Acknowledgment toReviewers IVolume9cgd.aacrjournals.org/cgi/issue_pdf/backmatter_pdf/9/12.pdf ·...
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Epstein, C.Ewen, M.
Cell Growth & Differentiation 1025
Acknowledgment to Reviewers I Volume 9
The Editor-in-Chief and Editorial Board gratefully acknowledge their colleagues who reviewed manuscripts for Cell
Growth & Differentiation, Volume 9.
AAaronson, A.Aitkin, A.
Arnold, H.Attisano, L
Azizkhan, J.
BBacchetti, S.Baldwin, A.Bartok, J.Basilico, C.Begley, C.G.Birchner, A.Bissell, M.Blasi, F.Blenis, J.Bohrnan, D.Bottaro, D.Brash, D.E.Broker, T.R.Brown, M.
Brugge, J.Bundy, D.Burke, D.
CCantley, LCarr, A.M.Cavenee, W.K.Chou, M.Clarke, A.Cleveland, J.Cobb, M.Cole, M.
Collins, S.Cooper, J.Cullen, B.Curran, T.
DDalla-Favera, A.Dang, C.Decker, T.DeGregori, J.Do Luca, LDenhardt, D.DePinho, A.Der, C.Do Vries, A.
Dickson, A.Donehower, LA.Dotto, P.Draotta, G.DressIer, G.Dyson, N.
F
Fanning, E.Famham, P.Fearon, E.Fidler, l.J.Fisher, 0.Freedman, LP.Freemont, P.Frisch, S.
GGallick, G.E.GaIlie, B.LGhosh, S.Giguiere, V.Gottesman, M.Grandon, C.Graves, B.Greene, LGreenberg, N.M.Groffen, J.Groner, B.Grosveld, G.Gruss, P.Gudas, L
HHandel, M.Hanks, S.K.Hannon, G.Hauschka, S.Hedrick, LHeintz, N.Hennighausen, LHerrlich, P.Hiebert, S.Hinds, P.Hinnebusch, A.Hockenbery, 0.Hong, W.K.Horwitz, S.Hynes, N.Hynes, A.
Inoue, J.Ip, M.Isaac, T.W.lsaacs, W.B.Israel, M.A.Isseroff, A.
JJaken, S.Johnson, P.
KKaolin, W.Kanno, T.Kaplan, D.A.Karin, M.Katze, M.Keene, J.
Kelly, P.Kemp, C.Keski-Oja, J.Kidd, V.Koeffler, P.Koff, A.Korsemeyer, S.Kowalik, T.F.Kraut, N.Knedberg, J.Krumm, T.Kufo, 0.Kurie, J.
LLand, H.Lane, D.P.Lane, T.Lanni, J.S.Lamer, A.Lassar, A.B.Lau, A.F.Lengyol, P.Levitt, M.
Levy, 0.Li, J-P.LJem, A.Liotta, L
Lipsick, J.Ljungman, M.Lotz, M.Lowe, S.Lutzkor, S.G.
M
Maness, P.F.Marais, A.Markby, D.Maronpot, R.A.Marshajl, C.McBumey, M.McCarthy, S.McMahon, M.Merlino, G.T.Michalopolous, G.Middlemas, 0.Miller, S.Minichiello, LMittnacht, S.Mochly-Rosen, D.Moll, U.Moran, E.
Morre, D.J.Morrison, 0.Morrison, A.S.Munger, K.Murre, K.
NNathan, C.Neckors, LM.Neel, B.Nister, M.
0
O’Bnan, C.A.O’Connor, P.M.Orlow, S.J.Osborne, BA.Oshirna, A.
PParada, L.Park, M.Parker, P.J.Parsons, 0.Parsons, T.Pavan, W.Pawelek, J.M.Pawson, T.Poles, E.Pendergast, A.M.Perry, M.E.Pickard, 0.Pitha-Rowe, P.Plowman, G.Poirior, G.Polakis, P.Pouyssegur, J.Postigo, A.Pnves, C.L
Q
Qu#{233}va,C.
RAauscher, F.Aeed, J.C.Aoed, 5.1.Reid, B.Roberts, A.Roberts, J.M.Rohrschneider, LA.Rosen, J.Rosenthal, N.A.Roussel, M.Rudnicki, M.A.Ruby, E.Ryan, M.
S
Salmon, T.Samuel, C.Schaffhausen, B.Schlessinger, J.Schmidt, E.V.Sears, A.Segal, S.Shackelford, 0.Shaw, A.S.Shaw, P.Shigesada, K.Sierra-Rivera, E.Silver, J.Srneal, T.Smoland, E.B.
1026 Acknowledgment to RevIewers / Volume 9
Smith, D.Sonenshein, 0.Spiegolman, B.Stanbndge, E.J.Stark, G.A.Staudt, LStokoe, 0.Studzinski, G.P.Sun, V.Sutherland, A.
TTaniguchi, T.Tapscott, S.Taylor, S.
Templeton, 0.Thompson, C.B.
Toker, A.Tsai, K.Tsai, LH.
VVerma, I.Vilcek, J.Vogt, P.Vousden, K.
w___Wahl, 0.Walsh, K.
Wang, J.Wang, J.Y.J.Wang, X-F.Waxman, S.Weber, B.LWeber, M.J.Weigel, A.Weinberg, B.Weinert, T.Weinstein, l.B.Weissman, B.E.Weitzman, J.B.White, E.Windle, J.J.Wohlgemuth, 0.
Xiong, V.
VYamasaki, LYamashiro, 0.Yaniv, M.Varden, V.Vee, A.Yeger, H.
zZantema, A.Zon, L
Gallego, M. I., 795Gansauge, F., 611
Cell Growth & Differentiation 1027
Author Index I Volume 9
AAaronson, S. A., 355Abdel-Malek, Z. A., 575Abe, K., 487Adachi, H., 267Adamo, S., 155Afrakhte, M., 983Agrawal, D., 847Ahn, N. G., 667Akhurst, A. J., 393Albee, L 0., II, 119Alfano, N., 651Andreeff, M., 105Angelotti, T., 247Apetlo, C., 929Arteaga, C. L, 345Auer, G., 565Austin, S., 267Azzam, E. I., 887
Babcock, G., 575Bafico, A., 355Baghen-Varmand, A., 497Balmain, A., 393Bao, T., 961Bardwell, W. M., 71Barrett, J. C., 545Basnett, A. K., 869Bassing, C. H., 223Bazarov, A. V., 367Beger, H. G., 611Biggs, J. A., 667Bilodeau, M., 165Bin#{233}truy,B., 565Blazquez, M-V., 277Bottaro, D. P., 355Boulukos, K. E., 929Bowes, A. C., Ill, 177Brickwood, J. A., 949Bromberg, J. F., 505Bromley, M., 1015Brown, C., 505Brown, T. L, 869Brun, G., 857
Byrnes, M. J., Ill, 197
CCance, W. G., 999Ca,iou, S., 165Carman, T. A., 545
Carstens, B. P., 119Catron, K. M., 949Cattloy, A. C., 815Champlin, A., 105Chang, V-C., 79Chang, V-N., 767Chellappan, S., 59Chen, H., 939Chen, K-D., 767Chin, E., 313Cho, V., 147Chow, L T., 313Christenson, J. G., 815
Christiansen-Weber, T., 139Cirafici, A. M., 97Cleveland, J. L, 59Consoli, U., 105Conti, C. J., 31Cornelius, J., 575Coss, M. C., 41Craven, A. J.,999Cr#{233}pin,M., 497Cnppen,C., 713Crowe, 0. L, 619Csete, M., 1Cui, W., 393Cumming, S. A., 393Cunha, 0. A., 777
DDai, W., 877Darnell, J. E., Jr., 505Datta, N. S., 639Davis, M. B., 575d’Avis, P. V., 71de Coupade, C., 327Deed,R.W., 1015DeGrogori,J., 113Deisseroth, A. B., 105Delmarre, C., 1007Deng, C., 557Derynck, A., 229, 777do Toledo, S. M., 887Do Vita, 0., 97Dewhirst, M. W., 49Dias, P., 699DiAugustine, A. P., 777Di Lauro, R., 97Dirnrneler, S., 415Dong, L, 177Donoghue, 0. J.,71Durett, A., 105
EEckhart, W., 13Endo, T., 487Espanel, X., 857Eto, K., 989Eventt, J., 405
FFahI, W. E., 523Falasca, M., 513Faller, 0. V., 465Fan, Z., 505Fischer, A. S., 209, 905Fitzpatrick, F. A., 687Flatt,P. M., 535Flower, A. J., 327Fowler, L, 177, 405
Franz#{233}n,B., 565Fukasawa, K., 877Fukumaki, V., 487Fusco, A., 97
Gansauge, S., 611Gazdar, A. F., 805Gillespie, 0. A. F., 677Gishizky, M. L, 939Glaiso, 0., 165Goheer, A., 475Goldsworthy, T. L, 815Gonzales, A. J., 815Gordon, A. E., 651Gorska, A. E., 229Graves, P. A., 197Greenspan, 0. 5., 423Grove, L E., 731Gudas, L J., 969Guenn, S., 929Guguen-Guillouzo, C., 165GuIding, K. M., 919Guo, W., 85Guo, X., 1007Guo, V., 185
HHaas,M., 139Hackney, J., 847Haendeler, J., 415Haggblom, C., 139Hanahan, 0., 557Hardman, A., 545Hauser, P. J., 847Heintz, N. H., 79Heitman, J., 223Heldin, N-E., 983Honnighausen, L, 795Herbst, A., 247Herlyn, M., 743Hiebert, S. W., 59Hirohashi, S., 337Hirose, T., 267Horn, V. K., 777Houghton, P. J.,699Howe, P. H., 869Huang, 0. V., 969Huang, T-S., 23Hubbard, K., 713Hussain, S., 677
Igarashi, H., 381Ikeda, M-a., 989Ilyin, 0. P., 165Im, S., 575Ireland, H., 393Isaacs, J. S., 545
lshov, A. M., 743Issack, P. S., 827, 837Itoh, H., 651
JJacks, T., 131, 287Jaken, S., 177, 405Jakoi, L, 113Joe, S-H., 23Jensen, D. E., 743Jotten, A. M., 267
Jiang, W., 13Johnson, 0. 0., 31Johnson, E. M., 651
Joseph, H., 229Jozefonvicz, J., 497
KKanemitsu, M. V., 13Kang, M. K., 85Kano, M., 381Kanovsky, M., 651Karisson, T., 757Kashii, V., 487Kastner, A., 857Kong, P., 887Kilbey, A., 677Kinto, K., 487Kishirnoto, T., 337Kiyokawa, H., 787Klein, M. G., 147Kleinrnan, H. K., 305, 355Koff, A., 787Kokura, K., 337Kornatsu, N., 487Kourbali, V., 497Kovalev, S., 897Kowalik, T. F., 113Kraft,A. S., 667
Kubota, V., 247Kudlow, J. E., 313Kujoth, G. C., 523Kullander, K., 757Kuo, M-L, 23Kyproos, K. E., 723Kypnanou, N., 185
LLaCava, M., 31Laderoute, K. A., 919Laifrenier, S., 887Lai, V-K., 767Lan, Z., 877Lane, C. M., 105LaQuaglia, M., 897Laudot, V., 1007Lauppe,M.J., 105Lee, D. C., 451Lee, V-S., 79Leone, G., 1 13, 297LJ,W., 877Li,V., 949Liddell, J., 393Ueu, C-H., 767Urn, W. H. B., 513Lin, P., 49Linder, S., 565Unnoila, A. I., 475Uttle, J. B., 887Uu, C-C., 767Uu, L N., 699Uu, A., 239
Uu, X., 795Uu, V., 961Ljungdahl, S., 565Long, M. W., 639
1028 Author Index I Volume 9
Loyer, P., 165Lu, K. K., 367Lucarelli, M., 155
Lucas, J., 165
M
Macho, A., 277Magae, J., 79Maheshwari, A. K., 305Maitra, A., 805Makino, V., 337Makri-Werzen, 0. M., 423Malinda, K. M., 355Malstrom, S., 513Manova, K., 787Marchenko, N., 897Masuda, M., 381Matzuk, M. M., 223Maul, G. G., 743McClatchey, A. I., 287Meadows, J., 877Modvedev, A., 267Melillo, A. M., 97Menard, M., 713Mendelsohn, J., 505Moyer, A. N., 71Michol, J. J., 435Minotti, S., 155Mitsui, V., 79Miura, V., 487Molinaro, M., 155Moll, U. M., 897Montesano, A., 355Mooro,A., 1015
Moos, P. J., 687Mor#{232}re,J. F.,497Morrison, 0. K., 41Moses, H. L, 229Muir, S., 223Mu#{241}oz,E., 277Muramatsu, M., 337
NNacht, M., 131Nakajima, T., 257Navas, P., 277Nervi, C., 155Nesbit, C. E., 731Nevins, J. A., 113, 297, 585Newman, M. J., 423Nowton,J.S., 1015Niodorfellnor, G., 247Ninomiya, V., 989Nip, J., 59Niwa, S-i., 337Nojima, H., 257Nordlund, J. J., 575Norton, J. D., 1015Nugont, M. A., 723Nusslor, A. K., 611
0Oberloy, L W., 239Oberloy, T. 0., 239
Oda, K., 257Ogg, S., 197Ohkawa, N., 337Ohmori, T., 345Okada, K., 487Olson, 0. C., 557Omura, S., 79Ota, M., 989Ouyang, B., 877Ozturk,M., 165
P__________Pan, H., 877Parekh, T. V., 423Parento, L, 327Park, M. S., 787Park, N-H., 85Parks, T. P., 949Paterson, A. J., 313Patil, S., 869Peng, C-V., 197Perry,M.E., 119Peters, K. G., 49Potkovich, M., 629Phelps, 0. E., 595Pietonpol, J. A., 535Pinar, H., 805Piwnica-Worms, H., 197Pledger, W. J., 847Pognonoc, P., 929Pollard, J. W., 787Polvonni, P. J., 49Ponco, M. L, 355Portella, G., 393Prasad, P. V., 305Pratt, M. A. C., 713Price, J. 0., 535Prochownik, E. V., 731Prywos, A., 513Puisioux, A., 165
Quinlan, M. P., 209, 905Quinn, T. Q., 49
RRathi, A., 805Aauschor, F. J., Ill, 743Richards, A. G., 777Robertson, S. C., 71Robinson, D. F., 523Robinson, G. W., 795Robles, A. I., 31Rodnguoz-Puebla, M. L, 31Rogers, B. B., 805Russo-Mane, F., 327
Sablitzky, F., 1015Sankar, S., 49Santoro, M., 97Saucodo, L J., 119Sause, A., 415
Scarpa, S., 155Schlossinger, J., 513Schroeder, J. A., 451Schulkos, A-K. A. M., 629Scicchitano, B. M., 155Seavey, S. E., 119Sebastian, J., 777Sedivy, J. M., 367Serra, A., 229Settleman,J., 513Sevilla, L, 929Shan, S-q., 49Shang, C., 949
Shannon, M. F., 949Shaw, A., 535Shaw, A. J., 287Shay, J. W., 805Shon, K., 961Shen, S-C., 23Shen, X., 961Shimizu, M., 257Shinjo, K., 487
Shoshan, M. C., 565Shou, W., 223Shuler, C. F., 619Sidhu, G. S., 305
Simok, S. L, 41Singh, A. K., 305Smith, E. J., 297Smith, G. H., 795Smith, L M., 41Soaros, V. C., 787Solito, E., 327Sonenshein, G. E., 723Sonnoveld, E., 629Soos, T. J.,787Sonano, J. V., 355Stephens, A. M., 41Stephenson, M. T., 197Stevens, J. L, 177, 405Stice, L, 465Strom, D. K., 59Suzuki, I., 575Swondeman, S., 897Szabo, E., 475
TTada, A., 575Takouchi, A., 257Talmage, 0. A., 147Tamura, T-a., 337Tanaka, K., 79Tejima, T., 79Thaloor, 0., 305Theodorescu, 0., 919Thoma, A. S., 197Thompson, J. A., 969Timmons, C. F., 805Tomizuka, H., 487
Tong, W., 787Tsichlis, P., 513Tsubota, V., 257
U_________UlInch, A., 247
Uson, A. A., 651
V_________Vanacker, J-M., 1007van den Brink, C. E., 629van dor Burg, B., 629van dor Loedo, B-j. M., 629van der Saag, P. T., 629van do Water, B., 177Vazin, C., 465VOgt,M., 139
w-Wagner, A., 1Walker, M. P., 777Wang, M. W-J., 105Wang, X. W., 423Wang, X-F., 223, 961Wang,V., 513Webster, M. K., 71Weissman, B. E., 545Welsh, M., 757Werb, Z., 777Westermark, B., 983Wiosen, J. F., 777Williams, J. L, 639Winterstein, D., 41Witschi, H., 475Wold, B. J., 1Wortman, M. J., 651Wright, W. E., 805Wu,X., 313Wu,Z., 197
xXie,W., 313Xiong, V., 435, 595Xu, L-H., 999
Vamada, M., 487Van, G. C., 939Van, Z-H., 267Vang, X., 999Vashima, K., 805Veargin, J., 139Vin, X., 731Voon, L S., 367Voshida, M., 337Voshikura, H., 381Vu,T-H., 767Vu,X., 1
zZabludoff, S. D., 1Zannini, M., 97Zoiher, A. M., 415Zhong, V., 209Ziff, E. B., 827, 837
Cell Growth & Differentiation 1029
Subject Index I Volume 9
A____________________________ Breast carcinoma ROR-y induction, 267A 549 cells CVP26, 629 angiogonic
differentiation Bubi inhibition by curcurnin, 305annexin 1 , 327 human hBubl , 877 annexin 1 , opitholial cells, 327
Actin Butyrate early myoloidcortical G1 arrest mechanisms, 465 CSF-1 and LIF synergistic effects,
adherens junctions regulation, 905 929a-Adducin � koratinocyte
renal tumor progression, 405 Cancer� see specific sites, types STAT3 activation and, 847
DAdducin Carboxymethyl benzylamide dextran myeloidrenal tumor progression, 405 tumor growth inhibition, 497 blOCkade by E2F-1 and E2F-3, 59
Adducins Carcinogens O&l�/� CSFI and LIF synergisticactivity, transformed cells, 177 nongenotoxic effects, 929
Adherens junctions apoptosis alteration, mouse myogonictargeting, 905 hepatocytes, 81 5 hormonal control, 155
Adipocytes Carcinoma: see specific sites, types nouronaldifferentiation Caspase Rb/E2F-1 protein complexes, quail
ROA-y induction, 267 inhibitor neural retina, 857Adipogenesis TGFp-induced apoptosis blockade, PKCa and PKCI3 functions, F9 cells,
CDK4 regulation, 595 869 147Angiogenesis CC1O retinoid X receptor, squamous cell
inhibition by curcumin, 305 neoplastic phenotype antagonism, carcinoma, 619Annexin I lung cancer cells, 475 reversible
epitholial cell differentiation, 327 CCAAT/enhancer binding protein �J cell cycle regulation, hepatoma cells,Antiapoptotic function ICAM-i gene regulation, 949 165
structural requirements, 939 cdc2 ATK-modiatodAPO-1/Fas rat promoter Pl3kinaso, FDC-P1 cells, 247
cell death silencer element, 257 Shb and, PC12 cells, 757inhibition by nitric oxide, 415 Cdc25C 5V40 enhancer repression by p300
Apoptosis serine 216 phosphorylation by C- and, undifferentiated F9 cells,alteration TAK1 , 197 989
nongonotoxic carcinogens, mouse Cell adhesion telomerase RNA expression, 805hepatocytes, 81 5 loss induction by FAK COOH-terminal thyroid
c-myc, 731 domain, 999 RET/PTC1 expression and, 97induction Cell cycle uncoupling growth arrest and, 787
E2F1 -specific, 1 13 arrest Wnt-1 and, PC12 cells, 837vanilloid compounds, 277 G1, butyrate-induced, 465 Cell growth: see also Tumor growth
inhibition checkpoint response arreststructural requirements, 939 keratinocytes vs fibroblasts, 535 G1 CDK activity inhibition,
L-myc, 731 G1 phase fibroblasts, 983N-myc, 731 butyrato-induced arrest, 465 uncoupling differentiation and, 787NO-induced, pancreatic carcinoma, CDK activity inhibition, fibroblasts, inhibition
61 1 983 EGF-induced, Stati and, 505rescue, hematopoietic cells, 105 Pura localization, CV-1 cells, 651 p1 07 accumulation control, 297taxane-modiated regulation p1 30 accumulation control, 297
signaling pathways, 687 mouse epidermis in vivo, 31 PCPE function andTaxol-induced reversibly differentiated hepatoma excisable rotroviral vectors, rat
MAPK role, U937 coils, 767 cells, 165 fibroblasts, 381TGF3-inducod typo V collagen, epithelial cells, 423 12-O-totradecanoylphorbol-1 3-acetate,
blockade by caspase inhibitor, 869 Cell cycle genes mouse skin, 31regulation Cell transformation
p53/p21���afl�dependent, diploid c-junB fibroblasts, 887 MEK1 -mediated loop support, 565Bax reversibly differentiated hepatoma hypertransformation
proteasome-mediated degradation, 79 cells, 165 Raci , epitholial cells, 209BD-fmk Cell death PKC activity, 177
TGFj3-induced apoptosis blockade, APO-1/Fas-mediatod Wnt-1869 inhibition by nitric oxide, 415 and HES-1 expression, PC12 cells,
Bladder cancer induction by FAK COOH-terminal 827motility domain, 999 c-foe
EGFA-regulated, 919 Cell densfty serum response elementB-Myb growth arrest activation by P13K and rho
al(l) collagen expression inhibition, G1 CDK activity inhibition, pathways, HeLa cells, 513723 fibroblasts, 983 cls-Diamminedichloroplatinum(ll)
BRCAI Cell differentiation PKC #{128}translocation andsubnuclear localization, 743 adipocyte phosphorylation, 345
F’
DI cellsdifferentiation
AOR-y induction, 267Development
telomerase RNA expression, 805Dextran
carboxymethyl benzylamidetumor growth inhibition, 497
1� Subject Index / Volume 9
Cisplatincytotoxicity
PKC #{128}and, 345c-jun
repression by v-Jun, 677transformation
MEK1 -mediated loop support, 565c-myc
apoptosis, 731Collagen
type Iexpression, B-Myb-modiated
inhibition, 723type V
epithelial cell cycle regulation by,423
Colon carcinomahuman
CVP26, 629Colony-stimulating factor I
synergy with LIF, early myeloid celldifferentiation, 929
Connexin 43phosphorylation, mitotic cells, 13
Cortical actin filamentsadherens junctions regulation, 905
c-Raf-IFKBP65 association, 41
c-sis/platelet-denved growth factor-BTATA neighboring sequence
binding by ETS factors, 523C-TAKI (Cdc25C associated protein
kinase)Cdc25C phosphorylation on senne
216, 197Cullin
CUL-ihuman SKP1 association, 435
Curcuminangiogenesis inhibition, 305
CV-I cellscycle
Pura localization, 651Cyclin
CDK2/cyclin complexesendomitosis, 639
Cyclin-dependent kinaseG1 activity
inhibition, fibroblasts, 983Cyclin-dependent kinase 2
cyclin complexesendomitosis, 639
CycIln-dependent kinase 4regulation
adipogenesis, 595Cytochrome P45026
human breast and colon carcinomacells, 629
Cytotoxicitycisplatin-induced
PKC #{128}and, 345
Diploid fibroblastsp53/p21�1-dependent cell cycle gene
regulation, 887DNA damage
checkpoint control by MmRad24, 961Dysplasia
thanatophonc type Imutations, FGFR3 activation, 71
EEIA
adherens junctions regulation, 905Embryonal carcinoma
muscle differentiationRXA-a expression and P19 cells,
713undifferentiated F9 cells
SV4O enhancer repression by p300,989
EndomitosisCDK2/cyclin complexes, 639
Endothelial cellshuman umbilical vein
angiogenic differentiation inhibitionby curcumin, 305
Endothelial tubulogenesisHGF isoform activity, 355
Endothelin-Imelanocyte regulation, 575
Epidermal growth factorgrowth arrest
Stati and, 505receptor
bladder cancer motility regulation,919
mammary gland morphogenesis,777
Epidermis
cell cycle regulation, mouse in vivo, 31development
erbB-2 and, 313Epithelial cells
cell cycle regulationtype V collagen, 423
differentiationannexin 1, 327
hyportransformationAaci, 209
mammary
endogenous TGFI3 role, 229renal proximal tubule, transformed
adducin activity, 177Epithellal tubulogenesis
HGF isoform activity, 355erbB-2
mammary gland morphogenesis, 777skin development and, 313
ERBB receptorsmouse mammary gland, 451
Erythropoiesisthrombopoietin and, human leukemia
cells, 587Estrogen receptor related a
osteopontin promoter activation, 1007Extracellular signal-regulated kinase
TATA-binding protein phosphorylation,667
FFas
cell deathinhibition by nitric oxide, 415
F9 cellsdifferentiation
PKCa and PKCI3 functions, 147undifferentiated
SV4O enhancer repression by p300,989
FDC-PI cellsdifferentiation, ATK-mediated
P13-kinase, 247Fibroblast growth factor
receptor 3activation by TDI mutations, 71
receptor 4function, islet cell carcinogenesis,
557Fibroblasts
cell cycle checkpoint response, 535c-jun transformation
MEK1 -mediated loop support, 565diploid
p53/p21W��depondont cell cyclegene regulation, 887
growthPCPE function and, rat, 381
growth arrestG1 CDK activity inhibition, 983
MyoD functionattenuation by phosphorylation, 699
senescenceinduction by pl6””� and p21CIP1,
139FK506 binding protein 12
TGF-p signaling regulation, 223FK506 binding protein 65
c-Raf-i association, 41Focal adhesion kinase
COOH-terminal domainadhesion loss and cell death
induction, 999
Genes: see also specific genescell cycle
p53/p2i��1-dopendent regulation,diploid fibroblasts, 887
reversibly differentiated hepatomacells, 165
Granulocytesdifferentiation
blockade by E2F-1 and E2F-3, 59Granulosa cells
luteal transitionuncoupling differentiation and
growth arrest, 787Growth factors
opidormalgrowth arrest, Stati and, 505receptor, bladder cancer motility
regulation, 919receptor, mammary gland
morphogenesis, 777fibroblast
receptor 3, activation by 101mutations, 71
receptor 4, islet cell carcinogenesis,557
hopatocyteisoform morphogenic activity, 355
insulin-likemyogenesis induction, 155
insulin-like, I
Infectionviral
BRCA1 nuclear redistribution, 743Insulin
antiapoptotic functionstructural requirements, 939
Insulin-like growth factormyogenesis induction, 155
Insulin-like growth factor I receptorantiapoptotic function
structural requirements, 939Intercellular adhesion molecule-I
regulation by ReIA and C/EBPI3, 949Interleukin 6
phorbol ester induction of annexin 1,327
transcription factorexpression, hopatocellular carcinomas,
337
Hepatocellular carcinomahepatocarcinogenesis-related
transcription factor expression,rats and humans, 337
Hepatocyte growth factorisoforms
morphogenic activity, 355Hepatocytes
apoptosis alteration by nongenotoxiccarcinogens, mouse, 815
Hepatomareversibly differentiated cells
cell cycle regulation, 165HES-I
MacrophagesMl 0+ differentiation
stimulation by CSF-1 , 929Mammary epithelium
endogenous TGFI3 role, 229Mammary gland
ERBB receptors, mouse, 451morphogonesis
EGFR and erbB-2, 777Mammary tissue
Stat5a compensating signals, 795MCF-7ras tumor growth
inhibitiondextran derivative, 497
Id proteinsexpression
stage- and subcellular-speciflc, 1015
Metastasisin vivo
TGFI3, mouse skin carcinoma, 393Mitogen-activated protein kinase
Taxol-induced apoptosis role, U937cells, 767
Mitotic cells
connexin 43 phosphorylation, 13Mitotic checkpoint kinase
human Bubi , 877MmRad24
DNA damage checkpoint control, 961Morphogenesis
HGF isoform activity, 355mammary
Cell Growth & Differentiation 1031
receptor, antiapoptotic function,structural requirements, 939
paracrineEl-i , melanocyte regulation, 575
platelet-derived, BTATA neighboring sequence binding
by ETS factors, 523transforming, j3
apoptosis blockade by caspaseinhibitor, 869
endogenous, mammary epithelium,229
signaling regulation by FKBP12, 223tumor invasion and metastasis in
vivo, 393transforming, �31
insensitivity, human prostate cancercells, 185
vascular epidermalsoluble receptor, tumor growth
inhibition, 49
HHair follicles
developmenterbB-2 and, 313
HeLa cellsc-fos SRE activation by P13K and rho
pathways, 513Hematopoietlc cells
rescue from apoptosis, 105Heoatocarclnoaenesis-related
expressionWnt-1 transformation and, PC12
cells, 827Homeobox genes
Hoxbl 3’ AAlDR� enhancerregulatory elements, 969
Hormonal control: see also specifichormones
myogenic differentiation, 155Human mitotic checkpoint kinase, 877Human umbilical vein endothelial cells
angiogenic differentiationinhibition by curcumin, 305
Hypertransformationepitholial
Raci, 209
Invasionin vivo
TGFIJ, mouse skin carcinoma, 393Islet cell carcinogenesis
FGFR4 function, 557
K
Keratinocytescell cycle checkpoint response, 535differentiation
STAT3 activation and, 847oral
roplicative senescence, telomeraseactivity and, 85
KinasesC-TAXi (Cdc twenty-five C associated
protein kinase)Cdc25C phosphorylation on serino
216, 197cyclin-dopendent
G1 activity inhibition, fibroblasts, 983cyclin-dependent, 2
cyclin complexes, endomitosis, 639cyclin-dependent, 4
regulation, adipogenesis, 595extracellular signal-regulated
TATA-binding proteinphosphorylation, 667
focal adhesionCOOH-terminal domain, adhesion
loss and cell death induction,999
human mitotic checkpoint, 877mitogen-activated protein
Taxol-induced apoptosis role, U937cells, 767
mitotic checkpointhuman Bubi , 877
p34cdc2
Taxol-induced activation, 23phosphatidylinositol 3-
EGFR-regulated bladder cancermotility mediation, 919
RTh-mediated FDC-P1differentiation, 247
protein, Cactivity, transformed cells, 177phosphorylation of a- and -y-
adducin, renal tumorprogression, 405
protein, Cafunction, F9 differentiation, 147
protein, C�function, F9 differentiation, 147
protein Ce
I
and cisplatin-induced cytotoxicity,345
translocation and phosphorylationby CDDP, 345
Raf-itemperature-sensitive mutations,
mammalian cells, 367receptor tyrosine
FDC-P1 differentiation, P13-kinase,247
Leukemiaerythropoiesis
thrombopoietin and, human coIls,
587Leukemia inhibitory factor
synergy with CSF-1 , early myoloid celldifferentiation, 929
L-mycapoptosis, 731
Lung cancerneoplastic phenotype
antagonism by CC1 0, 475Luteal cells
granulosa transitionuncoupling differentiation and
growth arrest, 787Lymphoma
thymicwithout Rag function, p53-deficient
mice, 131
MEKIautocrino loop
and c-jun transformation, 565Melanocytes
paracrino regulation by Er-i , 575Merlin
localization and functional domains,287
1� Subject Index I Volume 9
EGFR and erbB-2, 777 Osteopontin PhosphorylationMotility promoter connexin 43, mitotic coils, 13
EGFA-rogulatod, bladder cancer activation by estrogen receptor PKC #{128}
mediation by P13K, 919 related a, 1007 COOP, 345Murine double minute 2 TATA-binding protein
degradation p _____________________________ EAK kinaso, 667proteasome-modiated, 79 pl6INK4 Platelet-derived growth factor-B
induction by UV light, 1 19 senescence induction, fibroblasts, 139 TATA neighboring sequencep53-specific transcript binding by ETS factors, 523Muscle differentiation p21 Procollagen C-proteinase enhancer
induction by nitric oxide, pancreaticRXR-a expression and, P1 9 embryonal protein
carcinoma cells, 71 3 carcinoma, 611function
Mutations p21C� excisable rotroviral vector and, ratsenescence induction, fibroblasts, 139
fibroblasts, 381temperature-sensitive p2lWatl � carcinomaRaf-1 kinase, mammalian cells, 367
cell cycle gene regulation, diploid TGF-p1 insensitivity, 185thanatophoric dysplasia type I fibroblasts, 887
FGFA3 activation, 71 ProteasomeMyelold cells p27’�1 mdm2 and bax degradation mediation,
differentiation expression, myotomes, 1 79blockade by E2F-1 and E2F-3, 59 myogenesis and, 1 Protein kinase Cearly, CSF-1 and LIF synergistic � kinase activity, transformed cells, 177Taxol-inducod activation, 23
effects, 929 phosphorylation of a- and ‘y-adducin,MyoD p53 renal tumor progression, 405
accumulation �,�tein kinase Cafunctional attenuation by �F1 -specific induction, 1 13 function
phosphorylation, 699cell cycle gene regulation, diploid F9 differentiation, 147
Myogenesis fibroblasts, 887induction by vasopressin and lGFs, distribution, neuroblastoma cells, 545 Protein kinase C13
155 functionp27K� and, 1 MDM2 transcript F9 differentiation, 147
induction by UV light, 119 �tein kinase CeMyogenic cellsdifferentiation p73 and cisplatin-induced cytotoxicity, 345
nouroblastoma, 897hormonal control, 155 translocation and phosphorylation by
Myotomes p107 COOP, 345p27� expression, 1 accumulation control, cell growth, 297 Proto-oncogenes: see speciTh genes
p130 PTCIaccumulation control, cell growth, 297 expression
N ______________________________ p300 thyroid differentiation and, 97SV4O enhancer repression, PuraNeoplastic phenotype undifferentiated F9 cells, 989
antagonism by CC1 0, lung cancer Panereatic carcinoma localization, CV-1 cell cycle, 651cells, 475 NO-induced apoptosis, 611
Neuroblastoma Papillary thyroid carcinoma R __________________________p53 distribution, 545 RET/PTC1 RacIp73 gene, 897 expression, thyroid differentiation adhorens junctions regulation, 905
Neurofibromatosis type II tumor and, 97 epitholial hypertransformation, 209suppressor Paracnne growth factors Rad24
localization and functional domains, � mammalian MmRad24287 molanocyte regulation, 575 DNA damage checkpoint control,
Neuroretinal development � 961Rb/E2F-1 protein complexes, quail, RET/PTC1 expression and, 97 Radiation
857 PCI2 cells ultravioletNitric oxide differentiation melanocyte response, regulation by
APO-1/Fas-mediated cell death Shb and, 757 ET-1 , 575inhibition, 415 Wnt-1 and, 837 p53-specific MDM2 transcript
apoptosis, pancreatic carcinoma, 61 1 Wnt-1 transformation and HES-1 induction, 119p21 induction, pancreatic carcinoma, expr�ion, 827 Ref-I kinase
61 1 P19 cells temperature-sensitive mutations,Nitric oxide synthase muscle differentiation mammalian cells, 367
endothelial AXR-a expression and, 71 3 Ragexpression effects on tumor biology, Phenotypes function
239 nooplastic thymic lymphoma without, p53-N-myc antagonism by CC1O, lung cancer deficient mice, 131
apoptosis, 731 coIls, 475 Receptors: see specific receptors
Phorbol ester Receptor tyrosine kinasesannexin 1 induction FDC-P1 differentiation
0 IL-6, 327 P13-kinaso, 247
Oncogenes: see specific genes Phosphatidylinositol 3-kinase ReIAOral carcinoma EGFR-rogulated bladder cancer ICAM-1 gene regulation, 949
tumor biology motility mediation, 919 Renal proximal tubule epithelial cellseNOS expression effects, 239 RTK-mediated FOC-Pi differentiation, transformed
Oral keratinocytes 247 adducin activity, 177replicativo senescence serum response element activation, Renal tumors
telomeraso activity and, 85 HoLa cells, 513 progression, 405
Cell Growth & Differentiation 1033
Replicative senescence: see also 1 2-O-tetradecanoylphorbol-1 3- carcinomas, rats and humans,
Senescence acetate, mouse, 31 337normal human oral keratinocytes development Pax-8
telomerase activity and, 85 erbB-2 and, 31 3 RET/PTC1 expression and, 97Retinoblastoma Skin carcinoma hF-i
E2F-i protein complexes spindle cell conversion in vivo RET/PTC1 expression and, 97neuroretinal development, quail, 857 TGFI3, mouse, 393 Transforming growth factor (3
functional complexity, review, 585 SKPI apoptosis blockade by caspaseRetinoic acid 4-hydroxylase human inhibitor, 869
human breast and colon carcinoma CUL-i association, 435 endogonous, mammary epithelium,cells, 629 Spindle cell conversion 229
Retinoic acid-inducible enhancer in vivo regulation by FKBP12, 223Hoxbl 3’ TGFf3, mouse skin carcinoma, 393 tumor invasion and metastasis in vivo,
regulatory elements, 969 Squamous cell carcinoma 393Retinoid-like orphan receptor y differentiation by retinoid X receptor, Transforming growth factor (31
induction 61 9 insensitivity, human prostate canceradipocyte differentiation, 267 Statl cells, 185
Retinoid X receptor and EGF-induced growth inhibition, TTF-Idifferentiation, squamous cell 505 RET/PTC1 expression and, 97
carcinoma, 61 9 TubulogeneslsRetinoid X receptor a T____________________________ epithelial and endothelial
expression HGF isoform activity, 355and muscle differentiation, P19 TATA-binding protein Tumor biology
ombryonal carcinoma cells, 713 phosphorylation by ERK kinase, 667 eNOS expression effects, 239TaxaneRET/PTCI Tumor growth: see also Cell growth
apoptosis inhibitionexpression
thyroid differentiation and, 97 signaling pathways, 687 dextran derivative, 497Taxol
Retroviral vectors soluble VEGF receptor, 49excisable apoptosis Tumor invasion
MAPK role, U937 cells, 767 .and PCPE function, rat fibroblasts,in vivo
381 p34cdC2 kinase activation, 23 TGF(3, mouse skin carcinoma, 393Telomerase
RhabdomyosacomaMyoD function activity
and normal human oral keratinocyte Uattenuation by phosphorylation, 699
rho roplicative senescence, 85 U937 cellsANA Taxol-induced apoptosis
pathway response element activation, expression, development, 805 MAPK role, 767
HeLa cells, 513 TemPerature-sensitive mutations Ultraviolet radiationAaf-1 kinase, mammalian cells, 367 molanocyte response
12-O-Tetradecanoylphorbol-I3-acetate regulation by ET-i, 575cell proliferation, mouse skin, 31 p53-specific MDM2 transcript
Thanatophoric dysplasia type I induction, 119SCC-25 cells mutations Umbilical vein
tumor biology FGFR3 activation, 71 human, endothelial cellseNOS expression effects, 239 Thrombopoletin angiogenic differentiation inhibition
Senescence and erythropoiesis, human leukemia by curcumin, 305induction cells, 587
pl6”�’� and p2lCiPl fibroblasts, Thymic lymphoma V____________________________1 39 without Rag function Vanillold compounds
telomerase activity and p53-deficient mice, 131 apoptosis induction, 277normal human oral keratinocytes, 85 Thyroid differentiation Vasoular cell adhesion molecule I
Serine 216 RET/PTC1 expression and, 97 apoptosis rescue, hematopoietic cells,Cdc25C phosphorylation by C-TAK1 , 313-LI cells 105
197 differentiationSerum response element AOA-y induction, 267 Vascular epidermal growth factor
activation by P13K and rho pathways, Transcription factors receptor, solubleHeLa cells, 51 3 E2F tumor growth inhibition, 49
Shb functional complexity, review, 585 VasoPressinand PC12 cell differentiation, 757 E2F-1 myogenesis induction, 155
Signal transducers and activators of apoptosis induction, 1 1 3 Very late antigen 4apoptosis rescue, hematopoietic cells,
transcription myeloid cell differentiation blockade, 105STAT3 59
Viral infectionactivation, koratinocyte p53 accumulation induction, 1 13 BRCA1 nuclear redistribution, 743
differentiation, 847 Rb/E2F-1 protein complexes, v-JunStat5a neuroretinal development, 857 c-jun gene repression, 677
compensating signals, mammary E2F-3tissue, 795 myeloid cell differentiation blockade,
Simian virus 40 59 W_______________________enhancer ETS factors Wnt-I
repression by p300, undifferentiated PDGF-B TATA neighboring and PC12 cell differentiation, 837F9 cells, 989 sequence binding, 523 transformation
Skin hopatocarcinogenosis-related and HES-i expression, PCi 2 cells,cell proliferation expression in hepatocellular 827
Cell Growth & Differentiation i
Instructions for AuthorsAims and ScopeCELL GROWTH & DIFFERENTiATiON aims to publish significant, ong-inal studies that address any aspect of the molecular biology of cellgrowth and differentiation, particularly as it relates to oncogonesis.Papers should be written as concisely as possible and should present acornploto body of work. In addition to the publication of full researchpapers, thejoumal also publishes reviews and minireviews that pro�dea synopsis of recent experimental findings or meetings. Although manyare invited, proposals for reviews may be submitted to the Editor-in-Chief.
Editorial PolicyWhen a manuscript is received for consideration, the Editors assumethat no similar paper has been or will be submitted for publicationelsewhere. Further, it is understood that all authors listed on a rnanu-script have agreed to its submission. AACR policy requires thatauthors, reviewers, and Editorial Board rnernbers reveal to the Editor-in-Chief any relationship that they believe could be construed ascausing a conflict of interest with regard to the manuscript submittedfor review. Upon acceptance, authors must transfer copyright to theAmerican Association for Cancer Research, Inc., the publisher andcopyright owner of thejoumal, prior to publication. Once an article isaccepted for publication in CELL GROWrH & DIFFERENTiATiON,the information therein is embargoed from reporting by the mediauntil the mail date of the issue in which the article appears.
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Results and Discussion. The results and discussion sectionsmay be separate or combined into a single section. Subheadingsmay be used.
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Acknowledgments. Should include all relevant informationwith the exception of acknowledgments of financial support,which should be indicated in a footnote.
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Number references in the order of their first mention in the text.Cite only the number assigned to the reference. References must bedoublo-spacod.
Sample references:1 . Pillay, I., and Sharma, S. V. In vivo and in vitro sermno/throonine
phosphorylations of opidermal growth factor receptor upon entryinto the cell cycle. CoIl Growth Differ., 6: 39-49, 1995.
2. Cooper, J. A. The sic-family of protein tyrosine kinasos. In: B. E.Kemp (ed.), Peptides and Protein Phosphorylation, pp. 8�-113.Boca Raton, FL: CRC Press, 1990.
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Schedule of PublicationAuthors should expect to receive reviewers’ comments within 4 weeksof submission. If revisions are required, only one revised version will beconsidered. Most articles will be pubhshed within 5-7 weeks of accept-once.
BENEFITS OF MEMBERSHIP
Margaret Foti, Ph.D.Executive Director
AMERICAN ASSOCIATION FOR CANCER RESEARCH
GUIDELINES FOR APPLICATION FOR ACTIVE AND
CORRESPONDING MEMBERSHIP
The American Association for Cancer Research (AACR), a scientificsociety of over 13,500 laboratoiy and clinical cancer researchers, was foundedin 1907 to facilitate communication and dissemination of knowledge amongscientists and others dedicated to the cancer problem; to foster research incancer and related biomedical sciences; to encourage the presentation and
discussion of new and important observations in the field; to foster publiceducation, science education, and training; and to advance the understanding
of cancer etiology, prevention, diagnosis, and treatment throughout the world.
Members of the AACR enjoy the following benefits:
1. the privilege of sponsoring a proffered paper (abstract) for consider-ation for presentation at the AACR annual meeting;
2. subscriptions to the Association’s high�uality journals Cancer Re-search, Clinical Cancer Research, Cell Growth & D�fferentiation, andCancer Epidemiology, Biomarkers & Prevention at reduced memberrates;
3. an advance copy of the Program and Proceedings of the AmericanAssociation for Cancer Research that contains over 4,000 abstracts ofproffered papers presented at the annual meeting;
4. reduced registration rates at annual meetings;5. priority notice ofsmall, focussed meetings in the AACR’s exciting series
of Special Conferences in Cancer Research;6. substantially reduced registration rates for Special Conferences;
7. opportunities for participation in AACR meetings in North America and
abroad with other scientific societies around the world;8. receipt of AACR Newsletters and other important announcements;9. early notification of and reduced rates for participation in the AACR
Employment Register;10. an up-to-date Membership Directory of over 13,500 member researchers
in the cancer field;11. the professional benefits of the AACR’s public education activities con-
cerning funding for cancer research and press coverage of the latest
research findings;
12. the opportunity to participate in three Summer Workshops that fosterknowledge in the cancer field for young investigators;
13. the facilitation ofinformal scientific exchange with leading researchers inthe cancer field; and
14. many more ongoing benefits.
QUALIFICATIONS FOR MEMBERSHIP
Active membership in the AACR is open to investigators who live in theAmericas. Individuals who have conducted two years of research resulting inpeer-reviewed publications relevant to cancer, or who have made substantialcontributions to cancer research in an administrative or educational capacity,
are eligible. If a candidate has conducted research in an area of biomedicalscience related to cancer, he or she will qualify for membership. Evidence ofpatents relevant to cancer research may be submitted as qualifications formembership in lieu of peer-reviewed publications.
Corresponding membership is open to persons who are not residentsof the Americas. The qualifications for corresponding membership are the
same as those indicated above for active membership. Visiting scientists
from outside the Americas who intend to return to their countries of originby the anticipated time of election should apply for corresponding mem-bership. All other visiting scientists should apply for active membershipand transfer to corresponding status upon leaving the Americas.
Graduate and medical students, postdoctoral fellows, and physicians intraining who do not yet meet the above qualifications for active orcorresponding membership should apply for associate membership.
Forms for associate membership are available from the AACR Office.
PROCEDURES FOR APPLICATION
There are three deadlines for the receipt of a membership application:January 1, May I, and September 1 of each year. The Membership
Committee will review all complete applications for active membership
that have been received by these deadlines and will submit recommenda-tions on each candidate to the Board of Directors which formally elects all
members. The same procedure is followed by the Special MembershipsCommittee which receives applications for corresponding membership.Candidates will be notified according to the following schedule:
Receipt of Applicationin AACR Office Notification of Candidate
January 1 March
May I JulySeptember 1 November
A complete application consists of the following material:1 . 6 copies of the form on the opposite side of this page, with all requested
information provided.
2. 5 copies of the candidate’s most current curriculum vitae and bibliog-
raphy.3. 5 copies of a letter of recommendation from a nominator who is an
active, corresponding, emeritus, or honorary member of the AACR (at
least one copy must be a signed, original letter). This letter shoulddescribe the candidate’s achievements in laboratory research, clinicalinvestigations, or epidemiological research, and it should affirm thatthis research adheres to accepted ethical scientific standards. -OR- Thenominator may supply the responses requested at the bottom of theapplication form in the section entitled “STATEMENT OF SUP-
PORT “ (at least one copy of the form must be the signed original).4. 5 copies of a letter of recommendation as described in Item 3 above
from a seconder who is an active, corresponding, emeritus, or honorarymember of the AACR (at least one copy must be a signed, originalleuer). -OR-- The seconder may supply the responses requested at thebottom of the application form in the section entitled “STATEMENT OF
SUPPORT” (at least one copy of the form must be the signed original).5. 5 reprints of each of two publications on which the candidate appears as
author. As noted above, evidence of patents developed by the candidatemay be submitted in lieu of one or both of the publications. If submittingpatents, supply patent number and year awarded.
All material should be collated into five complete sets with the originalapplication form as a covering document and sent to the address givenbelow. Questions regarding procedures for membership application mayalso be directed to the following address:
Membership Services DepartmentAmerican Association for Cancer Research
Public Ledger Building, Suite 826
150 5. Independence Mall West
Philadelphia, PA 19106-3483Phone: 215/440-9300FAX: 215/440-9412
E-mail: [email protected]
RESPONSIBILITIES OF MEMBERSHIP
Candidates should be aware of the following responsibilities of mem-bership in the AACR. Active members must pay annual dues. In 1999annual dues for active members are $185, $105 of which is designated forAACR journal subscriptions. Newly elected members of the AACR whohave already purchased subscriptions to Cancer Research, Clinical Can-cer Research, Cell Growth & Differentiation, or Cancer Epidemiology,Biomarkers & Prevention at the higher, nonmember rates will receive
reimbursement of the unused portion of those subscriptions once their firstyear’s membership dues are paid in full.
Corresponding members are required to pay dues ($105 in 1999) and
may, if they wish, subscribe to Cancer Research, Clinical Cancer Re-search, Cell Growth & Differentiation, or Cancer Epidemiology, Biomar-kers & Prevention at reduced member rates.
Applicants elected in March will be responsible for payment of that
year’s dues; applicants elected in July and November will pay dues for the
following year. Applicants elected in March and July will be eligible tosponsor an abstract for the next annual meeting. Evcry effort will be madeto afford the same opportunity to applicants elected in November.
AMERICAN ASSOCIATION FOR CANCER RESEARCH, INC.
Public Ledger Building . Suite 826 . 150 5. Independence Mall West � Philadelphia, PA 19106-3483
APPLICATION FOR ACTIVE OR CORRESPONDING MEMBERSHIP
NAME OF CANDIDATE:_____________ _____________ _____ DATE OF BIRTh:___________
LAST FIRST M.I. Month/Day/Year
PRESENT POSITION/TITLE:
INSTITUTIONAL AFFILIATION:
INSTITUTIONAL ADDRESS:
(City) (State/Province) (Country) (Postal Code)
TELEPHONE NUMBER:____________________________ FAX NUMBER:_________________________
E-MAIL ADDRESS:
PRIMARY FIELD OF RESEARCH (Please check only one):Biochemistry and Biophysics Biostatistics Carcinogenesis
_____Cellular Biology and Genetics _____Clinical Investigations EndocrinologyEpidemiology Immunology Molecular Biology and GeneticsPreclinical Pharmacology and _____Virology Other:_________________________________
Experimental Therapeutics (Please specify)
ACADEMIC DEGREES (Including where and when granted)
EXPERIENCE SINCE HIGHEST DEGREE WAS GRANTED (Please list most recent first)
PUBLICATIONS (Reprints of two peer-reviewed articles on which the candidate appears as an author must accompany this application. For
these two articles list the authors, title, journal, volume, inclusive pages, and year. Do not submit abstracts. If submitting patents, supply patent
number and year awarded.)
CANDIDATE IS APPLYING FOR (Check one): E ACTIVE � CORRESPONDING MEMBERSHIP
CANDIDATE CANDIDATE
NOMINATED BY*:___________________________ SECONDED BY*:___________________________
(Please print) (Please print)
STATEMENT OF SUPPORTInstead of submitting letters of recommendation, either the nominator or the seconder or both may complete the following section:
I acknowledge by signing this statement of support that this candidate adheres to accepted ethical scientific standards and has or will make along-term contribution to cancer research.
Signature of Nominator* Date Signature of Seconder* Date
See Guidelines for Application on the reverse side of this form for further instructions.
*Both nominator and seconder must be active, corresponding, emeritus, or honorary members of the AACR in good standing.
(This form may be reproduced.) 1999
AMERICAN ASSOCIATION FOR CANCER RESEARCH
� GUIDELINES FOR APPLICATION FOR ASSOCIATE MEMBERSHIP
QUALIFICATIONS FOR MEMBERSHIP
Associate membership is open to graduate students, medical students,postdoctoral fellows, and physicians in training who are following acourse of study or who are working in a research program relevant tocancer. Scientists in training who already have a substantial record of
publications may wish to apply for active or corresponding membership
which confers full benefits of membership.
BENEFITS OF MEMBERSHIP
The American Association for Cancer Research (AACR), a scientific
society consisting of laboratory and clinical cancer researchers, was
founded in 1907 to facilitate communication and dissemination of knowl-
edge among scientists and others dedicated to the cancer problem; to
foster research in cancer and related biomedical sciences; to encouragepresentation and discussion of new and important observations in the
field; to foster public education, science education, and training; and to
advance the understanding of cancer etiology, prevention, diagnosis, and
treatment throughout the world. Associate members of the AACR enjoy
the following benefits:
1 . the privilege of sponsoring a proffered paper (abstract) for consider-ation for presentation at the AACR annual meeting provided that (a)
the associate member is the presenter of the paper and (b) an active,
corresponding, emeritus, or honorary member in good standing of the
AACR also signs the abstract of the paper in support of the work. (Inthis instance, the member who cosigns the abstract does not lose his
or her own sponsorship privilege.);
2. optional subscriptions to the Association’s high-quality journals:
Cancer Research, Clinical Cancer Research, Cell Growth & Differ-entiation, and Cancer Epidemiology, Biomarkers & Prevention at
reduced member rates; beginning in I 998 associate members will be
able to purchase AACR journals for half the price of a regular membersubscription;
3. the privilege of registering for the annual meeting at the low associate
member rate;4. the privilege of electing an Associate Member Council that organizes
programs benefiting associate members and that presents their con-
cerns to the AACR Board of Directors:
5. the opportunity to stand for election to the Associate Member Coun-
cil;
6. preferred access to the AACR Employment Register;
7. priority notification of events in the AACR’s series of specialconferences on timely subjects in the field;
8. substantially reduced registration rates at special conferences;9. the receipt of AACR newsletters, meeting announcements, and an
up-to-date Membership Directory;
10. the opportunity to participate in three Summer Workshops that fosterknowledge in the cancer field for young investigators; and
1 1 . the facilitation of informal scientific exchange with leading research-ers in the cancer field.
PROCEDURES FOR APPLICATION
Persons wishing to apply for associate membership must use the
official application form on the reverse side of these instructions. Each
candidate for associate membership must be nominated by an active,
corresponding, emeritus, or honorary member in good standing of the
AACR. Three completed copies of the form should be submitted: at least
one of these copies must carry the original signatures of both the candidate
and the nominator. In addition, the candidate should submit one copy of
his or her curriculum vitae. The application form may be submitted to the
Association Office at any time.
After review of applications for associate membership, the Executive
Director will notify candidates of their election or deferral within onemonth of the receipt of the application form. A check for one year’s duespayment must accompany the application. Dues for 1998 and 1999 are$55 for associate members residing in the Americas and $65 for residentsof other countries. This fee will be refunded to any candidate deemed to
be ineligible for associate membership. Checks should be in U.S. cur-
rency, made payable to AACR, Inc., and drawn on a U.S. bank. Send thethree copies of the application form and the appropriate dues payment to:
Membership Services Department
American Association for Cancer Research
Public Ledger Building, Suite 826150 S. Independence Mall West
Philadelphia, PA 19106-3483Phone: 215/440-9300
Fax: 215/440-9412E-mail: [email protected]
RESPONSIBILITIES OF MEMBERSHIP
Associate members must pay annual dues in an amount to be deter-mined by the AACR Board of Directors. Dues for I 999 have been set at$55 per year for residents of the Americas and $65 for residents of other
countries. If an application is submitted by August 3 1, the accompanying
dues payment will be credited to the current year. Candidates submitting
applications between September 1 and December 3 1 may indicate whether
they wish their dues payments credited to the current or forthcoming year.
Candidates should be aware, however, that associate members may spon-
sor an abstract for the annual meeting only if their dues for the current year
are paid. For example, an associate member submitting an abstract in
November 1998 for the forthcoming annual meeting must have paid duesfor 1998. Any newly elected associate members of the AACR who havealready purchased subscriptions to Cancer Research, Clinical Cancer
Research, Cell Growth & Differentiation, or Cancer Epidemiology, Bio-
markers & Prevention at the higher, nonmember rate will receive a refund
for the unused portion of that subscription upon receipt of their paymentfor a member’s subscription.
Each Fall the AACR will send to current associate members an invoice
for dues for the forthcoming year. Payment of this invoice must be
accompanied by a statement signed by the associate member’s currentregistrar, dean, or department head, verifying the member’s current aca-
demic status. The Association’s By-Laws state that dues are payable foreach year in advance by January 1 of the year to which they should be
applied. An individual may be an associate member for a maximum offive years. Each year in which an individual pays dues will count as onefull year of associate membership. Thus, an associate member who pays
dues for 1999 may retain associate membership until December 31, 2003.The Board of Directors may terminate the membership of an associate
member whose dues are in arrears for two years.
Margaret Foti, Ph.D.Executive Director
I APPLICATIONFOR ASSOCIATE MEMBERSHIP
NAME OF CANDIDATE:_______________
MI.
DATE OF B1RTH:________________
INSTITUTIONAL
INSTITUTIONAL ADDRESS:
LAST FIRST
AFFILIATION:________________________________________________________________
Month/Day/Year
(City) (StatefProvince) (Country) (Postal Code)
Carcinogenesis
Endocrinology
______Molecular Biology and Genetics
Other:
(Please specify)
(This form may be reproduced.) I 999
AMERICAN ASSOCIATION FOR CANCER RESEARCH, INC.
Public Ledger Building ‘ Suite 826 ‘ 150 5. Independence Mall West ‘ Philadelphia, PA 19106-3483
TELEPHONE NUMBER: FAX NUMBER:
P
E-MAIL ADDRESS:
PRESENT ACADEMIC STATUS/TITLE (Please check only one):
______Graduate Student ______Medical Student
Physician in Training Postdoctoral Fellow Gender: E Male E Female
PRIMARY FIELD OF RESEARCH (Please check only one):
Biochemistry and Biophysics Biostatistics ______
______Cellular Biology and Genetics ______Clinical Investigations
Epidemiology Immunology
_____Preclinical Pharmacology and _____Virology
Experimental Therapeutics
ACADEMIC DEGREES (Please indicate degree(s) acquired to date along with the name ofthe academic institution and date ofreceipt. Provide
information on degree currently being sought and the anticipated date of completion of this degree program.)
RELEVANT RESEARCH EXPERIENCE NOT RELATED TO COURSE WORK (Please list most recent first.)
PUBLICATIONS (List the authors, title, journal, volume, inclusive pages, and year of any article in a peer-reviewed journal on which thecandidate appears as an author. Do not list abstracts. Continue on a separate sheet, if necessary.)
CANDIDATE NOMINATED BY*:(Please print)
SIGNATURESI hereby apply for associate membership in the American Association for Cancer Research. I have read the instructions on the reverse side of
this form, and I understand the privileges and responsibilities of this class of membership. I certify that the statements on this application are
true.
Signature of Candidate:.
I recommend this candidate for associate membership in the American Association for Cancer Research. To the best of my knowledge, the
candidate is qualified tbr this class of membership. and the statements on this application are true.
Signature of Nominator* :_______________________________________________________________________ Date:_____________________
Submit three copies of this form. At least one copy must contain the original signatures of the candidate and the nominator. In addition, submit
one copy of your curriculum vitae. Enclose a check in U.S. funds, made payable to AACR, Inc., and drawn on a U.S. bank for one year’s dues.
For 1998 and 1999, dues are $55 for associate members residing in the Americas and $65 for residents of other countries.
Check one of the following boxes only if this tbrm is being submitted between September 1 and December 3 1:
The enclosed dues payment should be applied to the E current E forthcoming calendar year.
(NOTE: If dues are applied to the forthcoming year, membership will take effect on January 1, but the candidate will not be eligible to sponsor
an abstract for presentation at the annual meeting in March or April of that year.) See Guidelines for Application on the reverse side of this
form for further instructions.
*Nominator must be active, corresponding. emeritus, or honorary member of the AACR in good standing.
Guidelines for Submitting Disksto
American Association for Cancer Research Publications
The word processing packages that we prefer are as follows:
MacWrite WordPerfect (DOS, Windows,
Microsoft Word (DOS, Windows, and Macintosh)
and Macintosh) XyWrite (DOS and Windows)
Also acceptable:
Ability Mass 1 1 SoloWriterAmiPro MS Windows Write SprintAM S-T�X MS Works StxAppleworks MS Works WP Mac SunWnteArborT�X Multimate SymphonyArborText Multimate Advantage TEXClarisWorks WP Nibia T�X78CPT 8000 Nisus (to ASCII file) Text EXecutiveCTOS Notewnter TexturesDiablo Obun Total WordDisplayWrite OfficeWriter TroffDuet PC Write p�T�XEinstein PFS First Choice VolkswriterEnable Professional Write VuWriterEXP Q&A Write Wang 015Final Word Quark XPress Wang WPSFullWrite RagTime MS Works Wang WriterGemWord Plus (to ASCII file) Window WorksIBM Writing Assistant Rich Text Format Windows WriteInterleaf RSG (to ASCII file) WiziWordLATEX Signature Wordstar
Latex SLITEX Wordstar 2000Leading Edge SmartWhere WriteNowLotus Manuscript SmartWnte II XeroxLotus Write
Software packages that we are unable to translate:
FrameMaker Ready, Set, GoPageMaker Scientific Writer
Disks produced on IBM or IBM-compatible computers are preferred, but those produced on some Apple orWang computers can also be converted. Because of the file structures and internal coding, we cannot acceptdisks created on desktop publishing systems or those created on proprietary typesetting systems. We alsocannot guarantee that all special characters can be translated. Tabular and mathematical material, such asequations, will not be captured from the disk but will be rekeyed.
To expedite work and for your own security, we do require that you submit a hard copy printout of the disk
file. The tables and equations will be keyed from this hard copy. We also need to know the name of the fileto be converted, the type of hardware (e.g., IBM PC) on which the files were created, the operating system(e.g., DOS 3.3), and the version of the software (e.g., WordPerfect 5.1) used to create the file.
PLEASE FILL OUT ALL INFORMATION ON REVERSE SIDE AND SUBMIT THIS FORM WITH YOUR DISK.
DISKS WILL NOT BE PROCESSED WITHOUT THIS INFORMATION.
DISK SUBMISSION FORM
AACR journals are now using personal computers to copyedit manuscripts accepted for publication. Whensubmitting a revised manuscript, authors are encouraged to submit an electronic disk of the paper along with
the required four hard copy printouts. Disks will ultimately be returned to the authors.
I See reverse for the word processing packages that can be accepted.
File preparation
Please be sure that the file you send is the most recent version of the manuscript and that it matches the mostrecently submitted printed copy. The file should contain all the parts of the manuscript in one file. Mathe-matical and tabular material, however, will be processed in the traditional manner and may be excluded fromthe disk file.
Note: AACR does not assume responsibility for errors in conversion of customized software, newly releasedsoftware, or special characters.
Please label the outside of the disk with the joumal name, the first author’s name, a partial title of themanuscript, and the name of the computer file used to access the manuscript on disk. To process your diskefficiently, we need the following information. Please be sure to provide ALL the information.
Name used to access paper on disk: ____________________
Name of computer used (e.g., IBM/PS2):
Operating system and version (e.g., DOS 3.3):
Word processing program and version (e.g., WordPerfect 5.0):
[See reverse for acceptable programs.]
Manuscript number: _________________________________
First author: ________________________________________
Corresponding author (if different from first author):
Telephone/FAX numbers: ____________________________
This form (both sides) may be reproduced.
P
AMERICAN ASSOCIATION FOR CANCER RESEARCH SCIENTIFIC CONFERENCES
JANUARY 8-12, 1999
The Steroid Receptor Superfamily
Chairpersons: Michael G. Rosenfeld, La Jolla, CA,and Christopher K. Glass, La Jolla, CA
Renaissance Esmeralda Resort, Indian Wells (Palm
Springs), CA
JANUARY 31- FEBRUARY 5, 1999
Cancer Biology and the Mutant Mouse: NewMethods, New Models, New Insights
Chairpersons: Tyler Jacks, Cambridge, MA, andRonald A. DePinho, Boston, MA
Keystone Resort, Keystone, CO
MARCH 4.8, 1999
Molecular Determinants of Sensitivity toAntitumor Agents
Chairpersons: Michael B. Kastan, Memphis, TN, andI. David Goldman, Bronx, NY
Whistler Resort and Conference Centre, Whistler,
British Columbia, Canada
OCTOBER 6.10, 1999
The Molecular and Genetic Basis ofChemoprevention and Early Detection ofCancer
Chairpersons: David Sidransky, Baltimore, MD, andFrank L. Meyskens, Jr. , Irvine, CA
Sheraton Bal Harbour Resort, BaI Harbour, FL
OCTOBER 20-24, 1999
Genetic and Functional Consequences of Cell
Cycle Alterations in CancerChairpersons: Steven I. Reed, La Jolla, CA, and Joan
Ruderman, Boston, MASheraton San Diego Hotel & Marina, San Diego, CA
NOVEMBER 1999
Disrupted Transcription Factors in Cancer
Chairpersons: Peter K. Vogt, La Jolla, CA, and
Frank J. Rauscher III, Philadelphia, PA
Exact dates and location to be determined
APRIL 10-14, 1999
9O�” Annual Meeting
Chairperson: Waun Ki Hong, Houston, TX
Co-Chairpersons: Carol W. Greider, Cold SpringHarbor, NY; Leroy F. Liu, Piscataway, NJ; andJoseph F. Fraumeni, Jr., Bethesda, MD
Pennsylvania Convention Center, Philadelphia, PA
SEPTEMBER 22-26, 1999
Molecular Aspects of Metastasis
Chairpersons: Ruth J. Muschel, Philadelphia, PA;Additional Chairperson to be Announced
Snowmass Village Resort, Snowmass, CO
AACR members will receive brochures on the aboveconferences as soon as they are available.
Nonmembers should call or write:
American Association for Cancer Research
Public Ledger Building, Suite 826I 50 South Independence Mall WestPhiladelphia, PA 19106-3483
21 5-440-9300 #{149}21 5-440-931 3 (FAX)E-Mail: [email protected] regular updates to this list visit the AACR ‘sWebsite, http://www.aacr.org
AMERICAN ASSOCIATION FOR CANCER RESEARCH
CAREER DEVELOPMENT AWARDSNew Program to SuppoiY the Professional Development ofJunior Faculty
Available to Cancer Researchers Around the World
Purpose: The AACR Career Development Awards in Cancer Research will be presented for the first
time in 1999. These two-year, international awards support research by junior, tenure-track
scientists, at the level of Assistant Professor, who are engaged in meritorious cancer research
at an academic institution anywhere in the world. The AACR-National Foundation for
Cancer Research Career Development Award is restricted to proposals in basic research
related to any type ofcancer. The AACR-Susan G. Komen Breast Cancer Foundation Career
Development Award is restricted to proposals for basic, clinical, or translational research
related to breast cancer, including epidemiological and prevention studies.
Support: The two-year, international grants provide $50,000 per year. The grant covers direct research
expenses, which may include payments to research assistants. The grant is not intended to
replace or supplement the salary ofthe primary investigator.
Sponsor: The AACR Career Development Awards are generously sponsored by the National Cancer
Research Foundation and the Susan G. Komen Breast Cancer Foundation.
Eligibility
At the time of application, candidates must be in the first or second year of a full-time, tenure-tracked
faculty appointment, at the level of Assistant Professor, in an academic institution anywhere in the world.
Candidates must also have completed productive postdoctoral research and demonstrated independent,
investigator-initiated research. Employees of a national government and employees ofprivate industry are
not eligible. Candidates must be nominated by a member ofAACR and must be an AACR member or
apply for membership by the time the fellowship application is submitted. AACR Associate Members
may not be nominators.
Selection Process
Applications are evaluated by a prestigious, multi-disciplinary committee consisting ofAACR Members
who are experts in basic, clinical, prevention, and translational research. The application deadline isJanuary 15, 1999.
More Information
The application form and complete guidelines can be requested by contacting AACR at the address
below. The materials will soon be available at the AACR’s websit#{231}www.aacr.org.
American Association for Cancer ResearchPublic Ledger Building, Suite 826
I 50 South Independence Mall WestPhiladelphia, PA 19106-3483
ph: (2 15) 440-9300; f: (21 5) 440-9372e-mail: horst�aacr.org
Attn: Jenny Anne Horst-Martz