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492 results on '"Potter, V."'

1. Sequential vs myeloablative vs reduced intensity conditioning for patients with myelodysplastic syndromes with an excess of blasts at time of allogeneic haematopoietic cell transplantation: a retrospective study by the chronic malignancies working party of the EBMT

Author

Potter, V., Gras, L., Koster, L., Kroger, N., Sockel, K., Ganser, A., Finke, J., Labussiere-Wallet, H., Peffault de Latour, R., Koc, Y., Salmenniemi, U., Smidstrup Friis, L., Jindra, P., Schroeder, T., Tischer, J., Arat, M., Pascual Cascon, M., de Wreede, L. C., Hayden, P., Raj, K., Drozd-Sokolowska, J., Scheid, C., McLornan, D. P., Robin, M., and Yakoub-Agha, I.

Published
2024
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2. Risk of Bowel Obstruction in Patients Undergoing Neoadjuvant Chemotherapy for High-risk Colon Cancer: A Nested Case-control Matched Analysis of an International, Multi-centre, Randomised Controlled Trial (FOxTROT)

Author

Glasbey, James, Glasbey, James, Beggs, Andrew, Glimelius, Bengt, Gray, Richard, Handley, Kelly, Laurberg, Søren, Magill, Laura, Murakami, Keigo, Palmer, Andy, Quirke, Philip, Seligman, Jenny, Seymour, Matt, Sinha, Yash, West, Nick, Morton, Dion, Glasbey, James, Handley, Kelly, Palmer, Andy, Morton, Dion, Crosby, T., Olliff, J., Peto (Chair), R., Brown, Gina, Ferry, David, Glimelius, Bengt, Gray, Richard, Handley, Kelly, Ismail, Tariq, Laurberg, Søren, Magill, Laura, Morton, Dion, Oliver, Alf, Quirke, Phil, Seymour, Matt, Scott, Nigel, Seligman, Jenny, Swift, Ian, Warren, Bryan, West, Nick, Northover, J., Parmar (Chair), M., Slevin, M., Magill, Laura, Gray, Richard, Handley, Kelly, Wilcockson, Adrian, Gray, Zoe, Lancaster, Dominic, Brown, James, Palmer, Andrew, Adie, Ladan, Kennedy, Georgia, Eld, M., Holt, G., Yilmaz, M., Spendler, K. Garm, Hansen, F., Laurberg, S., Rosenkilde, M., Ahlstrom, H., Glimelius, B., Abgamu, D., Day, N., Walsh, C., Bannister, J., Furniss, D., Morgan, S., Walkington, L., Yates, S., Branagan, G., Mustajab, A., O’Neil, H., Rees, C., Geh, I., Hendrickse, C., Langman, G., Pallan, A., Conn, A., Lowe, A., Ostrowski, J., Steward, M., Callaway, M., Falk, S., Thomas, M., Wong, N., Cast, J., Hartley, J., Roy, R., Tiam, R., Blunt, D., Cleator, S., Dawson, P., Goldin, R., Gujral, D., Lowdell, C., Ziprin, P., Clenton, S., Dewdney, A., Euinton, H., Furniss, D., Gupta, R., Tarapowewalla, D., Wilshaw, V., Braun, M., Chakrabarty, B., Hill, J., Laasch, H., Saunders, M., Cruickshank, N., Davies, M., Muzaffar, S., Orme, A., Punia, P., Rea, D., Campbell, F., Hughes, M., Palmer, D., Rooney, P., Abbott, G., Hamid, B., Vimalachandran, D., Berry, J., Hinson, F., Maarouf, Z., Nicoll, J., Adams, C., Denson, J., Jackson, S., Sherriff, D., Kweka, E., McAdam, G., Peters, M., Roy, R., Khaira, M., Kurien, G., Robinson, J., Wadsley, J., White, D., Young, R., Dega, R., Lamparelli, M., Orbell, J., Osborne, R., Taylor, P., Thomas, T., Gopalakrishnan, K., Jadhav, V., Scott-Brown, M., Baijal, S., Chapman, M., Glaholm, J., Nelson, C., Singh, R., Harrison, J., Last, K., Scott, D., Scullion, D., Lind, P., Milosavljevic, Z., Dent, J., Ilsley, D., Littleford, S., Roberts, C., Crabtree, M., Orrell, J., Sherwin, E., Smith, S., Soomal, R., Braun, M., De, A., Khan, A., Khan, U., Lavin, V., McBain, C., Radharkrishna, G., Sil, R., Weerasinghe, S., Hill, J., Lee, S., Wright, P., Church, R., Holland, C., Kunene, V., Thompson, A., Glynne-Jones, R., Goh, V., Livingstone, J., Richman, P., Barlow, C., Burn, P., Geraghty, J., Walther, J., Grumett, S., Mangalika, S., Qaiyum, M., Williams, G., Borgstein, R., Bridgewater, J., Melville, D., Rees, J., Coxon, F., Hainsworth, P., Needham, S., Scott, J., Asmussen, J., Hansen, T., Jensen, K., Pfeiffer, P., Alkhaldi, A., Brittenden, J., Jackson, A., Kamposioras, K., Kumaran, G., Macklin, C., Alexander, J., Harle, A., Hickish, T., Talbot, R., Tarver, D., Bridgewater, J., Partridge, W., Sundaresan, V., Vivekanandan, S., Agrawal, N., Higginson, A., Muthuramalingam, S., O’Leary, D., Devarajan, G., Gulati, M., Kerwat, R., Maisey, N., Mikhaeel, G., Ismail, T., Middleton, G., Page, A., Steven, N., Taniere, P., Gutmann, J., Huang, J., Raouf, S., Dunn, W., Escola, C. Lopez, Potter, V., Scholefield, J., Walker, G., Zaitoun, A., Eason, D., McPhail, N., Mmeka, W., Stenhouse, G., Watson, A., Fozard, B., Hickish, T., Snape, S., Ellis, R., Faux, W., Jenkins, R., Maskell, G., Kulkarni, R., Lund, J., Menon, S., Singh, R., Chandler, I., Daniels, I., Harries, S., Osborne, M., Bell, J., Krell, D., Mayer, A., Ogunbiyi, O., Watkins, J., Bronder, C., Eaton, D., Taylor, A., Brown, G., Cunningham, D., Tekkis, P., Wotherspoon, A., Dobson, M., Mitchell, P., Pitt, M., Scott, N., Susnerwala, S., Adab, F., Britton, I., Ghiridaran, S., Howitt, C., Kirby, R., Biddlestone, L., Dalton, S., De Winton, E., Phillips, A., Ferry, D., Grumett, S., Kawesha, A., Maleki, K., Momtahan, N., Burnett, H., Hayes, S., Soop, M., Branagan, G., Cook, I., Cook, S., Iveson, T., Shablak, A., Coup, A., Hamid, A., Moore, P., O’Toole, L., Pai, D., Bateman, A., Bateman, A., Blaquiere, R., Nichols, P., Chappell, M., Dworkin, M., Jain, S., Tsang, D., Hopkins, K., Loveday, E., Lyons, A., Rooney, N., Ali, N., Chatterjee, M., Chiphang, A., Dundas, S., Myint, A. Sun, Zeiderman, M., Beharry, N., Chong, H., Lofts, F., Melville, D., Finan, P., Seymour, M., Tolan, D., West, N., Anyamene, N., Burling, D., Kennedy, R., Moorghen, M., Agrawal, S., Hasan, J., Mehta, S., Saeed, M., Burgess, P., John, L., Lowndes, S., Planner, A., Campbell, F., Hughes, M., Rooney, P., Smith, D., Hochhauser, D., Obichere, A., Rodriguez-Justo, M., Shiu, K., Taylor, S., Correa, P., James, S., Shatwell, W., Williams, N., Brady, J., Lanaspre, E., Mikhaeel, G., Ahmad, M., Gill, T., Wilson, D., Adams, R., Beehen, R., Morgan, M., Lindh, B., Adams, R., Morgan, M., Ford, A., Gopal, K., Pranesh, N., Shareef, D., Tighe, M., Busby, K., Correa, P., Sanders, S., Sinha, R., Ahmad, R., Desai, S., Ramesh, S., Hilman, S., Lott, M., O’Brien, J., Radstone, D., West, D., Amin, S., Hampton, J., Hornbuckle, J., Kitsanta, P., Ali, M., Desai, A., Hadaki, M., Hall, M., Arul, D., Hochhauser, D., Leonard, P., Mukhtar, H., Murray, D., Baxter, A., Churn, M., Farrugia, D., Lake, S., Smith, G., Bansal, A., Chandran, P., Corr, C., Gollins, S., Davenport, A., Saunders, M., Sukumar, S., Bathurst, N., Beaumont, E., Cooper, E., Francis, N., Sephton, M., Sparrow, G., Clarke, A., Haselden, J., Last, K., Woodcock, N., Atkinson, M., Gollins, S., Gupta, M., Maw, A., Abdullah, N., Bale, C., and Lord, M.

Published
2023
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5. Haplotype motif-based models for KIR-genotype informed selection of hematopoietic cell donors fail to predict outcome of patients with Myelodysplastic Syndromes or secondary Acute Myeloid Leukemia (vol 11,& nbsp;584520, 2021)

Author

Schetelig, J., Baldauf, H., Koster, L., Kuxhausen, M., Heidenreich, F., Wreede, L.C. de, Spellman, S., Gelder, M. van, Bruno, B., Onida, F., Lange, V., Massalski, C., Potter, V., Ljungman, P., Schaap, N., Hayden, P., Lee, S.P.N.J., Kroeger, N., Hsu, K.T.Y., Schmidt, A.H., Yakoub-Agha, I., and Robin, M.

Subjects
KIR3DL1, unrelated donor, hematopoietic stem cell transplantation, donor selection, KIR2DS1, KIR
Published
2021

26. Safety and Efficacy of Autologous Stem Cell Transplantation in Dialysis-Dependent Myeloma Patients – the Diadem Study from the Chronic Malignancies Working Party of the EBMT

Author

Gyan, E, Schroyens, W, Potter, V, Nikolousis, M, Basak, GW, Sever, M, Baurmann, H, Bulabois, CE, ARAT, MUTLU, Ills, A, Dreger, P, Snowden, JA, ÖZKURT, ZÜBEYDE NUR, Guffroy, B, Sirait, T, Wreede, LC, Wang, J, Anna, WG, Hayden, PJ, Serna, J, BEKSAÇ, MERAL, Gorkom, GV, Schönland, SO, and YakoubAgha, I

Published
2019

27. Impact of primary disease on outcome after allogeneic stem cell transplantation for transformed secondary acute leukaemia

Author

Kroger, N., Eikema, D.J., Koster, L., Beelen, D., Wreede, L.C. de, Finke, J., Koenecke, C., Niederwieser, D., Bornhauser, M., Schoenland, S., Potter, V., Wolschke, C., Maertens, J., Theobald, M., Kobbe, G., Itala-Remes, M., Wulf, G., Kahls, P., Forcade, E., Greinix, H., Masszi, T., Yakoub-Agha, I., Chalandon, Y., Robin, M., and European Soc Blood Marrow Transpla

Subjects
Male, Chronic myelomonocytic leukaemia, myeloproliferative neoplasm, Medizin, Myeloproliferative neoplasm, Graft vs Host Disease, Gastroenterology, 0302 clinical medicine, allogeneic stem cell transplantation, hemic and lymphatic diseases, MDS, Medicine, Cumulative incidence, ddc:616, Hematopoietic Stem Cell Transplantation, Leukemia, Myelomonocytic, Chronic, Hematology, Middle Aged, Haematopoiesis, Leukemia, Myeloid, Acute, 030220 oncology & carcinogenesis, Acute Disease, Disease Progression, Female, Stem cell, chronic myelomonocytic leukaemia, Adult, medicine.medical_specialty, Adolescent, Transplantation, Autologous, Disease-Free Survival, 03 medical and health sciences, Young Adult, Median follow-up, Statistical significance, Internal medicine, Humans, Aged, Secondary acute myeloid leukaemia, Myeloproliferative Disorders, secondary acute myeloid leukaemia, business.industry, Myelodysplastic syndromes, medicine.disease, Allogeneic stem cell transplantation, Transplantation, Myelodysplastic Syndromes, Chronic Disease, Neoplasm Recurrence, Local, business, 030215 immunology
Abstract

Myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN) and chronic myelomonocytic leukaemia (CMML) can progress to secondary acute myeloid leukaemia (sAML). We compared the outcome of 4214 sAML patients who received allogeneic haematopoietic stem cell transplantation (allo-HSCT) from an unrelated (62%) or human leucocyte antigen (HLA)-identical sibling donor (38%) according the underlying disease: MDS (n = 3541), CMML (n = 251) or MPN (n = 422). After a median follow up of 46·5 months, the estimated 3-year progression-free (PFS) and overall survival (OS) for the entire group was 36% (34-37%) and 41% (40-43%), respectively. The cumulative incidence of relapse and non-relapse mortality (NRM) was 37% (35-39%) and 27% (26-29%), respectively. In a multivariable analysis for OS, besides age (P

Published
2019

28. Human parainfluenza virus type 3 infections in a haemato-oncology unit: social distancing measures needed in outpatient clinics.

Author

Anton-Vazquez, V., Smith, M., Mehra, V., Avenoso, D., Krishnamurthy, P., Kulasekararaj, A., Potter, V., Pagliuca, A., and Zuckerman, M.

Abstract

Background: Human parainfluenza virus type 3 (HPIV3) infections are associated with high mortality in immunocompromised settings, especially in bone marrow transplant recipients. Asymptomatic infection and lack of effective antiviral treatment makes HPIV3 prevention and treatment a real challenge.Aim: To retrospectively investigate the epidemiological characteristics, clinical characteristics and outcomes of 51 haematology patients with confirmed HPIV3 infections, detected between February and May 2019 in the haematology unit at King's College Hospital, London.Methods: Between February and May 2019, HPIV3 RNA was detected in combined nose and throat swab samples collected from 51 symptomatic haematology patients, 41 of whom attended the haematology outpatient unit. Clinical data were reviewed retrospectively and a timeline of patients' appointments drawn up to investigate transmission. Sequencing analysis was performed on 14 stored samples.Findings: Fifty-one patients were identified with HPIV3 infection. Mean age was 54 years (SD: 12; range: 19-72) and 60% (31/51) were male. There were 41 (80%) bone marrow transplant recipients, 24 had an allograft, and 17 an autograft. Thirty-day and 3-month mortality post HPIV3 was 6% and 14%, respectively. Lower respiratory tract infection and inpatient acquisition were associated with higher mortality (6/7 vs 1/7, P = 0.010; and 5/7 vs 2/7, P = 0.031). Onset of HPIV3 infection in patients within 6 days of attending the clinic was associated with the clusters identified in phylogenetic analysis (64% (9/14) vs 21% (8/37); odds ratio: 6.5 (confidence interval: 95% 1.7-25); P = 0.006).Conclusion: Timelines suggested community transmission, but also possible transmission patterns within the outpatients and subsequent nosocomial transmission within the same ward. Early recognition of HPIV3 infection and the use of polymerase chain reaction and sequence analysis is fundamental in identifying respiratory virus outbreaks and person-to-person transmission. Careful planning of outpatient clinic attendance is required to minimize contact and prevent respiratory virus transmission in immunosuppressed patients. [ABSTRACT FROM AUTHOR]

Published
2021
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29. Mixed T Cell Chimerism After Allogeneic Hematopoietic Stem Cell Transplantation for Severe Aplastic Anemia Using an Alemtuzumab-Containing Regimen Is Shaped by Persistence of Recipient CD8 T Cells

Author

Grimaldi F., Potter V., Perez-Abellan P., Veluchamy J. P., Atif M., Grain R., Sen M., Best S., Lea N., Rice C., Pagliuca A., Mufti G. J., Marsh J. C. W., Barber L. D., Grimaldi, F., Potter, V., Perez-Abellan, P., Veluchamy, J. P., Atif, M., Grain, R., Sen, M., Best, S., Lea, N., Rice, C., Pagliuca, A., Mufti, G. J., Marsh, J. C. W., and Barber, L. D.

Subjects
Adult, Male, Transplantation Chimera, Transplantation Conditioning, Adolescent, Cell Survival, Graft Survival, Hematopoietic Stem Cell Transplantation, T cell, Anemia, Aplastic, T-Lymphocyte Subset, CD8-Positive T-Lymphocyte, Middle Aged, Chimerism, Immunosuppressive Agent, Young Adult, Treatment Outcome, Retrospective Studie, Female, Aplastic anemia, Alemtuzumab, Whole-Body Irradiation, Human
Abstract

Prevention of graft-versus-host disease (GVHD) is paramount for allogeneic hematopoietic stem cell transplantation (HSCT) to treat nonmalignant diseases. We previously reported that allogeneic HSCT for severe aplastic anemia (SAA) using the fludarabine, cyclophosphamide, and alemtuzumab (Campath-1H) (FCC) regimen is associated with a very low risk of GVHD and excellent clinical outcomes. We now report a single-center study of 45 patients with longer follow-up and investigation of lymphocyte recovery. Overall survival (OS) was 93%, and event-free survival (EFS) was 90.7%. Acute and chronic GVHD each occurred in 6 patients (13.3%), and only 1 case was severe. Mixed T cell chimerism was frequent and persisted after cessation of immunosuppression. T cells were extensively depleted, representing only 11.3% of lymphocytes at day 30 and rising to 43.8% by 1 year, but still significantly below normal levels (67.2%; P = .018), and deficiency persisted after immunosuppressive therapy (IST) withdrawal. Depletion of CD4 T cells was particularly profound, causing inversion of the normal CD4:CD8 T cell ratio. T cell subset composition was also abnormal, with memory and effector T cells predominating for at least 6 months after FCC HSCT. Analysis of T cell subset chimerism showed that CD4 T cells were predominantly donor-derived at 1 year, whereas recipient-derived CD8 T cells shaped mixed chimerism with a notable contribution of recipient effector CD8 T cells. The prolonged mixed T cell chimerism after IST withdrawal and low incidence of GVHD indicates the establishment of mutual tolerance, but the low incidence of viral disease suggests maintenance of antiviral immunity. Our study shows that despite the abnormal T cell profile after allogeneic HSCT for SAA using the FCC regimen, this regimen is conducive to an excellent clinical outcome.

Published
2017

31. Cardiopoietic cell therapy for advanced ischemic heart failure : results at 39 weeks of the prospective, randomized, double blind, sham-controlled CHART-1 clinical trial

Author

Bartunek, Jozef, Terzic, Andre, Davison, Beth A, Filippatos, Gerasimos S, Radovanovic, Slavica, Beleslin, Branko, Merkely, Bela, Musialek, Piotr, Wojakowski, Wojciech, Andreka, Peter, Horvath, Ivan G, Katz, Amos, Dolatabadi, Dariouch, El Nakadi, Badih, Arandjelovic, Aleksandra, Edes, Istvan, Seferovic, Petar M, Obradovic, Slobodan, Vanderheyden, Marc, Jagic, Nikola, Petrov, Ivo, Atar, Shaul, Halabi, Majdi, Gelev, Valeri L, Shochat, Michael K, Kasprzak, Jaroslaw D, Sanz Ruiz, Ricardo, Heyndrickx, Guy R, Nyolczas, Noémi, Legrand, Victor, Guédès, Antoine, Heyse, Alex, Moccetti, Tiziano, Fernandez Aviles, Francisco, Jimenez Quevedo, Pilar, Bayes Genis, Antoni, Hernandez Garcia, Jose Maria, Ribichini, Flavio, Gruchala, Marcin, Waldman, Scott A, Teerlink, John R, Gersh, Bernard J, Povsic, Thomas J, Henry, Timothy D, Metra, Marco, Hajjar, Roger J, Tendera, Michal, Behfar, Atta, Alexandre, Bertrand, Seron, Aymeric, Stough, Wendy Gattis, Sherman, Warren, Cotter, Gad, Wijns, W. i. l. l. i. a. m. Collaborators Clinical investigators, Dens, sites Belgium: Ziekenhuis Oost Limburg: J., Dupont, M., Mullens, W., Janssens, M., Dolatabadi, Hoˆpital Civil de Charleroi: D., De Bruyne, Y., Lalmand, J., Dubois, P., El Nakadi, B., Aminian, A., De Vuyst, E., Gurnet, P., Gujic, M., Blankoff, I., Guedes, CHU Mont Godinne UCL: A., Gabriel, L., Seldrum, S., Doyen, C., Andre´, M., Heyse, AZ Glorieux: A., Van Durme, F., Verschuere, J., Legrand, Domaine Universitaire du Sart Tilman: V., Gach, O., D’Orio, V., Davin, L., Lancellotti, P., Baudoux, E., Ancion, A., Dulgheru, R., Vanderheyden, OLV Ziekenhuis Aalst – Cardiologie: M., Bartunek, J., Wijns, W., Verstreken, S., Penicka, . M., Gelev, P. Meeus Bulgaria: Tokuda Hospital Sofia: V., Zheleva Kichukova, I., Parapunova, R., Melamed, R., Sardovski, S., Radev, O., Yordanov, A., Radinov, A., Nenov, D., Amine, I., Petrov, City Hospital Clinic Cardiology Center: I., Kichukov, K., Nikitasov, L., Stankov, Z., Stoyanov, H., Tasheva Dimitrova, I., Angelova, M., Dimitrov, E., Minchev, M., Garvanski, I., Botev, C., Polomski, P., Alexandrovska University Hospital, Vassilev, Sofia: D., Karamfiloff, K., Tarnovska Kadreva, R., Vladimirova, L., Dimitrov, G., Hadzhiev, E., Tzvetkova, G., Andreka, . M. Atanasova Hungary: Gottsegen Gyo¨ rgy Orszagos Kardiologiai Inte´zet: P., Fontos, G., Fabian, J., Csepregi, A., Uzonyi, G., Gelei, A., Edes, Debreceni Egyetem Orvos e´s Ege´szse´gtudomanyi Centrum Altalanos Orvostudomanyi Kar Kardiologia Inte´zet: I., Balogh, L., Vajda, G., Darago, A., Gergely, S., Fulop, T., Jenei, C., Horvath, Pe´csi Tudomanyegyetem Klinikai Ko¨zpont Szıvgyogyaszati Klinika: I., Magyari, B., Nagy, A., Cziraki, A., Faludi, R., Kittka, B., Alizadeh, H., Merkely, Semmelweis Egyetem Varosmajori Szıv e´s Ergyogyaszati Klinika: B., Geller, L., Farkas, P., Szombath, G., Foldes, G., Skopal, J., Kovacs, A., Kosztin, A., Gara, E., Sydo, N., Nyolczas, MH Ege´szse´gu¨gyi Ko¨zpont Kardiologiai Osztaly: N., Kerecsen, G., Korda, A., Kiss, . M., Borsanyi, T., Polgar, B., Muk, B., Sharif, Z. Bari Ireland: HRB Clinical Research Facility: F., Atar, Y. M. Smyth Israel:Western Galilee Hospital: S., Shturman, A., Akria, L., Kilimnik, M., Brezins, M., Halabi, Ziv Medical Center: M., Dally, N., Goldberg, A., Aehab, K., Rosenfeld, I., Levinas, T., Saleem, D., Katz, Barzilai Medical Center: A., Plaev, T., Drogenikov, T., Nemetz, A., Barshay, Y., Jafari, J., Orlov, I., Nazareth Hospital EMMS: M. Omory, N. Kogan Nielsen, Shochat, Hillel Yaffe Medical Center: M., Shotan, A., Frimerman, A., Meisel, S., Asif, A., Sofer, O., Blondheim, D. S., Vazan, A., Metra, L. Arobov Italy: A. O. Spedali Civili di Brescia: M., Bonadei, I., Inama, L., Chiari, E., Lombardi, C., Magatelli, M., Russo, D., Lazzarini, V., Carubelli, V., Vassanelli, AOUI Verona – Borgo Trento Hospital: C., Ribichini, Flavio Luciano, Bergamini, C., Krampera, Mauro, Cicoria, M. A., Zanolla, L., Dalla Mura, D., Gambaro, A., Rossi, A., Pesarini Poland: Jagiellonian University Department of Cardiac, G., Musialek, Vascular Diseases at John Paul II Hospital in Krakow: P., Mazurek, A., Drabik, L., Ka˛dzielski, A., Walter, Z., Dzieciuch Rojek, M., Rubis, P., Plazak, . W., Tekieli, L., Podolec, J., Orczyk, W., Sutor, U., Zmudka, K., Olszowska, M., Podolec, P., Gruchala, Uniwersyteckie Centrum Kliniczne: M., Ciecwierz, D., Mielczarek, M., Burakowski, S., Chmielecki, M., Zielinska, M., Frankiewicz, A., Wdowczyk, J., Stopczynska, I., Bellwon, J., Mosakowska, K., Nadolna, R., Wroblewska, J., Rozmyslowska, M., Rynkiewicz, M., Marciniak, I., Raczak, G., Tarnawska, M., Taszner, M., Kasprzak, Bieganski Hospital: J., Plewka, M., Fiutowska, D., Rechcinski, T., Lipiec, P., Sobczak, M., Weijner Mik, P., Wraga, M., Krecki, R., Markiewicz, M., Haval Qawoq, D., Wojakowski, Gornosla˛skie Centrum Medyczne Sla˛skie j. Akademii Medycznej: W., Ciosek, J., Dworowy, S., Gaszewska Zurek, E., Ochala, A., Cybulski, W., Jadczyk, T., Wanha, W., Parma, Z., Kozlowski, M., Dzierzak, M., Markiewicz Serbia: Clinical Hospital Center Zvezdara, M., Arandjelovic, Cardiology Clinic: A., Sekularac, N., Boljevic, D., Bogdanovic, A., Zivkovic, S., Cvetinovic, N., Loncar, G., Clinical Centre of Serbia, Beleslin, Cardiology Clinic: B., Nedeljkovic, M., Trifunovic, D., Giga, V., Banovic, M., Nedeljkovic, I., Stepanovic, J., Vukcevic, V., Djordjevic Dikic, A., Dobric, M., Obrenovic Kircanski, B., Seferovic, Cardiology Clinic: P., Orlic, D., Tesic, M., Petrovic, O., Milinkovic, I., Simeunovic, D., Jagic, Clinical Center of Kragujevac: N., Tasic, M., Nikolic, D., Miloradovic, V., Djurdjevic, P., Sreckovic, M., Zornic, N., Clinical Hospital Center Bezanijska Kosa, Radovanovic, Cardiology Department: S., Saric, J., Hinic, S., Djokovic, A., Ðordevic, S., Bisenic, V., Markovic, O., Stamenkovic, S., Malenkovic, V., Tresnjak, J., Misic, G., Cotra, D., Tomovic, L., Vuckovic, V., Clinic of Emergency Internal Medicine, Obradovic, Military Medical Academy: S., Jovic, Z., Vukotic, S., Markovic, D., Djenic, N., Ristic Andjelkov, A., Bayes Genis, D. Ljubinka Spain: Hospital Universitario Germans Trias I. Pujol: A., Rodriguez Leor, O., Labata, C., Vallejo, N., Ferrer, E., Batlle, M., Fernandez Aviles, Hospital General Universitario Gregorio Mara~non: F., Sanz Ruiz, R., Casado, A., Loughlin, G., Zatarain, E., Anguita, J., Ferna ndez Santos, M. E., Pascual, C., Bermejo, J., Hernandez Garcia, Hospital Clinico Universitario Virgen de la Victoria: J. M., Jimenez Navarro, M., Dominguez, A., Carrasco, F., Mu~noz, A., Garcia Pinilla, J. M., Ruiz, J., Queipo de Llano, M. P., Hernandez, A., Fernandez, A., Jimenez Quevedo, Hospital Clinico San Carlos: P., Guerra, R., Biagioni, C., Gonzalez, R. A., Gomez deDiego, J. J., Mansson Broberg, L. Perez de Isla Sweden: Karolinska University Hospital: A., Sylve´n, C., Leblanc, K., Winter, R., Blomberg, P., Gunyeli, E., Ruck, A., Silva, C., Fo¨rstedt Switzerland: CardioCentro Ticino, J., Moccetti, Switzerland: T., Rossi, M., Pasotti, E., Petrova, I., Crljenica, C., Monti, C., Murzilli, R., Su¨rder, D., Moccetti, M., Turchetto, L., Locicero, V., Chiumiento, L., Maspoli, S., Mombelli, M., Anesini, A., Biggiogero, M., Ponti, G., Camporini, C., Polledri, S., Hill, G. Dolci United Kingdom: Kings College Hospital: J., Plymen, C., Amin Youssef, G., Mcdonagh, T., Drasar, E., Mijovic, A., Jouhra, F., Mcloman, D., Dworakowski, R., Webb, I., Byrne, J., and Potter, V.

Subjects
0301 basic medicine, Male, Cardiopoiesis, Cardiovascular disease, Disease severity, Marker, Precision medicine, Regenerative medicine, Stem cell, Target population, Adult, Aged, Double-Blind Method, Female, Heart Failure, Humans, Mesenchymal Stem Cell Transplantation, Middle Aged, Myocardial Ischemia, Prospective Studies, Treatment Outcome, Young Adult, Cardiology and Cardiovascular Medicine, Cell- and Tissue-Based Therapy, mesenchymal stem-cells, 030204 cardiovascular system & hematology, Cardiorespiratory Medicine and Haematology, outcomes, Fast-Track Clinical Research, Sudden cardiac death, 0302 clinical medicine, Ischemia, cardiovascular disease, Clinical endpoint, target population, CHART Program, Ejection fraction, bone-marrow, Heart Failure/Cardiomyopathy, 3. Good health, Cohort, Cardiology, Fast Track, disease severity, delivery, medicine.medical_specialty, precision medicine, Clinical Sciences, regenerative medicine, 03 medical and health sciences, cardiopoiesis, Internal medicine, medicine, Adverse effect, marker, disease, business.industry, medicine.disease, mortality, Confidence interval, Clinical trial, stem cell, Editor's Choice, 030104 developmental biology, predictors, Cardiovascular System & Hematology, Heart failure, business
Abstract

Altres ajuts: This work was supported by Celyad, SA (Mont-Saint-Guibert, Belgium). Celyad has received research grants from the Walloon Region (Belgium, DG06 funding). Cardiopoietic cells, produced through cardiogenic conditioning of patients' mesenchymal stem cells, have shown preliminary efficacy. The Congestive Heart Failure Cardiopoietic Regenerative Therapy (CHART-1) trial aimed to validate cardiopoiesis-based biotherapy in a larger heart failure cohort. This multinational, randomized, double-blind, sham-controlled study was conducted in 39 hospitals. Patients with symptomatic ischaemic heart failure on guideline-directed therapy (n = 484) were screened; n = 348 underwent bone marrow harvest and mesenchymal stem cell expansion. Those achieving > 24 million mesenchymal stem cells (n = 315) were randomized to cardiopoietic cells delivered endomyocardially with a retention-enhanced catheter (n = 157) or sham procedure (n = 158). Procedures were performed as randomized in 271 patients (n = 120 cardiopoietic cells, n = 151 sham). The primary efficacy endpoint was a Finkelstein–Schoenfeld hierarchical composite (all-cause mortality, worsening heart failure, Minnesota Living with Heart Failure Questionnaire score, 6-min walk distance, left ventricular end-systolic volume, and ejection fraction) at 39 weeks. The primary outcome was neutral (Mann–Whitney estimator 0.54, 95% confidence interval [CI] 0.47–0.61 [value > 0.5 favours cell treatment], P = 0.27). Exploratory analyses suggested a benefit of cell treatment on the primary composite in patients with baseline left ventricular end-diastolic volume 200–370 mL (60% of patients) (Mann–Whitney estimator 0.61, 95% CI 0.52–0.70, P = 0.015). No difference was observed in serious adverse events. One (0.9%) cardiopoietic cell patient and 9 (5.4%) sham patients experienced aborted or sudden cardiac death. The primary endpoint was neutral, with safety demonstrated across the cohort. Further evaluation of cardiopoietic cell therapy in patients with elevated end-diastolic volume is warranted.

Published
2017

32. CAR T treatment access and outcomes in patients with large B‐cell lymphoma according to ethnicity and socioeconomic deprivation.

Author

Dragoi, D., Cusworth, S., Amrith, M., Sanderson, R., Paneesha, S., Patten, P., Potter, V., Hardefeldt, P., Yallop, D., Chaganti, S., Burns, D., and Kuhnl, A.

Subjects
HEALTH services accessibility, TREATMENT effectiveness, ETHNICITY, LYMPHOMAS, ETHNIC groups, MOTION sickness
Abstract

However, patients from more deprived areas had inferior overall survival and access to post-CAR T therapies, underscoring healthcare inequalities in these patients. B Background: b CAR T-cell therapy has revolutionised treatment of relapsed/refractory (r/r) large B-cell lymphoma (LBCL), but it is unclear whether access and clinical benefit is equal for ethnic minorities and deprived communities. CAR T treatment access and outcomes in patients with large B-cell lymphoma according to ethnicity and socioeconomic deprivation. [Extracted from the article]

Published
2023
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33. Outcome and biomarker analysis from a multi-centre phase 2 study of ipilimumab in combination with carboplatin and etoposide (ICE) as first line therapy for extensive stage small cell lung cancer

Author

Arriola, E., Wheater, M., Galea, I., Cross, N., Maishman, T., Hamid, D., Stanton, L., Cave, J., Geldart, T., Mulatero, C., Potter, V., Danson, S., Woll, P.J., Griffiths, R., Nolan, L., and Ottensmeier, C.

Abstract

BACKGROUND: To evaluate safety and efficacy of ipilimumab combined with standard first-line chemotherapy for patients with extensive stage SCLC.METHODS: Chemotherapy-naïve extensive stage SCLC patients were treated with carboplatin and etoposide up to six cycles. Ipilimumab 10 mg/kg was given on day 1 of cycles 3-6 and every 12 weeks. Response was assessed by RECIST v1.0 and immune related response criteria (irRC). The primary endpoint was 1-year progression-free survival (PFS) according to RECIST. Secondary endpoints included PFS by irRC (irPFS) and overall survival (OS). Autoantibody serum levels were evaluated and correlated with clinical outcomes.RESULTS: 42 patients were enrolled between September 2011-April 2014, 39 evaluable for safety and 38 for efficacy. 6/38 patients (15.8% [95% CI: 7.4%-30.4%]) were alive and progression-free at 1-year by RECIST. Median PFS was 6.9 months (95%CI: 5.5-7.9). Median irPFS was 7.3 months (95% CI: 5.5-8.8). Median OS was 17.0 months (95% CI: 7.9-24.3). In patients evaluable for response, 21/29 patients (72.4%) achieved an objective response by RECIST and 28/33 (84.8%) by irRC. All patients experienced at least one adverse event; 35/39 (89.7%) patients developed at least one toxicity ? Grade 3; in 27 (69.2%) this was related to ipilimumab. Five deaths were reported to be related to ipilimumab. The positivity of an autoimmune profile at baseline was associated with improved outcomes and severe neurological toxicity.CONCLUSION: Ipilimumab in combination with carboplatin and etoposide might benefit a subgroup of patients with advanced SCLC. Autoantibody analysis correlates with treatment benefit and toxicity and warrants further investigation.

Published
2016

37. P1444: IMPACT OF CO‐MORBIDITIES ON NON‐RELAPSE MORTALITY AND CYTOKINE‐RELEASE SYNDROME AFTER CD19 CAR‐T CELL THERAPY ‐ A RETROSPECTIVE STUDY FROM THE TCWP OF THE EBMT AND GOCART COALITION.

Author

Basak, G., Peczynski, C., Koenecke, C., Terwel, S., Cabrerizo, Y., Penack, O., Moiseev, I., Schoemans, H., Fegueux, N., Potter, V., Zeerleder, S., Yakoub‐Agha, I., Collin, M., Schanz, U., Dreger, P., Blaise, D., Besley, C., Glass, B., Mohty, M., and Chabannon, C.

Published
2022
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39. Effects of a maternal high-fat diet on offspring behavioral and metabolic parameters in a rodent model.

Author

Johnson, S. A., Javurek, A. B., Painter, M. S., Murphy, C. R., Conard, C. M., Gant, K. L., Howald, E. C., Ellersieck, M. R., Wiedmeyer, C. E., Vieira-Potter, V. J., and Rosenfeld, C. S.

Abstract

Maternal diet-induced obesity can cause detrimental developmental origins of health and disease in offspring. Perinatal exposure to a high-fat diet (HFD) can lead to later behavioral and metabolic disturbances, but it is not clear which behaviors and metabolic parameters are most vulnerable. To address this critical gap, biparental and monogamous oldfield mice (Peromyscus polionotus), which may better replicate most human societies, were used in the current study. About 2 weeks before breeding, adult females were placed on a control or HFD and maintained on the diets throughout gestation and lactation. F1 offspring were placed at weaning (30 days of age) on the control diet and spatial learning and memory, anxiety, exploratory, voluntary physical activity, and metabolic parameters were tested when they reached adulthood (90 days of age). Surprisingly, maternal HFD caused decreased latency in initial and reverse Barnes maze trials in male, but not female, offspring. Both male and female HFD-fed offspring showed increased anxiogenic behaviors, but decreased exploratory and voluntary physical activity. Moreover, HFD offspring demonstrated lower resting energy expenditure (EE) compared with controls. Accordingly, HFD offspring weighed more at adulthood than those from control fed dams, likely the result of reduced physical activity and EE. Current findings indicate a maternal HFD may increase obesity susceptibility in offspring due to prenatal programming resulting in reduced physical activity and EE later in life. Further work is needed to determine the underpinning neural and metabolic mechanisms by which a maternal HFD adversely affects neurobehavioral and metabolic pathways in offspring. [ABSTRACT FROM PUBLISHER]

Published
2017
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47. Treatment decisions and survival for people with small-cell lung cancer.

Author

Powell, H A, Tata, L J, Baldwin, D R, Potter, V A, Stanley, R A, Khakwani, A, and Hubbard, R B

Abstract

Background: Chemotherapy improves survival for many patients with SCLC, and hence it is important to understand variations in practice and outcomes for this treatment strategy.Methods: We used the National Lung Cancer Audit and Hospital Episodes Statistics to determine the proportion of patients who received chemotherapy for SCLC, and assess the effects of patient and organisational factors on the odds of receiving chemotherapy and of completing four cycles. We calculated median survival and used Cox regression to determine factors that predicted survival.Results: Of 15 091 cases of SCLC, 70% received at least one cycle of chemotherapy. More deprived people were less likely to receive chemotherapy, but patients were more likely to receive chemotherapy, and to complete ≥ four cycles, if they were referred to the lung cancer team by their GP. Median survival for those treated with chemotherapy was 12.9 months for limited and 7.3 months for extensive stage disease.Conclusions: The Linked NLCA and HES data provide real-life measures of survival in people treated with chemotherapy and show how this is influenced by patient and tumour characteristics. These data show the characteristics of patients who are less likely to complete a full course of treatment, an adverse predictor of survival. [ABSTRACT FROM AUTHOR]

Published
2014
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48. Sleep and cognition in older adults with cardiovascular disease.

Author

Kociuba C, Szabo A, Gunstad J, Spitznagel MB, Potter V, Hughes J, Waechter D, Josephson R, and Rosneck J

Abstract

BACKGROUND: Sleep problems are common in the normal population and likely to be especially prevalent in persons with cardiovascular disease. PURPOSE: We examined the prevalence of sleep difficulties and their impact on cognitive function in 77 persons (mean age, 62.8 [SD, 12.5] years; 24% female) presenting for perfusion stress scan at an outpatient cardiology center. METHODS: Participants completed the Pittsburgh Sleep Quality Index and Modified Mini-Mental State Examination as part of a larger project. RESULTS: Analyses showed that approximately 94% of participants met the criteria for 'poor' sleep (ie, Pittsburgh Sleep Quality Index global score >=5). Poorer reported sleep was associated with reduced cognitive function as measured by the Modified Mini-Mental State Examination after adjusting for age, depression, and cardiovascular fitness (ie, estimated metabolic equivalents; R² change = 0.08, F = 7.17; P <.001). CONCLUSION: These findings indicate that sleep problems are common in cardiovascular disease and extend previous research by demonstrating they negatively impact cognitive function. Further work is needed to identify other consequences of poor sleep in this population and optimal treatment. [ABSTRACT FROM AUTHOR]

Published
2010
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49. Selective determinants of inositol 1,4,5-trisphosphate and adenophostin A interactions with type 1 inositol 1,4,5-trisphosphate receptors.

Author

Rossi, Ana M, Sureshan, Kana M, Riley, Andrew M, Potter, Barry VL, Taylor, Colin W, and Potter, V L

Subjects
INOSITOL phosphates, MOLECULAR structure, CATIONS, ION-ion collisions, GENETIC mutation, CARRIER proteins, CALCIUM metabolism, PROTEIN metabolism, ADENOSINES, ANIMAL experimentation, COMPARATIVE studies, RESEARCH methodology, MEDICAL cooperation, PROTEINS, RATS, RESEARCH, RESEARCH funding, VASOCONSTRICTORS, EVALUATION research
Abstract

Background and Purpose: Adenophostin A (AdA) is a potent agonist of inositol 1,4,5-trisphosphate receptors (IP(3) R). AdA shares with IP(3) the essential features of all IP(3) R agonists, namely structures equivalent to the 4,5-bisphosphate and 6-hydroxyl of IP(3) , but the basis of its increased affinity is unclear. Hitherto, the 2'-phosphate of AdA has been thought to provide a supra-optimal mimic of the 1-phosphate of IP(3) .Experimental Approach: We examined the structural determinants of AdA binding to type 1 IP(3) R (IP(3) R1). Chemical synthesis and mutational analysis of IP(3) R1 were combined with (3) H-IP(3) binding to full-length IP(3) R1 and its N-terminal fragments, and Ca(2+) release assays from recombinant IP(3) R1 expressed in DT40 cells.Key Results: Adenophostin A is at least 12-fold more potent than IP(3) in functional assays, and the IP(3) -binding core (IBC, residues 224-604 of IP(3) R1) is sufficient for this high-affinity binding of AdA. Removal of the 2'-phosphate from AdA (to give 2'-dephospho-AdA) had significantly lesser effects on its affinity for the IBC than did removal of the 1-phosphate from IP(3) (to give inositol 4,5-bisphosphate). Mutation of the only residue (R568) that interacts directly with the 1-phosphate of IP(3) decreased similarly (by ~30-fold) the affinity for IP(3) and AdA, but mutating R504, which has been proposed to form a cation-π interaction with the adenine of AdA, more profoundly reduced the affinity of IP(3) R for AdA (353-fold) than for IP(3) (13-fold).Conclusions and Implications: The 2'-phosphate of AdA is not a major determinant of its high affinity. R504 in the receptor, most likely via a cation-π interaction, contributes specifically to AdA binding. [ABSTRACT FROM AUTHOR]

Published
2010
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