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28 results on '"Keohane, Clodagh"'

9. Treatment patterns and outcomes of unfit and elderly patients with Mantle cell lymphoma unfit for standard immunochemotherapy: A UK and Ireland analysis

Author

Rampotas, Alexandros, primary, Wilson, Matthew R., additional, Lomas, Oliver, additional, Denny, Nicholas, additional, Leary, Heather, additional, Ferguson, Graeme, additional, McKay, Pamela, additional, Ebsworth, Tim, additional, Miller, Jonathan, additional, Shah, Nimish, additional, Martinez‐Calle, Nicolas, additional, Bishton, Mark, additional, Everden, Angharad, additional, Tucker, David, additional, El‐Hassad, Ezzat, additional, Hennessy, Brian, additional, Doherty, Dearbhla, additional, Prideaux, Steve, additional, Faryal, Rehman, additional, Hayat, Amjad, additional, Keohane, Clodagh, additional, Marr, Helen, additional, Gibb, Adam, additional, Pocock, Rachael, additional, Lambert, Jonathan, additional, Lacey, Rachel, additional, Elmusharaf, Nagah, additional, Clifford, Ruth, additional, and Eyre, Toby A., additional

Published
2021
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11. High grade non-germinal centre-like diffuse large Bcell lymphoma double expressor presenting as a hydrocoele.

Author

Hogan, Donnacha, Hayes, Brian, Keohane, Clodagh, and Hennessey, Derek Barrry

Abstract

A 72-year-old man was referred to our urology outpatient department with a left hemi-scrotal swelling increasing in size over a matter of weeks, initially suspicious for a left hydrocoele. Initial investigation with ultrasound (US) identified a heterogenous enlargement of the left testis and epididymis with a soft tissue mass extending through the inguinal canal. Subsequent CT detected this soft tissue mass to extend along the left gonadal vein to the level of the left renal vein. A biopsy of the retroperitoneal mass confirmed a diagnosis of diffuse large B-cell lymphoma. Immunohistochemical staining further categorised this lymphoma as double expressor but not double hit. Through multidisciplinary team involvement the patient was treated with combination steroids and chemotherapy. Given the scrotal involvement this was considered a sanctuary site for chemotherapy therefore the patient also received radiotherapy to the scrotum. He recovered well following his treatment. This case highlights how early specialist referral can identify rare variants of disease. Essential preoperative imaging with US prior to treating a presumed hydrocoele prevented inappropriate surgical excision. A multidisciplinary team approach improved the patient’s outcome and is hoped to have improved his chances of recurrence-free survival. [ABSTRACT FROM AUTHOR]

Published
2021
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12. Essential thrombocythaemia treated with recombinant interferon: ‘real world' United Kingdom referral centre experience

Author

Desterro, Joana, primary, McLornan, Donal P., additional, Curto Garcia, Natalia, additional, O'Sullivan, Jennifer, additional, Alimam, Samah, additional, Keohane, Clodagh, additional, Woodley, Claire, additional, Francis, Yvonne, additional, Kordasti, Shahram, additional, Radia, Deepti H., additional, and Harrison, Claire N., additional

Published
2019
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13. A multicenter report on the natural history of myelodysplastic syndromes in very old patients (aged over 85 years)

Author

McDonald, Laura S., primary, McCarthy, Peter, additional, Khan, Mohammad, additional, Hogan, Patrick, additional, Kelleher, Eileen, additional, Murphy, Philip T., additional, Quinn, John, additional, Desmond, Ronan, additional, McHugh, John, additional, Strickland, Melanie, additional, O'Connell, Elizabeth, additional, Cahill, Mary, additional, Maung, Su W., additional, Keohane, Clodagh, additional, O'Neill, Desmond, additional, Ryan, Dan, additional, Mykytiv, Vitaliy, additional, and Enright, Helen, additional

Published
2019
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14. Should Myelodysplastic Syndromes in Very Old Patients be More Actively Managed? Clinical Characteristics, Management and Outcomes for Patients 85 Years and Older

Author

McDonald, Laura, primary, McCarthy, Peter, additional, Khan, Mohammad, additional, Hogan, Patrick, additional, Kelleher, Eileen C., additional, Murphy, Philip, additional, Quinn, John, additional, Desmond, Ronan, additional, McHugh, Johnny, additional, Strickland, Melanie, additional, Cahill, Mary, additional, Maung, Su Wai, additional, Keohane, Clodagh, additional, O'Neill, Desmond, additional, Ryan, Daniel, additional, Mykytiv, Vitaliy, additional, and Enright, Helen, additional

Published
2018
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15. Treatment and management of myelofibrosis in the era of JAK inhibitors

Author

Harrison, Claire, Deepti Radia,Deepti, and Keohane,Clodagh

Subjects
hemic and lymphatic diseases, Targets and Therapy [Biologics]
Abstract

Clodagh Keohane, Deepti H Radia, Claire N HarrisonDepartment of Haematology, Guy's and St Thomas' NHS Foundation Trust, London, UKAbstract: Myelofibrosis (MF) can present as a primary disorder or evolve from polycythemia vera (PV) or essential thrombocythemia (ET) to post-PV MF or post-ET MF, respectively. MF is characterized by bone marrow fibrosis, splenomegaly, leukoerythroblastosis, extramedullary hematopoiesis, and a collection of debilitating symptoms. Until recently, the therapeutic options for patients with MF consisted of allogeneic hematopoietic stem cell transplant (alloHSCT), the use of cytoreductive agents (ie, hydroxyurea), splenectomy and splenic irradiation for treatment of splenomegaly, and management of anemia with transfusions, erythropoiesis-stimulating agents (ESAs), androgens, and immunomodulatory agents. However, with increased understanding of the pathogenesis of MF resulting from dysregulated Janus kinase (JAK) signaling, new targeted JAK inhibitor therapies, such as ruxolitinib, are now available. The purpose of this article is to review the clinical features of MF, discuss the use and future of JAK inhibitors, reassess when and how to use conventional MF treatments in the context of JAK inhibitors, and provide a perspective on the future of MF treatment.Keywords: myelofibrosis, ruxolitinib, JAK inhibitorCorrigendum for this article has been published

Published
2013

16. Treatment and management of myelofibrosis in the era of JAK inhibitors [Corrigendum]

Author

Keohane,Clodagh, Radia,Deepti H, Harrison,Claire N, Keohane,Clodagh, Radia,Deepti H, and Harrison,Claire N

Abstract

Keohane C, Radia DH, Harrison CN. Biologics: Targets and Therapy. 2013;7:189–198. On page 193 note that the paragraph beginning "Pacritinib (SB1518; Cell Technology, Inc, Mountain View, CA, USA) is a JAK2 and FLT3 inhibitor currently being evaluated at a dose of 400 mg daily in a Phase II study (N=34) that included patients with low platelet counts (<50 × 109/L)." should have been "Pacritinib (SB1518; Cell Therapeutics, Inc, Seattle, WA, USA) is a JAK2 and FLT3 inhibitor which was evaluated at a dose of 400 mg daily in a Phase II study (N=34) that included patients with low platelet counts (<50 × 109/L)." On page 193 in the same paragraph note that "Post-Essential Thrombocythemia Myelofibrosis: PERSIST)." should have been "Post-Essential Thrombocythemia Myelofibrosis-1: PERSIST-1)."Read the original article

Published
2013

17. Treatment and management of myelofibrosis in the era of JAK inhibitors

Author

Keohane,Clodagh, Radia,Deepti H, Harrison,Claire N, Keohane,Clodagh, Radia,Deepti H, and Harrison,Claire N

Abstract

Clodagh Keohane, Deepti H Radia, Claire N HarrisonDepartment of Haematology, Guy's and St Thomas' NHS Foundation Trust, London, UKAbstract: Myelofibrosis (MF) can present as a primary disorder or evolve from polycythemia vera (PV) or essential thrombocythemia (ET) to post-PV MF or post-ET MF, respectively. MF is characterized by bone marrow fibrosis, splenomegaly, leukoerythroblastosis, extramedullary hematopoiesis, and a collection of debilitating symptoms. Until recently, the therapeutic options for patients with MF consisted of allogeneic hematopoietic stem cell transplant (alloHSCT), the use of cytoreductive agents (ie, hydroxyurea), splenectomy and splenic irradiation for treatment of splenomegaly, and management of anemia with transfusions, erythropoiesis-stimulating agents (ESAs), androgens, and immunomodulatory agents. However, with increased understanding of the pathogenesis of MF resulting from dysregulated Janus kinase (JAK) signaling, new targeted JAK inhibitor therapies, such as ruxolitinib, are now available. The purpose of this article is to review the clinical features of MF, discuss the use and future of JAK inhibitors, reassess when and how to use conventional MF treatments in the context of JAK inhibitors, and provide a perspective on the future of MF treatment.Keywords: myelofibrosis, ruxolitinib, JAK inhibitorCorrigendum for this article has been published

Published
2013

18. The Genomic Landscape of Myeloproliferative Neoplasms: Somatic Calr Mutations in the Majority of JAK2-Wildtype Patients

Author

Nangalia, Jyoti, primary, Massie, Charles, additional, Baxter, E Joanna, additional, Nice, Francesca L, additional, Gundem, Gunes, additional, Wedge, David, additional, Avezov, Edward, additional, Li, Juan, additional, Kollmann, Karoline, additional, Kent, David G., additional, Aziz, Athar, additional, Godfrey, Anna L, additional, Hinton, Jonathan, additional, Martincorena, Inigo, additional, Van Loo, Peter, additional, Jones, Amy V, additional, Guglielmelli, Paola, additional, Tarpey, Patrick, additional, Harding, Heather P, additional, Fitzpatrick, John D, additional, Goudie, Calum T, additional, Ortmann, Christina A, additional, Loughran, Stephen J, additional, Raine, Keiran, additional, Jones, David, additional, Butler, Adam, additional, Teague, Jon W, additional, O'Meara, Sarah, additional, McLaren, Stuart, additional, Bianchi, Michele, additional, Silber, Yvonne, additional, Dimitropolou, Danai, additional, Bloxham, David, additional, Mudie, Laura J, additional, Maddison, Mark, additional, Robinson, Ben, additional, Keohane, Clodagh, additional, MacLean, Cathy, additional, Hill, Kate, additional, Orchard, Kim H., additional, Tauro, Sudhir, additional, Du, Ming-Qing, additional, Greaves, Mel, additional, Bowen, David, additional, Huntly, Brian, additional, Harrison, Claire N, additional, Cross, Nicholas C.P., additional, Ron, David, additional, Vannucchi, Alessandro M, additional, Papaemmanuil, Elli, additional, Campbell, Peter J., additional, and Green, Anthony R, additional

Published
2013
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24. Myeloproliferative neoplasms.

Author

Houstoun, Conal and Keohane, Clodagh

Subjects
THERAPEUTIC use of interferons, DISEASE progression, BONE marrow cancer, MYELOFIBROSIS, MYELOPROLIFERATIVE neoplasms, ASPIRIN, SYMPTOMS
Published
2022

25. JAK Inhibition Reduces CD25 highCD27+FOXp3+T Regulatory Cells and Causes a Silencing Of T Effector Cells In Patients With Myeloproliferative Neoplasms Whilst Promoting a TH17 Phenotype

Author

Keohane, Clodagh, Kordasti, Shahram Y, Seidl, Thomas, Abellan, Pilar Perez, Thomas, Nicholas Shaun B., Mufti, Ghulam J, Harrison, Claire N, and McLornan, Donal

Abstract

The myeloproliferative neoplasms (MPN), in particular myelofibrosis, are associated with elevated levels of inflammatory cytokines and constitutional symptoms. Treatment with JAK inhibitors (JAKi) have lead to marked improvement in symptoms and splenomegaly. Signaling through the JAK pathway is critical for T cell development and differentiation. However the baseline immune signature remains largely undescribed in MPN as does the effect of JAK inhibition on the immune subsets in this disease.

Published
2013
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26. The effects of JAK inhibitor therapy upon novel markers of thrombosis In myeloproliferative neoplasms.

Author

Keohane C, McLornan DP, Sanchez K, Connor C, Radia D, and Harrison CN

Subjects
Aspirin administration & dosage, Biomarkers blood, Female, Humans, Male, Middle Aged, Nitriles, Pyrimidines, Warfarin administration & dosage, Hematologic Neoplasms, Janus Kinase 2 antagonists & inhibitors, Janus Kinase 2 blood, Janus Kinase 2 genetics, Polycythemia Vera blood, Polycythemia Vera drug therapy, Polycythemia Vera genetics, Pyrazoles administration & dosage, Pyrrolidines administration & dosage, Sulfonamides administration & dosage, Thrombocythemia, Essential blood, Thrombocythemia, Essential genetics, Thrombosis blood, Thrombosis drug therapy
Published
2015
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27. Resolution of bone marrow fibrosis in a patient receiving JAK1/JAK2 inhibitor treatment with ruxolitinib.

Author

Wilkins BS, Radia D, Woodley C, Farhi SE, Keohane C, and Harrison CN

Subjects
Aged, Humans, Male, Nitriles, Pyrazoles pharmacology, Pyrimidines, Treatment Outcome, Janus Kinase 1 antagonists & inhibitors, Janus Kinase 2 antagonists & inhibitors, Primary Myelofibrosis diagnosis, Primary Myelofibrosis drug therapy, Pyrazoles therapeutic use
Abstract

Unlabelled: Ruxolitinib, a JAK1/JAK2 inhibitor, is currently the only pharmacological agent approved for the treatment of myelofibrosis. Approval was based on findings from two phase 3 trials comparing ruxolitinib with placebo (COMFORT-I) and with best available therapy (COMFORT-II) for the treatment of primary or secondary myelofibrosis. In those pivotal trials, ruxolitinib rapidly improved splenomegaly, disease-related symptoms, and quality of life and prolonged survival compared with both placebo and conventional treatments. However, for reasons that are currently unclear, there were only modest histomorphological changes in the bone marrow, and only a subset of patients had significant reductions in JAK2 V617F clonal burden. Here we describe a patient with post-polycythemia vera myelofibrosis who received ruxolitinib at our institution (Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom) as part of the COMFORT-II study. While on treatment, the patient had dramatic improvements in splenomegaly and symptoms shortly after starting ruxolitinib. With longer treatment, the patient had marked reductions in JAK2 V617F allele burden, and fibrosis of the bone marrow resolved after approximately 3 years of ruxolitinib treatment. To our knowledge, this is the first detailed case report of resolution of fibrosis with a JAK1/JAK2 inhibitor., Trial Registration: ClinicalTrials.gov Identifier: NCT00934544.

Published
2013
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28. Treatment and management of myelofibrosis in the era of JAK inhibitors.

Author

Keohane C, Radia DH, and Harrison CN

Abstract

Myelofibrosis (MF) can present as a primary disorder or evolve from polycythemia vera (PV) or essential thrombocythemia (ET) to post-PV MF or post-ET MF, respectively. MF is characterized by bone marrow fibrosis, splenomegaly, leukoerythroblastosis, extramedullary hematopoiesis, and a collection of debilitating symptoms. Until recently, the therapeutic options for patients with MF consisted of allogeneic hematopoietic stem cell transplant (alloHSCT), the use of cytoreductive agents (ie, hydroxyurea), splenectomy and splenic irradiation for treatment of splenomegaly, and management of anemia with transfusions, erythropoiesis-stimulating agents (ESAs), androgens, and immunomodulatory agents. However, with increased understanding of the pathogenesis of MF resulting from dysregulated Janus kinase (JAK) signaling, new targeted JAK inhibitor therapies, such as ruxolitinib, are now available. The purpose of this article is to review the clinical features of MF, discuss the use and future of JAK inhibitors, reassess when and how to use conventional MF treatments in the context of JAK inhibitors, and provide a perspective on the future of MF treatment.

Published
2013
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