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Your search keyword '"Gill, Harinder"' showing total 344 results
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344 results on '"Gill, Harinder"'

3. Loss of symmetric cell division of apical neural progenitors drives DENND5A-related developmental and epileptic encephalopathy

Author

Banks, Emily, Francis, Vincent, Lin, Sheng-Jia, Kharfallah, Fares, Fonov, Vladimir, Lévesque, Maxime, Han, Chanshuai, Kulasekaran, Gopinath, Tuznik, Marius, Bayati, Armin, Al-Khater, Reem, Alkuraya, Fowzan S., Argyriou, Loukas, Babaei, Meisam, Bahlo, Melanie, Bakhshoodeh, Behnoosh, Barr, Eileen, Bartik, Lauren, Bassiony, Mahmoud, Bertrand, Miriam, Braun, Dominique, Buchert, Rebecca, Budetta, Mauro, Cadieux-Dion, Maxime, Calame, Daniel G., Cope, Heidi, Cushing, Donna, Efthymiou, Stephanie, Elmaksoud, Marwa Abd, El Said, Huda G., Froukh, Tawfiq, Gill, Harinder K., Gleeson, Joseph G., Gogoll, Laura, Goh, Elaine S.-Y., Gowda, Vykuntaraju K., Haack, Tobias B., Hashem, Mais O., Hauser, Stefan, Hoffman, Trevor L., Hogue, Jacob S., Hosokawa, Akimoto, Houlden, Henry, Huang, Kevin, Huynh, Stephanie, Karimiani, Ehsan G., Kaulfuß, Silke, Korenke, G. Christoph, Kritzer, Amy, Lee, Hane, Lupski, James R., Marco, Elysa J., McWalter, Kirsty, Minassian, Arakel, Minassian, Berge A., Murphy, David, Neira-Fresneda, Juanita, Northrup, Hope, Nyaga, Denis M., Oehl-Jaschkowitz, Barbara, Osmond, Matthew, Person, Richard, Pehlivan, Davut, Petree, Cassidy, Sadleir, Lynette G., Saunders, Carol, Schoels, Ludger, Shashi, Vandana, Spillmann, Rebecca C., Srinivasan, Varunvenkat M., Torbati, Paria N., Tos, Tulay, Zaki, Maha S., Zhou, Dihong, Zweier, Christiane, Trempe, Jean-François, Durcan, Thomas M., Gan-Or, Ziv, Avoli, Massimo, Alves, Cesar, Varshney, Gaurav K., Maroofian, Reza, Rudko, David A., and McPherson, Peter S.

Published
2024
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6. Management of classical Philadelphia chromosome-negative myeloproliferative neoplasms in Asia: consensus of the Asian Myeloid Working Group

Author

Gill, Harinder, Leung, Garret M. K., Ooi, Melissa G. M., Teo, Winnie Z. Y., Wong, Chieh-Lee, Choi, Chul Won, Wong, Gee-Chuan, Lao, Zhentang, Rojnuckarin, Ponlapat, Castillo, Ma. Rosario Irene D., Xiao, Zhijian, Hou, Hsin-An, Kuo, Ming-Chung, Shih, Lee-Yung, Gan, Gin-Gin, Lin, Chien-Chin, Chng, Wee-Joo, and Kwong, Yok-Lam

Published
2023
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10. Genome-wide sequencing and the clinical diagnosis of genetic disease: The CAUSES study

Author

Elliott, Alison M., Adam, Shelin, du Souich, Christèle, Lehman, Anna, Nelson, Tanya N., van Karnebeek, Clara, Alderman, Emily, Armstrong, Linlea, Aubertin, Gudrun, Blood, Katherine, Boelman, Cyrus, Boerkoel, Cornelius, Bretherick, Karla, Brown, Lindsay, Chijiwa, Chieko, Clarke, Lorne, Couse, Madeline, Creighton, Susan, Watts-Dickens, Abby, Gibson, William T., Gill, Harinder, Tarailo-Graovac, Maja, Hamilton, Sara, Heran, Harindar, Horvath, Gabriella, Huang, Lijia, Hulait, Gurdip K., Koehn, David, Lee, Hyun Kyung, Lewis, Suzanne, Lopez, Elena, Louie, Kristal, Niederhoffer, Karen, Matthews, Allison, Meagher, Kirsten, Peng, Junran J., Patel, Millan S., Race, Simone, Richmond, Phillip, Rupps, Rosemarie, Salvarinova, Ramona, Seath, Kimberly, Selby, Kathryn, Steinraths, Michelle, Stockler, Sylvia, Tang, Kaoru, Tyson, Christine, van Allen, Margot, Wasserman, Wyeth, Mwenifumbo, Jill, and Friedman, Jan M.

Published
2022
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11. Implications of Clonal Hematopoiesis in Hematological and Non-Hematological Disorders.

Author

Zhang, Qi, Yim, Rita, Lee, Paul, Chin, Lynn, Li, Vivian, and Gill, Harinder

Abstract

Simple Summary: Clonal hematopoiesis (CH) predicts the development of myeloid neoplasms and other hematological malignancies. CH is also implicated as a risk factor for adverse outcomes in cardio-metabolic conditions. Future management of CH should target the somatic mutations associated with CH and the selection pressure that provide an advantage to hematopoietic stem and progenitor cells (HSCPs) that harbor significant CH-related somatic mutations. Clonal hematopoiesis (CH) is associated with an increased risk of developing myeloid neoplasms (MNs) such as myelodysplastic neoplasm (MDS) and acute myeloid leukemia (AML). In general, CH comprises clonal hematopoiesis of indeterminate potential (CHIP) and clonal cytopenia of undetermined significance (CCUS). It is an age-related phenomenon characterized by the presence of somatic mutations in hematopoietic stem cells (HSCs) and hematopoietic stem and progenitor cells (HSPCs) that acquire a fitness advantage under selection pressure. Individuals with CHIP have an absolute risk of 0.5–1.0% per year for progressing to MDS or AML. Inflammation, smoking, cytotoxic therapy, and radiation can promote the process of clonal expansion and leukemic transformation. Of note, exposure to chemotherapy or radiation for patients with solid tumors or lymphomas can increase the risk of therapy-related MN. Beyond hematological malignancies, CH also serves as an independent risk factor for heart disease, stroke, chronic obstructive pulmonary disease, and chronic kidney disease. Prognostic models such as the CH risk score and MN-prediction models can provide a framework for risk stratification and clinical management of CHIP/CCUS and identify high-risk individuals who may benefit from close surveillance. For CH or related disorders, therapeutic strategies targeting specific CH-associated mutations and specific selection pressure may have a potential role in the future. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Clinical delineation, sex differences, and genotype–phenotype correlation in pathogenic KDM6A variants causing X-linked Kabuki syndrome type 2

Author

Faundes, Víctor, Goh, Stephanie, Akilapa, Rhoda, Bezuidenhout, Heidre, Bjornsson, Hans T., Bradley, Lisa, Brady, Angela F., Brischoux-Boucher, Elise, Brunner, Han, Bulk, Saskia, Canham, Natalie, Cody, Declan, Dentici, Maria Lisa, Digilio, Maria Cristina, Elmslie, Frances, Fry, Andrew E., Gill, Harinder, Hurst, Jane, Johnson, Diana, Julia, Sophie, Lachlan, Katherine, Lebel, Robert Roger, Byler, Melissa, Gershon, Eric, Lemire, Edmond, Gnazzo, Maria, Lepri, Francesca Romana, Marchese, Antonia, McEntagart, Meriel, McGaughran, Julie, Mizuno, Seiji, Okamoto, Nobuhiko, Rieubland, Claudine, Rodgers, Jonathan, Sasaki, Erina, Scalais, Emmanuel, Scurr, Ingrid, Suri, Mohnish, van der Burgt, Ineke, Matsumoto, Naomichi, Miyake, Noriko, Benoit, Valérie, Lederer, Damien, and Banka, Siddharth

Published
2021
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22. RAPIDOMICS: rapid genome-wide sequencing in a neonatal intensive care unit—successes and challenges

Author

Elliott, Alison M., du Souich, Christèle, Lehman, Anna, Guella, Ilaria, Evans, Daniel M., Candido, Tara, Tooman, Leah, Armstrong, Linlea, Clarke, Lorne, Gibson, William, Gill, Harinder, Lavoie, Pascal M., Lewis, Suzanne, McKinnon, Margaret L., Nikkel, Sarah M., Patel, Millan, Solimano, Alfonso, Synnes, Anne, Ting, Joseph, van Allen, Margot, Christilaw, Jan, Farrer, Matthew J., Friedman, Jan M., and Osiovich, Horacio

Published
2019
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28. A Phase 2 Study of the LSD1 Inhibitor Bomedemstat (IMG-7289) for the Treatment of Advanced Myelofibrosis (MF): Updated Results and Genomic Analyses

Author

Pettit, Kristen M., Gill, Harinder, Yacoub, Abdulraheem, Bradley, Terrence, Gerds, Aaron T., Tatarczuch, Maciej, Shortt, Jake, Curtin, Natasha Joan, Rossetti, James M., Burbury, Kate, Mead, Adam J, Göthert, Joachim R, Koschmieder, Steffen, Reyer, Matt, Siranosian, Benjamin, Natsoulis, Georges, Stevenson, William S, Ewing, Joanne, Chacko, Joseph M., Rumi, Elisa, Halpern, Anna B., Palandri, Francesca, Vianelli, Nicola, Passamonti, Francesco, Mesa, Ruben, Marchetti, Monia, Harrison, Claire, Vannucchi, Alessandro M., Watts, Justin, Ross, David M, Talpaz, Moshe, and Rienhoff, Hugh Young, Jr.

Published
2022
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29. A Phase 2 Study of the LSD1 Inhibitor Bomedemstat (IMG-7289) for the Treatment of Essential Thrombocythemia (ET)

Author

Gill, Harinder, Palandri, Francesca, Ross, David M, Cochrane, Tara, Tate, Courtney, Lane, Steven W, Larsen, Stephen R, Gerds, Aaron T., Halpern, Anna B., Shortt, Jake, Rossetti, James M., Pettit, Kristen M., Liang, James, Mead, Adam J, Marchetti, Monia, Vannucchi, Alessandro M., Wilson, Andrew J, Göthert, Joachim R, Hanna, Merit, Passamonti, Francesco, Stevenson, William S, Harrison, Claire, Talpaz, Moshe, Vianelli, Nicola, and Rienhoff, Hugh Young, Jr.

Published
2022
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31. Prevalence and architecture of de novo mutations in developmental disorders

Author

McRae, Jeremy F., Clayton, Stephen, Fitzgerald, Tomas W., Kaplanis, Joanna, Prigmore, Elena, Rajan, Diana, Sifrim, Alejandro, Aitken, Stuart, Akawi, Nadia, Alvi, Mohsan, Ambridge, Kirsty, Barrett, Daniel M., Bayzetinova, Tanya, Jones, Philip, Jones, Wendy D., King, Daniel, Krishnappa, Netravathi, Mason, Laura E., Singh, Tarjinder, Tivey, Adrian R., Ahmed, Munaza, Anjum, Uruj, Archer, Hayley, Armstrong, Ruth, Awada, Jana, Balasubramanian, Meena, Banka, Siddharth, Baralle, Diana, Barnicoat, Angela, Batstone, Paul, Baty, David, Bennett, Chris, Berg, Jonathan, Bernhard, Birgitta, Bevan, Paul A., Bitner-Glindzicz, Maria, Blair, Edward, Blyth, Moira, Bohanna, David, Bourdon, Louise, Bourn, David, Bradley, Lisa, Brady, Angela, Brent, Simon, Brewer, Carole, Brunstrom, Kate, Bunyan, David J., Burn, John, Canham, Natalie, Castle, Bruce, Chandler, Kate, Chatzimichali, Elena, Cilliers, Deirdre, Clarke, Angus, Clasper, Susan, Clayton-Smith, Jill, Clowes, Virginia, Coates, Andrea, Cole, Trevor, Colgiu, Irina, Collins, Amanda, Collinson, Morag N., Connell, Fiona, Cooper, Nicola, Cox, Helen, Cresswell, Lara, Cross, Gareth, Crow, Yanick, D’Alessandro, Mariella, Dabir, Tabib, Davidson, Rosemarie, Davies, Sally, de Vries, Dylan, Dean, John, Deshpande, Charu, Devlin, Gemma, Dixit, Abhijit, Dobbie, Angus, Donaldson, Alan, Donnai, Dian, Donnelly, Deirdre, Donnelly, Carina, Douglas, Angela, Douzgou, Sofia, Duncan, Alexis, Eason, Jacqueline, Ellard, Sian, Ellis, Ian, Elmslie, Frances, Evans, Karenza, Everest, Sarah, Fendick, Tina, Fisher, Richard, Flinter, Frances, Foulds, Nicola, Fry, Andrew, Fryer, Alan, Gardiner, Carol, Gaunt, Lorraine, Ghali, Neeti, Gibbons, Richard, Gill, Harinder, Goodship, Judith, Goudie, David, Gray, Emma, Green, Andrew, Greene, Philip, Greenhalgh, Lynn, Gribble, Susan, Harrison, Rachel, Harrison, Lucy, Harrison, Victoria, Hawkins, Rose, He, Liu, Hellens, Stephen, Henderson, Alex, Hewitt, Sarah, Hildyard, Lucy, Hobson, Emma, Holden, Simon, Holder, Muriel, Holder, Susan, Hollingsworth, Georgina, Homfray, Tessa, Humphreys, Mervyn, Hurst, Jane, Hutton, Ben, Ingram, Stuart, Irving, Melita, Islam, Lily, Jackson, Andrew, Jarvis, Joanna, Jenkins, Lucy, Johnson, Diana, Jones, Elizabeth, Josifova, Dragana, Joss, Shelagh, Kaemba, Beckie, Kazembe, Sandra, Kelsell, Rosemary, Kerr, Bronwyn, Kingston, Helen, Kini, Usha, Kinning, Esther, Kirby, Gail, Kirk, Claire, Kivuva, Emma, Kraus, Alison, Kumar, Dhavendra, Ajith Kumar, V. K., Lachlan, Katherine, Lam, Wayne, Lampe, Anne, Langman, Caroline, Lees, Melissa, Lim, Derek, Longman, Cheryl, Lowther, Gordon, Lynch, Sally A., Magee, Alex, Maher, Eddy, Male, Alison, Mansour, Sahar, Marks, Karen, Martin, Katherine, Maye, Una, McCann, Emma, McConnell, Vivienne, McEntagart, Meriel, McGowan, Ruth, McKay, Kirsten, McKee, Shane, McMullan, Dominic J., McNerlan, Susan, McWilliam, Catherine, Mehta, Sarju, Metcalfe, Kay, Middleton, Anna, Miedzybrodzka, Zosia, Miles, Emma, Mohammed, Shehla, Montgomery, Tara, Moore, David, Morgan, Sian, Morton, Jenny, Mugalaasi, Hood, Murday, Victoria, Murphy, Helen, Naik, Swati, Nemeth, Andrea, Nevitt, Louise, Newbury-Ecob, Ruth, Norman, Andrew, O’Shea, Rosie, Ogilvie, Caroline, Ong, Kai-Ren, Park, Soo-Mi, Parker, Michael J., Patel, Chirag, Paterson, Joan, Payne, Stewart, Perrett, Daniel, Phipps, Julie, Pilz, Daniela T., Pollard, Martin, Pottinger, Caroline, Poulton, Joanna, Pratt, Norman, Prescott, Katrina, Price, Sue, Pridham, Abigail, Procter, Annie, Purnell, Hellen, Quarrell, Oliver, Ragge, Nicola, Rahbari, Raheleh, Randall, Josh, Rankin, Julia, Raymond, Lucy, Rice, Debbie, Robert, Leema, Roberts, Eileen, Roberts, Jonathan, Roberts, Paul, Roberts, Gillian, Ross, Alison, Rosser, Elisabeth, Saggar, Anand, Samant, Shalaka, Sampson, Julian, Sandford, Richard, Sarkar, Ajoy, Schweiger, Susann, Scott, Richard, Scurr, Ingrid, Selby, Ann, Seller, Anneke, Sequeira, Cheryl, Shannon, Nora, Sharif, Saba, Shaw-Smith, Charles, Shearing, Emma, Shears, Debbie, Sheridan, Eamonn, Simonic, Ingrid, Singzon, Roldan, Skitt, Zara, Smith, Audrey, Smith, Kath, Smithson, Sarah, Sneddon, Linda, Splitt, Miranda, Squires, Miranda, Stewart, Fiona, Stewart, Helen, Straub, Volker, Suri, Mohnish, Sutton, Vivienne, Swaminathan, Ganesh Jawahar, Sweeney, Elizabeth, Tatton-Brown, Kate, Taylor, Cat, Taylor, Rohan, Tein, Mark, Temple, Karen I., Thomson, Jenny, Tischkowitz, Marc, Tomkins, Susan, Torokwa, Audrey, Treacy, Becky, Turner, Claire, Turnpenny, Peter, Tysoe, Carolyn, Vandersteen, Anthony, Varghese, Vinod, Vasudevan, Pradeep, Vijayarangakannan, Parthiban, Vogt, Julie, Wakeling, Emma, Wallwark, Sarah, Waters, Jonathon, Weber, Astrid, Wellesley, Diana, Whiteford, Margo, Widaa, Sara, Wilcox, Sarah, Wilkinson, Emily, Williams, Denise, Williams, Nicola, Wilson, Louise, Woods, Geoff, Wragg, Christopher, Wright, Michael, Yates, Laura, Yau, Michael, Nellåker, Chris, Parker, Michael, Firth, Helen V., Wright, Caroline F., FitzPatrick, David R., Barrett, Jeffrey C., and Hurles, Matthew E.

Published
2017
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32. Disseminated infections with talaromyces marneffei in non-AIDS patients given monoclonal antibodies against CD20 and Kinase inhibitors

Author

Chan, Jasper F.W., Chan, Thomas S.Y., Gill, Harinder, Lam, Frank Y.F., Trendell-Smith, Nigel J., Sridhar, Siddharth, Tse, Herman, Lau, Susanna K.P., Hung, Ivan F.N., Yuen, Kwok-Yung, and Woo, Patrick C.Y.

Subjects
Health
Abstract

Talaromyces (formerly Penicillium) marneffei is a pathogenic, thermal dimorphic fungus that causes systemic mycosis in Southeast Asia. T. marneffei infection is characterized by fungal invasion of multiple organ systems, especially [...]

Published
2015
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35. Targeting and Monitoring Acute Myeloid Leukaemia with Nucleophosmin-1 (NPM1) Mutation.

Author

Chin, Lynn, Wong, Chantelle Ye Gwen, and Gill, Harinder

Subjects
ACUTE myeloid leukemia, DNA topoisomerase I, NUCLEOPHOSMIN, DNA topoisomerase II, MUTANT proteins, POLYMERASE chain reaction, NUCLEOTIDE sequencing, RNA polymerases
Abstract

Mutations in NPM1, also known as nucleophosmin-1, B23, NO38, or numatrin, are seen in approximately one-third of patients with acute myeloid leukaemia (AML). A plethora of treatment strategies have been studied to determine the best possible approach to curing NPM1-mutated AML. Here, we introduce the structure and function of NPM1 and describe the application of minimal residual disease (MRD) monitoring using molecular methods by means of quantitative polymerase chain reaction (qPCR), droplet digital PCR (ddPCR), next-generation sequencing (NGS), and cytometry by time of flight (CyTOF) to target NPM1-mutated AML. Current drugs, now regarded as the standard of care for AML, as well as potential drugs still under development, will also be explored. This review will focus on the role of targeting aberrant NPM1 pathways such as BCL-2 and SYK; as well as epigenetic regulators (RNA polymerase), DNA intercalators (topoisomerase II), menin inhibitors, and hypomethylating agents. Aside from medication, the effects of stress on AML presentation have been reported, and some possible mechanisms outlined. Moreover, targeted strategies will be briefly discussed, not only for the prevention of abnormal trafficking and localisation of cytoplasmic NPM1 but also for the elimination of mutant NPM1 proteins. Lastly, the advancement of immunotherapy such as targeting CD33, CD123, and PD-1 will be mentioned. [ABSTRACT FROM AUTHOR]

Published
2023
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42. Oral arsenic trioxide for treating acute promyelocytic leukaemia: Implications for its worldwide epidemiology and beyond.

Author

Kumana, Cyrus R., Yok-Lam Kwong, and Gill, Harinder

Abstract

This account describes how orally administered Arsenic-trioxide (ATO) therapy influences the epidemiology of acute promyelocytic leukaemia (APL), and how the experience that ensued may expand the indications for oral ATO as a treatment for diseases/disorders other than APL. Over the last two decades, experience with APL patients in Hong Kong treated with an oral regimen comprising ATO, all-trans retinoic acid (ATRA), and ascorbic acid (also known as “AAA”) has confirmed a dramatic improvement in overall survival. Over that period, there has been an estimated 60-fold increase in the prevalence of APL (proportion of surviving APL patients in the population on December 31 including those deemed to be ‘cured’). In contrast to regimens entailing intravenous (IV) ATO, the consequential therapeutic benefits of using oral ATO have been achieved with much less patient inconvenience and quality of life disruption, reduced burdens on health care facilities (hospitalisations and staff involvement), and much enhanced affordability (retail drug & other cost reductions). Numerous experimental and a few clinical studies suggest that ATO may also have a therapeutic role in many other diseases/disorders. Several such diseases (e.g. autoimmune disorders & idiopathic pulmonary fibrosis) are far more prevalent than APL, which means that very large numbers of patients may potentially benefit from ATO treatment, even if its efficacy is limited to selected populations with these diseases. The known safety of oral ATO and its advantages over repeated long-term IV delivery suggests that this route be used in future clinical studies of its possible role in treating such patients. If the clinical utility of oral ATO treatment is validated for patients enduring any such non-APL diseases, very large numbers of patients may stand to benefit. [ABSTRACT FROM AUTHOR]

Published
2022
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47. Bomedemstat (IMG-7289), an LSD1 Inhibitor, Manages the Signs and Symptoms of Essential Thrombocythemia (ET) While Reducing the Burden of Cells Homozygous for Driver Mutations

Author

Goethert, Joachim R., Gill, Harinder, Palandri, Francesca, Ross, David M., Cochrane, Tara, Larsen, Stephen R., Halpern, Anna B., Shortt, Jake, Rossetti, James M., Liang, James, Marchetti, Monia, Wilson, Andrew J., Innes, Andrew, Hanna, Merit, Stevenson, William S., Vannucchi, Alessandro M., Kleppe, Maria, Natsoulis, Georges, Harrison, Claire N, and Rienhoff Jr., Hugh Young

Published
2023
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