of chromosomal loss in 13q in many MMs, implicating the involvement of a TSG that is critical to the pathogenesis of this malignancy. In contrast, the lower incidence and diffuse pattern of allelic losses in 14q suggest that several TSGs in this chromosome arm may contribute to tumorigenic progression in a subset of MMs. Genes Chromosomes Cancer 28:337-341, 2000., (Copyright 2000 Wiley-Liss, Inc.)
- Published
- 2000
46. Monoclonality of multifocal myxoid liposarcoma: confirmation by analysis of TLS-CHOP or EWS-CHOP rearrangements.
- Author
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Antonescu CR, Elahi A, Healey JH, Brennan MF, Lui MY, Lewis J, Jhanwar SC, Woodruff JM, and Ladanyi M
- Subjects
- Adult, Aged, Chromosomes, Human, Pair 12, Chromosomes, Human, Pair 16, Clone Cells, DNA Damage, DNA, Neoplasm isolation & purification, Female, Heterogeneous-Nuclear Ribonucleoproteins, Humans, Liposarcoma chemistry, Liposarcoma pathology, Male, Middle Aged, Neoplasms, Multiple Primary chemistry, Neoplasms, Multiple Primary pathology, RNA-Binding Protein EWS, RNA-Binding Protein FUS, RNA-Binding Proteins genetics, Reverse Transcriptase Polymerase Chain Reaction, Transcription Factor CHOP, Transcription, Genetic, Translocation, Genetic, CCAAT-Enhancer-Binding Proteins genetics, Gene Rearrangement, Liposarcoma genetics, Neoplasms, Multiple Primary genetics, Ribonucleoproteins genetics, Transcription Factors genetics
- Abstract
Multifocal presentation, defined as the presence of tumor at two or more anatomically separate sites, before the manifestation of disease in sites where sarcomas usually metastasize (e.g., lungs) occurs in about 1% of extremity soft tissue sarcomas (STSs). Debate still persists whether multifocal STSs represent an unusual pattern of metastasis or multiple separate primary tumors. Among STSs with multifocal presentation, myxoid liposarcoma is the predominant histological type. This subtype of liposarcoma contains the specific t(12;16) chromosomal translocation, which results in rearrangement of the TLS and CHOP genes that is clone specific at the DNA level. We, therefore, sought to address the question of clonality by molecular analysis in six patients who presented with either synchronous or metachronous multifocal myxoid liposarcoma. In all six cases, adequate frozen tumor was available for DNA extraction from at least two distinct anatomical sites. Southern blot analysis using CHOP, TLS, and EWS cDNA probes was performed on genomic DNA. Five cases contained a TLS-CHOP rearrangement, and one case had the variant EWS-CHOP fusion (seen in <5% of cases). The size of the rearranged CHOP fragment differed among the six patients, as expected, but was identical in all anatomically separate tumor samples from each patient. Likewise, the sizes of the rearranged bands observed with either the TLS or EWS probes supported the monoclonality of all cases. Our results confirm the monoclonal origin of multifocal myxoid liposarcoma, establishing the metastatic nature of distant soft tissue lesions in these cases. It remains unclear whether this unusual pattern of metastasis represents an intrinsic property of this subset of myxoid liposarcoma or merely a rare chance occurrence. The clinical outcomes observed in this small series suggest that the prognosis of multifocal myxoid liposarcoma is poor, regardless of its often bland or "low-grade" histological appearance.
- Published
- 2000
47. MUC1 is activated in a B-cell lymphoma by the t(1;14)(q21;q32) translocation and is rearranged and amplified in B-cell lymphoma subsets.
- Author
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Dyomin VG, Palanisamy N, Lloyd KO, Dyomina K, Jhanwar SC, Houldsworth J, and Chaganti RS
- Subjects
- B-Lymphocyte Subsets pathology, Base Sequence, Chromosome Mapping, Gene Expression Regulation, Neoplastic, Gene Rearrangement, Genetic Markers, Humans, Lymphoma, B-Cell pathology, Molecular Sequence Data, Chromosomes, Human, Pair 1, Chromosomes, Human, Pair 14, Lymphoma, B-Cell genetics, Mucins genetics, Translocation, Genetic
- Abstract
The band 1q21 is among the most common sites affected by chromosomal translocations in lymphoid, myeloid, epithelial, and sarcomatous lesions. In non-Hodgkin's lymphoma (NHL), translocations and duplications affecting this chromosomal site are frequently, but not exclusively, seen in association with primary abnormalities such as the t(14;18)(q32;q21) and t(8;14)(q24;q32) translocations, suggesting a role for 1q21 rearrangements in tumor progression. We report here the characterization and cloning of breakpoints in a case of extranodal ascitic B-cell lymphoma with a t(1;14)(q21;q32) translocation. The breakpoints on the der(1) and der(14) chromosomes were mapped by fluorescence in situ hybridization and Southern blot analysis and cloned using an IGHG (Cgamma) probe. The translocation linked the IGHG4 switch (Sgamma4) sequences of the productively rearranged allele to chromosome 1 sequences downstream of MUC1, leaving the MUC1 transcriptional unit intact. MUC1 was markedly overexpressed in the tumor at the mRNA and protein levels relative to lymphoma cell lines lacking a 1q21 rearrangement. Presumably, MUC1 transcription is aberrantly regulated by the IGHA (Calpha) 3' enhancer element retained on the same chromosome. Screening of a panel of B-cell lymphomas by Southern blot analysis identified a subset with a 3' MUC1 breakpoint and another with low-level amplification of MUC1. MUC-1 mucin has previously been shown to be frequently overexpressed in human epithelial cancers and to be associated with tumor progression and poor clinical outcome. Thus, MUC1 activation by chromosomal translocation, rearrangement, and amplification, identified here for the first time in NHL, is consistent with its suggested role in tumorigenesis. (Blood. 2000;95:2666-2671)
- Published
- 2000
48. Expression of GPC3, an X-linked recessive overgrowth gene, is silenced in malignant mesothelioma.
- Author
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Murthy SS, Shen T, De Rienzo A, Lee WC, Ferriola PC, Jhanwar SC, Mossman BT, Filmus J, and Testa JR
- Subjects
- Alleles, Animals, Cell Line, DNA Methylation, DNA, Complementary analysis, Down-Regulation, Female, Glypicans, Humans, Mesothelioma pathology, Promoter Regions, Genetic, Rats, Rats, Inbred F344, Heparan Sulfate Proteoglycans, Heparitin Sulfate genetics, Mesothelioma genetics, Proteoglycans genetics
- Abstract
Gene expression changes in rat asbestos-induced malignant mesothelioma (MM) cells were investigated by differential mRNA display. A mRNA transcript identified by this approach was abundant in normal rat mesothelial cells but not expressed in rat MM cell lines. Northern blot analysis confirmed that this transcript is uniformly silenced in rat MM cell lines and primary tumors. Nucleotide sequence analysis revealed that this transcript is encoded by the rat glypican 3 gene (GPC3), whose human homolog is mutated in the Simpson-Golabi-Behmel overgrowth syndrome. Allelic loss at the GPC3 locus was infrequent (6.9%) in MM cell lines, and no mutations were found. GPC3 transcript levels were markedly decreased in 16 of 18 primary tumors and 17 of 22 human MM cell lines. Most of the cell lines were shown to have aberrant methylation of the GPC3 promoter region. In two of four human MM cell lines tested, GPC3 expression was restored after 2-deoxy 5-azacytidine (DAC)-mediated demethylation of its promoter region. Ectopic expression of GPC3 inhibited in vitro colony formation of human MM cells. Collectively, these data suggest that down-regulation of GPC3 is a common occurrence in MM and that GPC3, an X-linked recessive overgrowth gene, may encode a negative regulator of mesothelial cell growth.
- Published
- 2000
- Full Text
- View/download PDF
49. Absence of BCL10 mutations in human malignant mesothelioma.
- Author
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Apostolou S, De Rienzo A, Murthy SS, Jhanwar SC, and Testa JR
- Subjects
- B-Cell CLL-Lymphoma 10 Protein, DNA, Neoplasm analysis, Genes, Tumor Suppressor, Humans, Loss of Heterozygosity, Polymorphism, Single-Stranded Conformational, Tumor Cells, Cultured, Adaptor Proteins, Signal Transducing, Mesothelioma genetics, Mutation, Neoplasm Proteins genetics
- Published
- 1999
- Full Text
- View/download PDF
50. Cytogenetic analysis of 363 consecutively ascertained diffuse large B-cell lymphomas.
- Author
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Cigudosa JC, Parsa NZ, Louie DC, Filippa DA, Jhanwar SC, Johansson B, Mitelman F, and Chaganti RS
- Subjects
- Chromosome Disorders, Humans, Karyotyping, Ploidies, Translocation, Genetic, Chromosome Aberrations genetics, Lymphoma, B-Cell genetics, Lymphoma, Large B-Cell, Diffuse genetics
- Abstract
Cytogenetic analysis was performed on 363 biopsy specimens with histologically confirmed diffuse large B-cell lymphoma (DLBCL), consecutively ascertained at the Memorial Sloan-Kettering Cancer Center, New York, between 1984 and 1994. Among 248 samples successfully karyotyped, clonal chromosomal abnormalities were noted in 215 (87%). The salient cytogenetic features of DLBCL from this analysis comprised the following. Breakpoints clustered, in decreasing frequency, at 10 recurring sites: 14q32, 18q21, 1q21, 3q27, 1p36, 8q24, 3p21, 6q21, 1p22, and 22q11. Of these, deletion breaks affecting bands 3p2 and 1p22 and translocation breaks affecting bands 14q32, 3q27, and 1q2 were frequent and distinctive for this subset of lymphomas. Translocations affecting band 14q32 were noted in 110 cases (51%) of which 42 (20%) had t(14;18)(q32;q21), 21 (10%) had t(8;14)(q24;q32) or t(8;22)(q24;q11), 14 (6.5%) had t(3;14)(q27;q32) or t(3;22)(q27;q11), and 33 (15%) had other rearrangements of 14q32. Among 144 new translocations detected in the entire group, the breakpoints in 19 were recurrent and clustered at three sites: 1q21, 3q27, and 14q32. Regions of common cytogenetic deletions were identified at 11 sites, 1p36, 1p33-34, 1p31, 1q32, 3p25-26, 3p21, 3q21, 6q15, 6q21, 6q23-24, and 7q32, suggesting possible loss of candidate tumor suppressor genes associated with DLBCL development. Of these, only those at 6q21, 6q23, and 7q32 have previously been described in lymphoid neoplasms. The group of DLBCL with translocations affecting band 14q32 showed a significantly different pattern of additional cytogenetic changes compared to the group lacking such translocation. This new comprehensive cytogenetic characterization provides the basis for investigations aimed at identifying molecular mechanisms as well as the clinical impact of cytogenetic changes in DLBCL.
- Published
- 1999
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