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.

It is understood that by publishing any work in CELL GROWTH &DIFFERENTiATION the authors agree to make freely available toother academic researchers any of the coIls, clones of cells, DNAclones, lines of genetically altered mice, antibodies, etc. that wereused in the research reported and that are not available from corn-mercial suppliers. Also, authors may be required to make primarydata available to the Editor-in-Chief in cases of dispute.

Submission of PapersAll papers should be submitted directly to the Editorial Office forconsideration (address below). The manuscript should be accompa-nied by a covering letter indicating that the paper is being submittedfor consideration for publication in CELL GROWTH & DIFFERENT!-AT1ON; the name and address of the corresponding author (includetelephone and FAX numbers and an E-mail address, if available); anda statement confirming that the paper has been reviewed by allauthors and is not under consideration elsewhere. If a manuscript isclosely related to papers that are in press or have been submittedseparately, copies of these papers also should be provided. Guide-lines for the organization of manuscripts are detailed below. Fourcopies ofthe manuscript and accompanying original illustrations (notphotocopies) should be submitted. Authors may suggest appropriatereviewers (suggestions are not limited to the Editorial Board), but thecomplete mailing addresses of any suggested reviewers, includingtelephone and FAX numbers, must be provided.

Editorial office address: Or. Joseph R. NevinsEditor-in-ChiefCell Growth & DifferentiationDuke University Medical CenterBox 3054CARL Building, Room 268Research DriveDurham, NC 27710

Organization and Preparation of ManuscriptsPapers should be written as concisely as possible in clear, gram-matical English and should not occupy more than 8-10 printedpages in the journal. This corresponds to approximately 32-40 dou-ble-spaced typescript pages (4 typed pages = 4 illustrations = 1journal page). Manuscripts should be double-spaced on 8#{189}x 11-inch paper and organized in the following manner

Title Page. A main title together with authors’ names andaffiliations and the address of the corresponding author. A run-ning title of no more than 50 characters in length should also beincluded.

Abstract. A single paragraph on a separate page of no morethan 150 words.

Introduction. A concise introduction to the body of the workwith no subheadings.

Results and Discussion. The results and discussion sectionsmay be separate or combined into a single section. Subheadingsmay be used.

Materials and Methods. Should contain sufficient detail toallow repetition of all procedures.

Acknowledgments. Should include all relevant informationwith the exception of acknowledgments of financial support,which should be indicated in a footnote.

Footnotes. On a page separate from the text. Designate foot-notes consecutively with superscript Arabic numerals.

Tables. On pages separate from the text, with descriptive titlesand legends.

Figure Legends. On pages separate from the text. Define allsymbols and include staining for halftones, where applicable.

References. Include only those articles that have been publishedor are in press. Unpublished data or personal communications mustbe cited as footnotes to the text. Personal communications should besubstantiated by a letter of permission.

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.

IllustrationsProvide four original sets of illustrations (whothor line-cut drawings orhalftones). Label each figure in pencil on the reverse side with the firstauthor’s name, figure number, and an arrow indicating top of figure.Letters and numbers on illustrations should not be smaller than6-point or larger than 12-point type. All illustrations will be publishedat a width of 3#{189}inches unless the author requests a greater width.

Indicate magnifications by moans ofa baron the photograph. Presentkaryotypes in the form of cardboard plates onto which chromosomesections from an original photomicrograph are pasted. Present nucleicacid sequences as glossy prints or original typescripts.

Authors are encouraged to submit color figures. The expense ofreproducing color photographs must be offset partially by theauthors. The cost of color reproduction charged to authors is $975per color figure. Submit color illustrations on flexible backing.

ProofsPage proofs must be returned to the office of the American Associ-ation for Cancer Research within 24 hours of receipt. Return proofsby ovemight mail. Proofs not received by the deadline will bepublished without the authors’ corrections. Accepted manu-scripts are regarded as final copy and should not be altered sub-stantially in proof. Extensive alterations could cause publication do-lays, and authors will be charged for excessive changes in proof.

Publication FeesA page charge of $50 per printed page will be levied on all manu-scripts accepted for publication. It is understood at the time ofsubmission that the author(s) agree to pay this charge in the event ofpublication. Under exceptional circumstances, when no other sourceof grant or other support exists, the author(s) may apply to Dr.Margaret Foti, Director of Publications, AACR Publications Depart-mont (see masthead page for address) at the time of submission fora waiver of the page charges. All such applications must be coun-torsigned by an appropriate institutional official stating that no fundsare available for the payment of page charges.

Typesetting Manuscripts from Computer DisksCELL GROWTH & DIFFERENTiATiON requests the submission ofdisks to expedite production of accepted manuscripts. When anarticle is accepted for publication, authors will receive instructionsregarding disk submission and a form which must be completed andreturned with the disk to the AACR Publications Department within48 hours of notification of acceptance. It is the author’s responsibilityto ensure that the material on the disk matches the final acceptedversion of the manuscript.

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: membership@aacr.org

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: membership@aacr.org

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: meetings@aacr.orgFor 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