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21. Civic Medicine

Author

Mendelsohn, J. Andrew, Kinzelbach, Annemarie, and Schilling, Ruth

Subjects
civic doctors, Early modern European medicine, transformative itineraries, urban polity
Abstract

Communities great and small across Europe for eight centuries have contracted with doctors. Physicians provided citizen care, helped govern, and often led in public life. Civic Medicine stakes out this timely subject by focusing on its golden age, when cities rivaled territorial states in local and global Europe and when civic doctors were central to the rise of shared, organized written information about the human and natural world. This opens the prospect of a long history of knowledge and action shaped more by community and responsibility than market or state, exchange or power.

Published
2020
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25. Civic Medicine

Author

Andrew Mendelsohn, J., primary, Kinzelbach, Annemarie, additional, and Schilling, Ruth, additional

Published
2019
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26. Acknowledgments

Author

Dierig, Sven, Lachmund, Jens, and Mendelsohn, J. Andrew

Published
2003

27. The conventional balance: A TKO for NATO?

Author

Mendelsohn, J. and Halverson, T.

Subjects
*WEAPONS
Abstract

Discusses the prevailing view on conventional force disparity and NATO's sense of inferiority to the Warsaw Pact's numerical superiority. NATO to Warsaw Pact comparison; Analysis. INSET: In the gift horse's mouth (Israeli acquisition of Soviet tanks)..

Published
1989
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31. Antiangiogenic and antitumor activity of anti-epidermal growth factor receptor C225 monoclonal antibody in combination with vascular endothelial growth factor antisense oligonucleotide in human GEO colon cancer cells

Author

Ciardiello, F., Bianco, R., Damiano, V., Fontanini, G., Caputo, R., Pomatico, G., Placido, S., Bianco, A. R., Mendelsohn, J., Giampaolo Tortora, Ciardiello, Fortunato, Bianco, R, Damiano, V, Fontanini, G, Caputo, R, Pomatico, G, DE PLACIDO, S, Bianco, Ar, Mendelsohn, J, and Tortora, G.

Subjects
Vascular Endothelial Growth Factor A, Lymphokines, Mice, Inbred BALB C, Dose-Response Relationship, Drug, Neovascularization, Pathologic, Vascular Endothelial Growth Factors, Blotting, Western, Antibodies, Monoclonal, Mice, Nude, Endothelial Growth Factors, Oligonucleotides, Antisense, Thionucleotides, Transforming Growth Factor alpha, Immunohistochemistry, Xenograft Model Antitumor Assays, ErbB Receptors, Mice, Colonic Neoplasms, Tumor Cells, Cultured, Animals, Humans, Female, Fibroblast Growth Factor 2
Abstract

Angiogenesis plays a key role in tumor growth and metastasis. The transforming growth factor alpha (TGF-alpha)-epidermal growth factor receptor (EGFR) autocrine pathway controls in part the production of angiogenic factors such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in cancer cells. In this study, we have evaluated the antiangiogenic and antitumor activity of monoclonal antibody (MAb) C225, an anti-EGFR chimeric human-mouse MAb, alone and in combination with a human VEGF antisense (AS) 21-mer phosphorothioate oligonucleotide (VEGF-AS) in human GEO colon cancer cells. MAb C225 treatment determined a dose-dependent inhibition of VEGF, bFGF, and TGF-alpha production by GEO cells in vitro. Treatment with VEGF-AS caused a selective inhibition in VEGF expression by GEO cells in vitro. Treatment of immunodeficient mice bearing established, palpable GEO xenografts for 3 weeks with VEGF-AS or with MAb C225 determined a cytostatic reversible inhibition of tumor growth. In contrast, a prolonged inhibition of tumor growth was observed in all mice treated with the two agents, in combination with a significant improvement in mice survival compared with controls (P.001), to MAb C225 (P.001), or to VEGF-AS (P.001) treated mice. All mice died within 4, 6, and 8 weeks after tumor cell injection in the control, VEGF-AS and MAb C225 groups, respectively. In contrast, 50% of mice treated with the combination of VEGF-AS and MAb C225 were alive at 13 weeks. Ten % of mice treated with VEGF-AS plus MAb C225 were alive at 20 weeks and had no histological evidence of GEO tumors. Immunohistochemical analysis of GEO tumor xenografts demonstrated a significant reduction of VEGF expression after treatment with VEGF-AS with a parallel reduction in microvessel count. MAb C225 treatment determined a reduction in the expression of VEGF, bFGF, and TGF-alpha with a reduction in microvessel count. Finally, a significant potentiation in inhibition of VEGF expression and little or no microvessels were observed in GEO tumors after the combined treatment with the two agents.

Published
2000

32. Antiangiogenic and antitumor activity of anti-EGFR C225 monoclonal antibody in combination with Vascular Endothelial Growth Factor antisense oligonucleotide in human GEO colon cancer cells

Author

Ciardiello, F, Bianco, R, Damiano, V, Fontanini, G, Caputo, R, Pomatico, G, DE PLACIDO, S, Bianco, Ar, Mendelsohn, J, Tortora, Giampaolo, Ciardiello, F, Bianco, Roberto, Damiano, Vincenzo, Fontanini, G, Caputo, R, Pomatico, G, DE PLACIDO, Sabino, Bianco, Ar, Mendelsohn, J, and Tortora, Giampaolo

Subjects
cetuximab, VEGF, EGFR
Published
2000

33. Antitumor activity of sequential treatment with topotecan and anti-epidermal growth factor receptor monoclonal antibody C225

Author

Fortunato Ciardiello, Bianco, R., Damiano, V., Lorenzo, S., Pepe, S., Placido, S., Fan, Z., Mendelsohn, J., Bianco, A. R., Tortora, G., Ciardiello, F, Bianco, Roberto, Damiano, Vincenzo, DE LORENZO, Sonya, Pepe, Stefano, DE PLACIDO, Sabino, Fan, Z, Mendelsohn, J, Bianco, A. R., Tortora, Giampaolo, Ciardiello, Fortunato, Bianco, R, Damiano, V, DE LORENZO, S, Pepe, S, DE PLACIDO, S, Bianco, Ar, and Tortora, G.

Subjects
Mice, Inbred BALB C, Dose-Response Relationship, Drug, EGFR, Antibodies, Monoclonal, Cetuximab, Mice, Nude, Antineoplastic Agents, Drug Synergism, Neoplasms, Experimental, Antibodies, Monoclonal, Humanized, Drug Administration Schedule, ErbB Receptors, Mice, Tumor Cells, Cultured, topotecan, cetuximab, Animals, Humans, Topotecan, Neoplasm Transplantation, Tumor Stem Cell Assay
Abstract

Epidermal growth factor (EGF)-related proteins such as transforming growth factor alpha (TGF-alpha) control cancer cell growth through autocrine and paracrine pathways. Overexpression of TGF-alpha and/or its receptor (EGFR) has been associated with a more aggressive disease and a poor prognosis. The blockade of EGFR activation has been proposed as a target for anticancer therapy. Monoclonal antibody (MAb) C225 is an anti-EGFR humanized chimeric mouse MAb that is presently in Phase II clinical trials in cancer patients. Previous studies have suggested the potentiation of the antitumor activity of certain cytotoxic drugs, such as cisplatin and doxorubicin, in human cancer cell lines by treatment with anti-EGFR antibodies. We have evaluated in human ovarian, breast, and colon cancer cell lines, which express functional EGFR, the antiproliferative activity of MAb C225 in combination with topotecan, a cytotoxic drug that specifically inhibits topoisomerase I and that has shown antitumor activity in these malignancies. A dose-dependent supraadditive increase of growth inhibition in vitro was observed when cancer cells were treated with topotecan and MAb C225 in a sequential schedule. In this respect, the cooperativity quotient, defined as the ratio between the actual growth inhibition obtained by treatment with topotecan followed by MAb C225 and the sum of the growth inhibition achieved by each agent, ranged from 1.2 to 3, depending on drug concentration and cancer cell line. Treatment with MAb C225 also markedly enhanced apoptotic cell death induced by topotecan. For example, in GEO colon cancer cells, 5 nM topotecan, followed by 0.5 microg/ml MAb C225, induced apoptosis in 45% cells as compared with untreated cells (6%) or to 5 nM topotecan-treated cells (22%). Treatment of mice bearing established human GEO colon cancer xenografts with topotecan or with MAb C225 determined a transient inhibition of tumor growth because GEO tumors resumed the growth rate of untreated tumors at the end of the treatment period. In contrast, an almost complete tumor regression was observed in all mice treated with the two agents in combination. This determined a prolonged life span of the mice that was significantly different as compared with controls (P0.001), to MAb C225-treated group (P0.001), or to the topotecan-treated group (P0.001). All mice of the topotecan plus MAb C225 group were the only animals alive 14 weeks after tumor cell injection. Furthermore, 20% of mice in this group were still alive after 19 weeks. The combined treatment with MAb C225 and topotecan was well tolerated by mice with no signs of acute or delayed toxicity. These results provide a rationale for the evaluation of the anticancer activity of the combination of topoisomerase I inhibitors and anti-EGFR blocking MAbs in clinical trials.

Published
1999

34. Synergistic growth inhibition and induction of apoptosis by a novel mixed backbone antisense oligonuclotide targeting CRIPTO in combination with C225 anti-EGFR monoclonal antibody and 8-Cl-cAMP in human GEO colon cancer cells

Author

Normanno, N, Tortora, Giampaolo, DE LUCA, A, Pomatico, G, Casamassimi, A, Agrawal, S, Mendelsohn, J, Bianco, Ar, Ciardiello, F., Normanno, N, Tortora, Giampaolo, DE LUCA, A, Pomatico, G, Casamassimi, A, Agrawal, S, Mendelsohn, J, Bianco, Ar, and Ciardiello, F.

Subjects
cetuximab, colon cancer cells, CRIPTO
Published
1999

35. Cooperative inhibitory effect of novel mixed backbone oligonucleotide targeting Protein Kinase A in combination with docetaxel and anti-EGFR-Receptor antibody on human breast cancer cell growth

Author

Tortora, Giampaolo, Caputo, R, Pomatico, G, Pepe, S, Bianco, A. R., Agrawal, S, Mendelsohn, J, Ciardiello, F., Tortora, Giampaolo, Caputo, R, Pomatico, G, Pepe, Stefano, Bianco, A. R., Agrawal, S, Mendelsohn, J, and Ciardiello, F.

Subjects
breast cancer, Protein Kinase A, anti-EGFR antibody
Published
1999

36. Growth inhibition of human colon carcinoma cells by combinations of anti-EGF-related growth factor antisense oligonucleotides

Author

Normanno, N., Bianco, C., Damiano, V., DE ANGELIS, E., Selvam, M. P., Grassi, M., Magliulo, G., Tortora, Giampaolo, Bianco, A. R., Mendelsohn, J., Salomon, D. S., Ciardiello, F., Normanno, N., Bianco, C., Damiano, V., de Angelis, E., Selvam, M. P., Grassi, M., Magliulo, G., Tortora, Giampaolo, Bianco, A. R., Mendelsohn, J., Salomon, D. S., and Ciardiello, F.

Subjects
colon cancer, EGF, antisense oligonucleotides
Published
1996

38. Cooperative antiproliferative effects of 8-chloro-cyclic AMP and 528 anti-epidermal growth factor receptor monoclonal antibody on human cancer cells

Author

CIARDIELLO, Fortunato, DAMIANO V, BIANCO C, DI ISERNIA G, RUGGIERO A, CARAGLIA, Michele, TAGLIAFERRI P, BASELGA J, MENDELSOHN J, BIANCO AR, Ciardiello, Fortunato, Damiano, V, Bianco, C, DI ISERNIA, G, Ruggiero, A, Caraglia, Michele, Tagliaferri, P, Baselga, J, Mendelsohn, J, and Bianco, Ar

Subjects
ErbB Receptors, Kinetics, Epidermal Growth Factor, Cell Cycle, Tumor Cells, Cultured, 8-Bromo Cyclic Adenosine Monophosphate, Antibodies, Monoclonal, Humans, Antineoplastic Agents, Breast Neoplasms, Female, DNA Fragmentation, Cell Division
Abstract

8-Chloro-cyclic AMP (8-Cl-cAMP), a site-selective cAMP analogue, is a specific inhibitor of type I cAMP-dependent protein kinase (PKAI) and induces growth inhibition in several human and rodent tumor cell lines. The anti-epidermal growth factor receptor (EGFR) mAb 528 is a blocking antibody able to inhibit the in vitro and in vivo growth of several human cancer cell lines that express functional EGFRs. Since enhanced levels of PKAI are generally found in tumor cells and an increase in PKAI expression is induced by transformation through a transforming growth factor alpha/EGFR autocrine pathway, we have evaluated whether treatment with mAb 528 in combination with 8-Cl-cAMP may have an additive or synergistic growth inhibitory effect on human cancer cells. A dose-dependent inhibition of monolayer cell growth was observed in two human colon cancer cell lines (GEO and CBS) and in a human breast cancer cell line (MDA-468) by treatment with either mAb 528 or 8-Cl-cAMP with 50% inhibitory concentration of 2-10 microgram/ml or 20-25 micrometer, respectively. The combined treatment with low noninhibitory doses of mAb 528 (0.25 microgram/ml) and with 8-Cl-cAMP had a more than additive growth inhibitory effect with a 3- to 5-fold reduction in the 8-Cl-cAMP 50% inhibitory concentration in all cell lines tested. This combined treatment was similarly effective in inhibiting the soft agar cloning efficiency of GEO cells. 8-Cl-cAMP treatment of GEO cells induced a dose-dependent increase in cell membrane-associated EGFRs with a maximum 3- to 4-fold increase within 48-72 h of treatment. These results suggest that a double blockade of the PKAI serine-threonine kinase-dependent and of the EGFR tyrosine kinase-dependent pathways is potentially useful in cancer therapy.

Published
1995

39. Start deals cut at Jackson Hole.

Author

Mendelsohn, J.

Subjects
*INTERNATIONAL cooperation on nuclear arms control
Abstract

Discusses the meeting between Secretary of State James Baker and Soviet Foreign Minister Eduard Shevardnadze that was held in late September in Jackson Hole, Wyoming. Overcoming impediments to a strategic arms reduction treaty (START); Sea-launched cruise missiles; Air-launched cruise missiles; Mobile missiles; Verification and stability; Timetables.

Published
1989
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40. 1 Feasibility of large-scale genomic testing to facilitate enrollment on genomically-matched clinical trials

Author

Meric-Bernstam, F., primary, Brusco, L., additional, Kopetz, S., additional, Davies, M., additional, Routbort, M.J., additional, Piha-Paul, S.A., additional, Alvarez, R., additional, Khose, S., additional, De Groot, J., additional, Ravi, V., additional, Janku, F., additional, Hong, D., additional, Li, Y., additional, Luthra, R., additional, Patel, K.P., additional, Broaddus, R., additional, Shaw, K., additional, Mendelsohn, J., additional, and Mills, G.B., additional

Published
2014
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42. Diabetes and risk of pancreatic cancer : a pooled analysis from the pancreatic cancer cohort consortium

Author

Elena, J. W., Steplowski, E., Yu, K., Hartge, P., Tobias, G. S., Brotzman, M. J., Chanock, S. J., Stolzenberg-Solomon, R. Z., Arslan, A. A., Bueno-De-Mesquita, H. B., Helzlsouer, K., Jacobs, E. J., Lacroix, A., Petersen, G., Zheng, W., Albanes, D., Allen, N. E., Amundadottir, L., Bao, Y., Boeing, H., Boutron-Ruault, M. -C, Buring, J. E., Gaziano, J. M., Giovannucci, E. L., Duell, E. J., Hallmans, Göran, Howard, B. V., Hunter, D. J., Hutchinson, A., Jacobs, K. B., Kooperberg, C., Kraft, P., Mendelsohn, J. B., Michaud, D. S., Palli, D., Phillips, L. S., Overvad, K., Patel, A. V., Sansbury, L., Shu, X. -O, Simon, M. S., Slimani, N., Trichopoulos, D., Visvanathan, K., Virtamo, J., Wolpin, B. M., Zeleniuch-Jacquotte, A., Fuchs, C. S., Hoover, R. N., Gross, M., Elena, J. W., Steplowski, E., Yu, K., Hartge, P., Tobias, G. S., Brotzman, M. J., Chanock, S. J., Stolzenberg-Solomon, R. Z., Arslan, A. A., Bueno-De-Mesquita, H. B., Helzlsouer, K., Jacobs, E. J., Lacroix, A., Petersen, G., Zheng, W., Albanes, D., Allen, N. E., Amundadottir, L., Bao, Y., Boeing, H., Boutron-Ruault, M. -C, Buring, J. E., Gaziano, J. M., Giovannucci, E. L., Duell, E. J., Hallmans, Göran, Howard, B. V., Hunter, D. J., Hutchinson, A., Jacobs, K. B., Kooperberg, C., Kraft, P., Mendelsohn, J. B., Michaud, D. S., Palli, D., Phillips, L. S., Overvad, K., Patel, A. V., Sansbury, L., Shu, X. -O, Simon, M. S., Slimani, N., Trichopoulos, D., Visvanathan, K., Virtamo, J., Wolpin, B. M., Zeleniuch-Jacquotte, A., Fuchs, C. S., Hoover, R. N., and Gross, M.

Abstract

Purpose: Diabetes is a suspected risk factor for pancreatic cancer, but questions remain about whether it is a risk factor or a result of the disease. This study prospectively examined the association between diabetes and the risk of pancreatic adenocarcinoma in pooled data from the NCI pancreatic cancer cohort consortium (PanScan). Methods: The pooled data included 1,621 pancreatic adenocarcinoma cases and 1,719 matched controls from twelve cohorts using a nested case-control study design. Subjects who were diagnosed with diabetes near the time (<2 years) of pancreatic cancer diagnosis were excluded from all analyses. All analyses were adjusted for age, race, gender, study, alcohol use, smoking, BMI, and family history of pancreatic cancer. Results: Self-reported diabetes was associated with a forty percent increased risk of pancreatic cancer (OR = 1.40, 95 % CI: 1.07, 1.84). The association differed by duration of diabetes; risk was highest for those with a duration of 2-8 years (OR = 1.79, 95 % CI: 1.25, 2.55); there was no association for those with 9+ years of diabetes (OR = 1.02, 95 % CI: 0.68, 1.52). Conclusions: These findings provide support for a relationship between diabetes and pancreatic cancer risk. The absence of association in those with the longest duration of diabetes may reflect hypoinsulinemia and warrants further investigation.

Published
2013
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44. Jeremiah Metzger Lecture. Targeted cancer therapy

Author

Mendelsohn, J.

Subjects
ErbB Receptors, Clinical Trials as Topic, Neovascularization, Pathologic, Neoplasms, Cell Cycle, Animals, Antibodies, Monoclonal, Humans, Antineoplastic Agents, Apoptosis, Neoplasm Metastasis, Combined Modality Therapy, Research Article
Abstract

I have reviewed here and elsewhere the preclinical data and the clinical trials which have demonstrated the efficacy of therapy with monoclonal antibodies that block activation of receptors for growth factors (12). Herceptin is now in clinical use. Our own antibody, C225 against the EGF receptor, shows great promise, but phase III trials need to be completed to prove its efficacy. The research efforts with C225 have involved scientists in academia, the pharmaceutical industry, and the National Cancer Institute, and contributions were made by many collaborators. I believe it is highly likely that blockade of growth factor-mediated signal transduction pathways, in combination with chemotherapy or radiotherapy, will enhance our ability to inhibit, and in some cases to eradicate, many of the common epithelial human malignancies (60).

Published
2000

48. OMICS AND PROGNSTIC MARKERS

Author

Adachi, K., primary, Sasaki, H., additional, Nagahisa, S., additional, Yoshida, K., additional, Hattori, N., additional, Nishiyama, Y., additional, Kawase, T., additional, Hasegawa, M., additional, Abe, M., additional, Hirose, Y., additional, Alentorn, A., additional, Marie, Y., additional, Poggioli, S., additional, Alshehhi, H., additional, Boisselier, B., additional, Carpentier, C., additional, Mokhtari, K., additional, Capelle, L., additional, Figarella-Branger, D., additional, Hoang-Xuan, K., additional, Sanson, M., additional, Delattre, J.-Y., additional, Idbaih, A., additional, Yust-Katz, S., additional, Anderson, M., additional, Olar, A., additional, Eterovic, A., additional, Ezzeddine, N., additional, Chen, K., additional, Zhao, H., additional, Fuller, G., additional, Aldape, K., additional, de Groot, J., additional, Andor, N., additional, Harness, J., additional, Lopez, S. G., additional, Fung, T. L., additional, Mewes, H. W., additional, Petritsch, C., additional, Arivazhagan, A., additional, Somasundaram, K., additional, Thennarasu, K., additional, Pandey, P., additional, Anandh, B., additional, Santosh, V., additional, Chandramouli, B., additional, Hegde, A., additional, Kondaiah, P., additional, Rao, M., additional, Bell, R., additional, Kang, R., additional, Hong, C., additional, Song, J., additional, Costello, J., additional, Nagarajan, R., additional, Zhang, B., additional, Diaz, A., additional, Wang, T., additional, Bie, L., additional, Li, Y., additional, Liu, H., additional, Luyo, W. F. C., additional, Carnero, M. H., additional, Iruegas, M. E. P., additional, Morell, A. R., additional, Figueiras, M. C., additional, Lopez, R. L., additional, Valverde, C. F., additional, Chan, A. K.-Y., additional, Pang, J. C.-S., additional, Chung, N. Y.-F., additional, Li, K. K.-W., additional, Poon, W. S., additional, Chan, D. T.-M., additional, Wang, Y., additional, Ng, H.-a. K., additional, Chaumeil, M., additional, Larson, P., additional, Yoshihara, H., additional, Vigneron, D., additional, Nelson, S., additional, Pieper, R., additional, Phillips, J., additional, Ronen, S., additional, Clark, V., additional, Omay, Z. E., additional, Serin, A., additional, Gunel, J., additional, Omay, B., additional, Grady, C., additional, Youngblood, M., additional, Bilguvar, K., additional, Baehring, J., additional, Piepmeier, J., additional, Gutin, P., additional, Vortmeyer, A., additional, Brennan, C., additional, Pamir, M. N., additional, Kilic, T., additional, Krischek, B., additional, Simon, M., additional, Yasuno, K., additional, Gunel, M., additional, Cohen, A. L., additional, Sato, M., additional, Aldape, K. D., additional, Mason, C., additional, Diefes, K., additional, Heathcock, L., additional, Abegglen, L., additional, Shrieve, D., additional, Couldwell, W., additional, Schiffman, J. D., additional, Colman, H., additional, D'Alessandris, Q. G., additional, Cenci, T., additional, Martini, M., additional, Ricci-Vitiani, L., additional, De Maria, R., additional, Larocca, L. M., additional, Pallini, R., additional, Theeler, B., additional, Lang, F., additional, Rao, G., additional, Gilbert, M., additional, Sulman, E., additional, Luthra, R., additional, Eterovic, K., additional, Routbort, M., additional, Verhaak, R., additional, Mills, G., additional, Mendelsohn, J., additional, Meric-Bernstam, F., additional, Yung, A., additional, MacArthur, K., additional, Hahn, S., additional, Kao, G., additional, Lustig, R., additional, Alonso-Basanta, M., additional, Chandrasekaran, S., additional, Wileyto, E. P., additional, Reyes, E., additional, Dorsey, J., additional, Fujii, K., additional, Kurozumi, K., additional, Ichikawa, T., additional, Onishi, M., additional, Ishida, J., additional, Shimazu, Y., additional, Kaur, B., additional, Chiocca, E. A., additional, Date, I., additional, Geisenberger, C., additional, Mock, A., additional, Warta, R., additional, Schwager, C., additional, Hartmann, C., additional, von Deimling, A., additional, Abdollahi, A., additional, Herold-Mende, C., additional, Gevaert, O., additional, Achrol, A., additional, Gholamin, S., additional, Mitra, S., additional, Westbroek, E., additional, Loya, J., additional, Mitchell, L., additional, Chang, S., additional, Steinberg, G., additional, Plevritis, S., additional, Cheshier, S., additional, Xu, J., additional, Napel, S., additional, Zaharchuk, G., additional, Harsh, G., additional, Gutman, D., additional, Holder, C., additional, Colen, R., additional, Dunn, W., additional, Jain, R., additional, Cooper, L., additional, Hwang, S., additional, Flanders, A., additional, Brat, D., additional, Hayes, J., additional, Droop, A., additional, Thygesen, H., additional, Boissinot, M., additional, Westhead, D., additional, Short, S., additional, Lawler, S., additional, Bady, P., additional, Kurscheid, S., additional, Delorenzi, M., additional, Hegi, M. E., additional, Crosby, C., additional, Faulkner, C., additional, Smye-Rumsby, T., additional, Kurian, K., additional, Williams, M., additional, Hopkins, K., additional, Palmer, A., additional, Williams, H., additional, Wragg, C., additional, Haynes, H. R., additional, Kurian, K. M., additional, White, P., additional, Oka, T., additional, Jalbert, L., additional, Elkhaled, A., additional, Jensen, R., additional, Salzman, K., additional, Schabel, M., additional, Gillespie, D., additional, Mumert, M., additional, Johnson, B., additional, Mazor, T., additional, Barnes, M., additional, Yamamoto, S., additional, Ueda, H., additional, Tatsuno, K., additional, Aihara, K., additional, Bollen, A., additional, Hirst, M., additional, Marra, M., additional, Mukasa, A., additional, Saito, N., additional, Aburatani, H., additional, Berger, M., additional, Taylor, B., additional, Popov, S., additional, Mackay, A., additional, Ingram, W., additional, Burford, A., additional, Jury, A., additional, Vinci, M., additional, Jones, C., additional, Jones, D. T. W., additional, Hovestadt, V., additional, Picelli, S., additional, Wang, W., additional, Northcott, P. A., additional, Kool, M., additional, Reifenberger, G., additional, Pietsch, T., additional, Sultan, M., additional, Lehrach, H., additional, Yaspo, M.-L., additional, Borkhardt, A., additional, Landgraf, P., additional, Eils, R., additional, Korshunov, A., additional, Zapatka, M., additional, Radlwimmer, B., additional, Pfister, S. M., additional, Lichter, P., additional, Joy, A., additional, Smirnov, I., additional, Reiser, M., additional, Shapiro, W., additional, Kim, S., additional, Feuerstein, B., additional, Jungk, C., additional, Friauf, S., additional, Unterberg, A., additional, Juratli, T. A., additional, McElroy, J., additional, Meng, W., additional, Huebner, A., additional, Geiger, K. D., additional, Krex, D., additional, Schackert, G., additional, Chakravarti, A., additional, Lautenschlaeger, T., additional, Kim, B. Y., additional, Jiang, W., additional, Beiko, J., additional, Prabhu, S., additional, DeMonte, F., additional, Sawaya, R., additional, Cahill, D., additional, McCutcheon, I., additional, Lau, C., additional, Wang, L., additional, Terashima, K., additional, Yamaguchi, S., additional, Burstein, M., additional, Sun, J., additional, Suzuki, T., additional, Nishikawa, R., additional, Nakamura, H., additional, Natsume, A., additional, Terasaka, S., additional, Ng, H.-K., additional, Muzny, D., additional, Gibbs, R., additional, Wheeler, D., additional, Zhang, X.-q., additional, Sun, S., additional, Lam, K.-f., additional, Kiang, K. M. Y., additional, Pu, J. K. S., additional, Ho, A. S. W., additional, Leung, G. K. K., additional, Loebel, F., additional, Curry, W. T., additional, Barker, F. G., additional, Lelic, N., additional, Chi, A. S., additional, Cahill, D. P., additional, Lu, D., additional, Yin, J., additional, Teo, C., additional, McDonald, K., additional, Madhankumar, A., additional, Weston, C., additional, Slagle-Webb, B., additional, Sheehan, J., additional, Patel, A., additional, Glantz, M., additional, Connor, J., additional, Maire, C., additional, Francis, J., additional, Zhang, C.-Z., additional, Jung, J., additional, Manzo, V., additional, Adalsteinsson, V., additional, Homer, H., additional, Blumenstiel, B., additional, Pedamallu, C. S., additional, Nickerson, E., additional, Ligon, A., additional, Love, C., additional, Meyerson, M., additional, Ligon, K., additional, Jalbert, L. E., additional, Nelson, S. J., additional, Bollen, A. W., additional, Smirnov, I. V., additional, Song, J. S., additional, Olshen, A. B., additional, Berger, M. S., additional, Chang, S. M., additional, Taylor, B. S., additional, Costello, J. F., additional, Mehta, S., additional, Armstrong, B., additional, Peng, S., additional, Bapat, A., additional, Berens, M., additional, Melendez, B., additional, Mollejo, M., additional, Mur, P., additional, Hernandez-Iglesias, T., additional, Fiano, C., additional, Ruiz, J., additional, Rey, J. 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Published
2013
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50. Formation of p27-CDK complexes during the human mitotic cell cycle

Author

Soos, Tj, Kiyokawa, H., Yan, Js, Rubin, Ms, Antonio Giordano, Deblasio, A., Bottega, S., Wong, Bm, Mendelsohn, J., and Koff, A.

Subjects
Tumor Suppressor Proteins, Blotting, Western, Cell Cycle, Cyclin-Dependent Kinase 2, G1 Phase, Mitosis, Cell Cycle Proteins, Cyclin-Dependent Kinase 6, Protein Serine-Threonine Kinases, Blotting, Northern, Cyclin-Dependent Kinases, Molecular Weight, Cricetinae, Cyclins, CDC2-CDC28 Kinases, Tumor Cells, Cultured, Animals, Humans, Cyclin D3, Enzyme Inhibitors, Microtubule-Associated Proteins, Cell Division, Cyclin-Dependent Kinase Inhibitor p27
Abstract

In eukaryotic cells, the coordinated activation of different cyclin-dependent kinases regulates entry into S-phase. In vitro and in nonproliferating cells, p27 associates with and inhibits cyclin/cycin-dependent kinase (CDK) holoenzymes containing either CDK4, CDK6, or CDK2. Although many different types of proliferating cells contain p27 protein, neither the interactions of p27 with cyclin/CDK complexes nor the consequences of this interaction during the mitotic cycle have been fully explored. We report that, in MANCA cells, the amount of p27 is constant during the cell cycle. In addition, p27 associates with three different CDKs: CDK2, CDK4, and CDK6. Furthermore, the amount of p27 is significantly lower than the amount of cyclin D3 in these cells. The amount of CDK4 and CDK6 associated with p27 does not change in a cell cycle-dependent fashion; in contrast, the amount of CDK2 associated with p27 is lowest in early G1 cells and increases to a maximum in mid-G1 phase, reaching a steady-state level in late G1-phase cells. After mid-G1 phase, the amount of each p27/CDK complex remains constant through the remainder of the cell cycle. p27-immunoprecipitates contain an Rb-kinase activity. The substrate specificity, the expression pattern of this kinase, and the ability to deplete 50% of this kinase activity with a CDK6-specific antibody suggest that the CDK6 protein mediates, in part, the p27-associated Rb-kinase activity. In contrast, p27 complexes containing CDK2 are incapable of phosphorylating histone H1. These data are consistent with a model wherein cyclin D/CDK complexes sequester the CDK2-dependent kinase inhibitory activity of p27.

Published
1996

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