keyword
MENU ▼
Read by QxMD icon Read
search

Markus Müschen

keyword
https://www.readbyqxmd.com/read/27479034/the-public-repository-of-xenografts-enables-discovery-and-randomized-phase-ii-like-trials-in-mice
#1
Elizabeth C Townsend, Mark A Murakami, Alexandra Christodoulou, Amanda L Christie, Johannes Köster, Tiffany A DeSouza, Elizabeth A Morgan, Scott P Kallgren, Huiyun Liu, Shuo-Chieh Wu, Olivia Plana, Joan Montero, Kristen E Stevenson, Prakash Rao, Raga Vadhi, Michael Andreeff, Philippe Armand, Karen K Ballen, Patrizia Barzaghi-Rinaudo, Sarah Cahill, Rachael A Clark, Vesselina G Cooke, Matthew S Davids, Daniel J DeAngelo, David M Dorfman, Hilary Eaton, Benjamin L Ebert, Julia Etchin, Brant Firestone, David C Fisher, Arnold S Freedman, Ilene A Galinsky, Hui Gao, Jacqueline S Garcia, Francine Garnache-Ottou, Timothy A Graubert, Alejandro Gutierrez, Ensar Halilovic, Marian H Harris, Zachary T Herbert, Steven M Horwitz, Giorgio Inghirami, Andrew M Intlekofer, Moriko Ito, Shai Izraeli, Eric D Jacobsen, Caron A Jacobson, Sébastien Jeay, Irmela Jeremias, Michelle A Kelliher, Raphael Koch, Marina Konopleva, Nadja Kopp, Steven M Kornblau, Andrew L Kung, Thomas S Kupper, Nicole R LeBoeuf, Ann S LaCasce, Emma Lees, Loretta S Li, A Thomas Look, Masato Murakami, Markus Muschen, Donna Neuberg, Samuel Y Ng, Oreofe O Odejide, Stuart H Orkin, Rachel R Paquette, Andrew E Place, Justine E Roderick, Jeremy A Ryan, Stephen E Sallan, Brent Shoji, Lewis B Silverman, Robert J Soiffer, David P Steensma, Kimberly Stegmaier, Richard M Stone, Jerome Tamburini, Aaron R Thorner, Paul van Hummelen, Martha Wadleigh, Marion Wiesmann, Andrew P Weng, Jens U Wuerthner, David A Williams, Bruce M Wollison, Andrew A Lane, Anthony Letai, Monica M Bertagnolli, Jerome Ritz, Myles Brown, Henry Long, Jon C Aster, Margaret A Shipp, James D Griffin, David M Weinstock
No abstract text is available yet for this article.
July 11, 2016: Cancer Cell
https://www.readbyqxmd.com/read/27071778/effects-of-pharmacological-and-genetic-disruption-of-cxcr4-chemokine-receptor-function-in-b-cell-acute-lymphoblastic-leukaemia
#2
Shubhchintan Randhawa, Byung S Cho, Dipanjan Ghosh, Mariela Sivina, Stefan Koehrer, Markus Müschen, Amnon Peled, Richard E Davis, Marina Konopleva, Jan A Burger
B cell acute lymphoblastic leukaemia (B-ALL) cells express high levels of CXCR4 chemokine receptors for homing and retention within the marrow microenvironment. Bone marrow stromal cells (BMSC) secrete CXCL12, the ligand for CXCR4, and protect B-ALL cells from cytotoxic drugs. Therefore, the therapeutic use of CXCR4 antagonists has been proposed to disrupt cross talk between B-ALL cells and the protective stroma. Because CXCR4 antagonists can have activating agonistic function, we compared the genetic and pharmacological deletion of CXCR4 in B-ALL cells, using CRISPR-Cas9 gene editing and CXCR4 antagonists that are in clinical use (plerixafor, BKT140)...
August 2016: British Journal of Haematology
https://www.readbyqxmd.com/read/27070704/the-public-repository-of-xenografts-enables-discovery-and-randomized-phase-ii-like-trials-in-mice
#3
Elizabeth C Townsend, Mark A Murakami, Alexandra Christodoulou, Amanda L Christie, Johannes Köster, Tiffany A DeSouza, Elizabeth A Morgan, Scott P Kallgren, Huiyun Liu, Shuo-Chieh Wu, Olivia Plana, Joan Montero, Kristen E Stevenson, Prakash Rao, Raga Vadhi, Michael Andreeff, Philippe Armand, Karen K Ballen, Patrizia Barzaghi-Rinaudo, Sarah Cahill, Rachael A Clark, Vesselina G Cooke, Matthew S Davids, Daniel J DeAngelo, David M Dorfman, Hilary Eaton, Benjamin L Ebert, Julia Etchin, Brant Firestone, David C Fisher, Arnold S Freedman, Ilene A Galinsky, Hui Gao, Jacqueline S Garcia, Francine Garnache-Ottou, Timothy A Graubert, Alejandro Gutierrez, Ensar Halilovic, Marian H Harris, Zachary T Herbert, Steven M Horwitz, Giorgio Inghirami, Andrew M Intlekoffer, Moriko Ito, Shai Izraeli, Eric D Jacobsen, Caron A Jacobson, Sébastien Jeay, Irmela Jeremias, Michelle A Kelliher, Raphael Koch, Marina Konopleva, Nadja Kopp, Steven M Kornblau, Andrew L Kung, Thomas S Kupper, Nicole LaBoeuf, Ann S LaCasce, Emma Lees, Loretta S Li, A Thomas Look, Masato Murakami, Markus Muschen, Donna Neuberg, Samuel Y Ng, Oreofe O Odejide, Stuart H Orkin, Rachel R Paquette, Andrew E Place, Justine E Roderick, Jeremy A Ryan, Stephen E Sallan, Brent Shoji, Lewis B Silverman, Robert J Soiffer, David P Steensma, Kimberly Stegmaier, Richard M Stone, Jerome Tamburini, Aaron R Thorner, Paul van Hummelen, Martha Wadleigh, Marion Wiesmann, Andrew P Weng, Jens U Wuerthner, David A Williams, Bruce M Wollison, Andrew A Lane, Anthony Letai, Monica M Bertagnolli, Jerome Ritz, Myles Brown, Henry Long, Jon C Aster, Margaret A Shipp, James D Griffin, David M Weinstock
More than 90% of drugs with preclinical activity fail in human trials, largely due to insufficient efficacy. We hypothesized that adequately powered trials of patient-derived xenografts (PDX) in mice could efficiently define therapeutic activity across heterogeneous tumors. To address this hypothesis, we established a large, publicly available repository of well-characterized leukemia and lymphoma PDXs that undergo orthotopic engraftment, called the Public Repository of Xenografts (PRoXe). PRoXe includes all de-identified information relevant to the primary specimens and the PDXs derived from them...
April 11, 2016: Cancer Cell
https://www.readbyqxmd.com/read/26974310/pten-opposes-negative-selection-and-enables-oncogenic-transformation-of-pre-b-cells
#4
Seyedmehdi Shojaee, Lai N Chan, Maike Buchner, Valeria Cazzaniga, Kadriye Nehir Cosgun, Huimin Geng, Yi Hua Qiu, Marcus Dühren von Minden, Thomas Ernst, Andreas Hochhaus, Giovanni Cazzaniga, Ari Melnick, Steven M Kornblau, Thomas G Graeber, Hong Wu, Hassan Jumaa, Markus Müschen
Phosphatase and tensin homolog (PTEN) is a negative regulator of the phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) signaling pathway and a potent tumor suppressor in many types of cancer. To test a tumor suppressive role for PTEN in pre-B acute lymphoblastic leukemia (ALL), we induced Cre-mediated deletion of Pten in mouse models of pre-B ALL. In contrast to its role as a tumor suppressor in other cancers, loss of one or both alleles of Pten caused rapid cell death of pre-B ALL cells and was sufficient to clear transplant recipient mice of leukemia...
April 2016: Nature Medicine
https://www.readbyqxmd.com/read/26958840/corrigendum-signalling-thresholds-and-negative-b-cell-selection-in-acute-lymphoblastic-leukaemia
#5
Zhengshan Chen, Seyedmehdi Shojaee, Maike Buchner, Huimin Geng, Jae Woong Lee, Lars Klemm, Björn Titz, Thomas G Graeber, Eugene Park, Ying Xim Tan, Anne Satterthwaite, Elisabeth Paietta, Stephen P Hunger, Cheryl L Willman, Ari Melnick, Mignon L Loh, Jae U Jung, John E Coligan, Silvia Bolland, Tak W Mak, Andre Limnander, Hassan Jumaa, Michael Reth, Arthur Weiss, Clifford A Lowell, Markus Müschen
No abstract text is available yet for this article.
June 2, 2016: Nature
https://www.readbyqxmd.com/read/26934650/inhibition-of-ire1%C3%AE-driven-pro-survival-pathways-is-a-promising-therapeutic-application-in-acute-myeloid-leukemia
#6
Haibo Sun, De-Chen Lin, Xiao Guo, Behzad Kharabi Masouleh, Sigal Gery, Qi Cao, Serhan Alkan, Takayuki Ikezoe, Chie Akiba, Ronald Paquette, Wenwen Chien, Carsten Müller-Tidow, Yang Jing, Konstantin Agelopoulos, Markus Müschen, H Phillip Koeffler
Survival of cancer cells relies on the unfolded protein response (UPR) to resist stress triggered by the accumulation of misfolded proteins within the endoplasmic reticulum (ER). The IRE1α-XBP1 pathway, a key branch of the UPR, is activated in many cancers. Here, we show that the expression of both mature and spliced forms of XBP1 (XBP1s) is up-regulated in acute myeloid leukemia (AML) cell lines and AML patient samples. IRE1α RNase inhibitors [MKC-3946, 2-hydroxy-1-naphthaldehyde (HNA), STF-083010 and toyocamycin] blocked XBP1 mRNA splicing and exhibited cytotoxicity against AML cells...
April 5, 2016: Oncotarget
https://www.readbyqxmd.com/read/26864341/normal-abl1-is-a-tumor-suppressor-and-therapeutic-target-in-human-and-mouse-leukemias-expressing-oncogenic-abl1-kinases
#7
Yashodhara Dasgupta, Mateusz Koptyra, Grazyna Hoser, Kanchan Kantekure, Darshan Roy, Barbara Gornicka, Margaret Nieborowska-Skorska, Elisabeth Bolton-Gillespie, Sabine Cerny-Reiterer, Markus Müschen, Peter Valent, Mariusz A Wasik, Christine Richardson, Oliver Hantschel, Heiko van der Kuip, Tomasz Stoklosa, Tomasz Skorski
Leukemias expressing constitutively activated mutants of ABL1 tyrosine kinase (BCR-ABL1, TEL-ABL1, NUP214-ABL1) usually contain at least 1 normal ABL1 allele. Because oncogenic and normal ABL1 kinases may exert opposite effects on cell behavior, we examined the role of normal ABL1 in leukemias induced by oncogenic ABL1 kinases. BCR-ABL1-Abl1(-/-) cells generated highly aggressive chronic myeloid leukemia (CML)-blast phase-like disease in mice compared with less malignant CML-chronic phase-like disease from BCR-ABL1-Abl1(+/+) cells...
April 28, 2016: Blood
https://www.readbyqxmd.com/read/26711339/mll-rearranged-acute-lymphoblastic-leukemias-activate-bcl-2-through-h3k79-methylation-and-are-sensitive-to-the-bcl-2-specific-antagonist-abt-199
#8
Juliana M Benito, Laura Godfrey, Kensuke Kojima, Leah Hogdal, Mark Wunderlich, Huimin Geng, Isabel Marzo, Karine G Harutyunyan, Leonard Golfman, Phillip North, Jon Kerry, Erica Ballabio, Triona Ní Chonghaile, Oscar Gonzalo, Yihua Qiu, Irmela Jeremias, LaKiesha Debose, Eric O'Brien, Helen Ma, Ping Zhou, Rodrigo Jacamo, Eugene Park, Kevin R Coombes, Nianxiang Zhang, Deborah A Thomas, Susan O'Brien, Hagop M Kantarjian, Joel D Leverson, Steven M Kornblau, Michael Andreeff, Markus Müschen, Patrick A Zweidler-McKay, James C Mulloy, Anthony Letai, Thomas A Milne, Marina Konopleva
Targeted therapies designed to exploit specific molecular pathways in aggressive cancers are an exciting area of current research. Mixed Lineage Leukemia (MLL) mutations such as the t(4;11) translocation cause aggressive leukemias that are refractory to conventional treatment. The t(4;11) translocation produces an MLL/AF4 fusion protein that activates key target genes through both epigenetic and transcriptional elongation mechanisms. In this study, we show that t(4;11) patient cells express high levels of BCL-2 and are highly sensitive to treatment with the BCL-2-specific BH3 mimetic ABT-199...
December 29, 2015: Cell Reports
https://www.readbyqxmd.com/read/26637659/infection-and-the-perils-of-b-cell-activation
#9
COMMENT
Mel Greaves, Markus Müschen
Recent studies have linked aberrant B-cell activation in the context of aberrant immune responses to infectious pathogens to malignant transformation and development of leukemia and lymphoma. A new study in this issue demonstrates that common infections can be drivers of clonal evolution of premalignant B-cell precursors toward childhood leukemia.
December 2015: Cancer Discovery
https://www.readbyqxmd.com/read/26324703/mapk-signaling-cascades-mediate-distinct-glucocorticoid-resistance-mechanisms-in-pediatric-leukemia
#10
MULTICENTER STUDY
Courtney L Jones, Christy M Gearheart, Susan Fosmire, Cristina Delgado-Martin, Nikki A Evensen, Karen Bride, Angela J Waanders, Faye Pais, Jinhua Wang, Teena Bhatla, Danielle S Bitterman, Simone R de Rijk, Wallace Bourgeois, Smita Dandekar, Eugene Park, Tamara M Burleson, Pillai Pallavi Madhusoodhan, David T Teachey, Elizabeth A Raetz, Michelle L Hermiston, Markus Müschen, Mignon L Loh, Stephen P Hunger, Jinghui Zhang, Michael J Garabedian, Christopher C Porter, William L Carroll
The outcome for pediatric acute lymphoblastic leukemia (ALL) patients who relapse is dismal. A hallmark of relapsed disease is acquired resistance to multiple chemotherapeutic agents, particularly glucocorticoids. In this study, we performed a genome-scale short hairpin RNA screen to identify mediators of prednisolone sensitivity in ALL cell lines. The incorporation of these data with an integrated analysis of relapse-specific genetic and epigenetic changes allowed us to identify the mitogen-activated protein kinase (MAPK) pathway as a mediator of prednisolone resistance in pediatric ALL...
November 5, 2015: Blood
https://www.readbyqxmd.com/read/26219304/targeting-casein-kinase-ii-restores-ikaros-tumor-suppressor-activity-and-demonstrates-therapeutic-efficacy-in-high-risk-leukemia
#11
Chunhua Song, Chandrika Gowda, Xiaokang Pan, Yali Ding, Yongqing Tong, Bi-Hua Tan, Haijun Wang, Sunil Muthusami, Zheng Ge, Mansi Sachdev, Shantu G Amin, Dhimant Desai, Krishne Gowda, Raghavendra Gowda, Gavin P Robertson, Hilde Schjerven, Markus Muschen, Kimberly J Payne, Sinisa Dovat
Ikaros (IKZF1) is a tumor suppressor that binds DNA and regulates expression of its target genes. The mechanism of Ikaros activity as a tumor suppressor and the regulation of Ikaros function in leukemia are unknown. Here, we demonstrate that Ikaros controls cellular proliferation by repressing expression of genes that promote cell cycle progression and the phosphatidylinositol-3 kinase (PI3K) pathway. We show that Ikaros function is impaired by the pro-oncogenic casein kinase II (CK2), and that CK2 is overexpressed in leukemia...
October 8, 2015: Blood
https://www.readbyqxmd.com/read/26196452/infectious-origins-of-childhood-leukemia
#12
EDITORIAL
Srividya Swaminathan, Markus Müschen
No abstract text is available yet for this article.
July 10, 2015: Oncotarget
https://www.readbyqxmd.com/read/26073130/erk-negative-feedback-control-enables-pre-b-cell-transformation-and-represents-a-therapeutic-target-in-acute-lymphoblastic-leukemia
#13
Seyedmehdi Shojaee, Rebecca Caeser, Maike Buchner, Eugene Park, Srividya Swaminathan, Christian Hurtz, Huimin Geng, Lai N Chan, Lars Klemm, Wolf-Karsten Hofmann, Yi Hua Qiu, Nianxiang Zhang, Kevin R Coombes, Elisabeth Paietta, Jeffery Molkentin, H Phillip Koeffler, Cheryl L Willman, Stephen P Hunger, Ari Melnick, Steven M Kornblau, Markus Müschen
Studying mechanisms of malignant transformation of human pre-B cells, we found that acute activation of oncogenes induced immediate cell death in the vast majority of cells. Few surviving pre-B cell clones had acquired permissiveness to oncogenic signaling by strong activation of negative feedback regulation of Erk signaling. Studying negative feedback regulation of Erk in genetic experiments at three different levels, we found that Spry2, Dusp6, and Etv5 were essential for oncogenic transformation in mouse models for pre-B acute lymphoblastic leukemia (ALL)...
July 13, 2015: Cancer Cell
https://www.readbyqxmd.com/read/25985233/mechanisms-of-clonal-evolution-in-childhood-acute-lymphoblastic-leukemia
#14
Srividya Swaminathan, Lars Klemm, Eugene Park, Elli Papaemmanuil, Anthony Ford, Soo-Mi Kweon, Daniel Trageser, Brian Hasselfeld, Nadine Henke, Jana Mooster, Huimin Geng, Klaus Schwarz, Scott C Kogan, Rafael Casellas, David G Schatz, Michael R Lieber, Mel F Greaves, Markus Müschen
Childhood acute lymphoblastic leukemia (ALL) can often be traced to a pre-leukemic clone carrying a prenatal genetic lesion. Postnatally acquired mutations then drive clonal evolution toward overt leukemia. The enzymes RAG1-RAG2 and AID, which diversify immunoglobulin-encoding genes, are strictly segregated in developing cells during B lymphopoiesis and peripheral mature B cells, respectively. Here we identified small pre-BII cells as a natural subset with increased genetic vulnerability owing to concurrent activation of these enzymes...
July 2015: Nature Immunology
https://www.readbyqxmd.com/read/25953975/ph-all-drawing-strength-from-a-benign-past
#15
COMMENT
Markus Müschen
In this issue of Blood, Mallampati et al report on the discovery of a new mechanism of tyrosine kinase inhibitor (TKI) resistance, which is mediated through TKI-mediated priming of mesenchymal stem cells (MSCs) in the bone marrow (BM).
May 7, 2015: Blood
https://www.readbyqxmd.com/read/25912253/hsp90-inhibitors-decrease-aid-levels-and-activity-in-mice-and-in-human-cells
#16
Damien Montamat-Sicotte, Ludivine C Litzler, Cecilia Abreu, Shiva Safavi, Astrid Zahn, Alexandre Orthwein, Markus Müschen, Pablo Oppezzo, Denise P Muñoz, Javier M Di Noia
Activation induced deaminase (AID) initiates somatic hypermutation and class switch recombination of the Ig genes in antigen-activated B cells, underpinning antibody affinity maturation and isotype switching. AID can also be pathogenic by contributing to autoimmune diseases and oncogenic mutations. Moreover, AID can exert noncanonical functions when aberrantly expressed in epithelial cells. The lack of specific inhibitors prevents therapeutic applications to modulate AID functions. Here, we have exploited our previous finding that the HSP90 molecular chaperoning pathway stabilizes AID in B cells, to test whether HSP90 inhibitors could target AID in vivo...
August 2015: European Journal of Immunology
https://www.readbyqxmd.com/read/25878119/rationale-for-targeting-the-pre-b-cell-receptor-signaling-pathway-in-acute-lymphoblastic-leukemia
#17
REVIEW
Markus Müschen
Inhibitors of B-cell receptor (BCR) and pre-BCR signaling were successfully introduced into patient care for various subtypes of mature B-cell lymphoma (e.g., ibrutinib, idelalisib). Acute lymphoblastic leukemia (ALL) typically originates from pre-B cells that critically depend on survival signals emanating from a functional pre-BCR. However, whether patients with ALL benefit from treatment with (pre-) BCR inhibitors has not been explored. Recent data suggest that the pre-BCR functions as tumor suppressor in the majority of cases of human ALL...
June 11, 2015: Blood
https://www.readbyqxmd.com/read/25799995/signalling-thresholds-and-negative-b-cell-selection-in-acute-lymphoblastic-leukaemia
#18
Zhengshan Chen, Seyedmehdi Shojaee, Maike Buchner, Huimin Geng, Jae Woong Lee, Lars Klemm, Björn Titz, Thomas G Graeber, Eugene Park, Ying Xim Tan, Anne Satterthwaite, Elisabeth Paietta, Stephen P Hunger, Cheryl L Willman, Ari Melnick, Mignon L Loh, Jae U Jung, John E Coligan, Silvia Bolland, Tak W Mak, Andre Limnander, Hassan Jumaa, Michael Reth, Arthur Weiss, Clifford A Lowell, Markus Müschen
B cells are selected for an intermediate level of B-cell antigen receptor (BCR) signalling strength: attenuation below minimum (for example, non-functional BCR) or hyperactivation above maximum (for example, self-reactive BCR) thresholds of signalling strength causes negative selection. In ∼25% of cases, acute lymphoblastic leukaemia (ALL) cells carry the oncogenic BCR-ABL1 tyrosine kinase (Philadelphia chromosome positive), which mimics constitutively active pre-BCR signalling. Current therapeutic approaches are largely focused on the development of more potent tyrosine kinase inhibitors to suppress oncogenic signalling below a minimum threshold for survival...
May 21, 2015: Nature
https://www.readbyqxmd.com/read/25759025/self-enforcing-feedback-activation-between-bcl6-and-pre-b-cell-receptor-signaling-defines-a-distinct-subtype-of-acute-lymphoblastic-leukemia
#19
Huimin Geng, Christian Hurtz, Kyle B Lenz, Zhengshan Chen, Dirk Baumjohann, Sarah Thompson, Natalya A Goloviznina, Wei-Yi Chen, Jianya Huan, Dorian LaTocha, Erica Ballabio, Gang Xiao, Jae-Woong Lee, Anne Deucher, Zhongxia Qi, Eugene Park, Chuanxin Huang, Rahul Nahar, Soo-Mi Kweon, Seyedmehdi Shojaee, Lai N Chan, Jingwei Yu, Steven M Kornblau, Janetta J Bijl, B Hilda Ye, K Mark Ansel, Elisabeth Paietta, Ari Melnick, Stephen P Hunger, Peter Kurre, Jeffrey W Tyner, Mignon L Loh, Robert G Roeder, Brian J Druker, Jan A Burger, Thomas A Milne, Bill H Chang, Markus Müschen
Studying 830 pre-B ALL cases from four clinical trials, we found that human ALL can be divided into two fundamentally distinct subtypes based on pre-BCR function. While absent in the majority of ALL cases, tonic pre-BCR signaling was found in 112 cases (13.5%). In these cases, tonic pre-BCR signaling induced activation of BCL6, which in turn increased pre-BCR signaling output at the transcriptional level. Interestingly, inhibition of pre-BCR-related tyrosine kinases reduced constitutive BCL6 expression and selectively killed patient-derived pre-BCR(+) ALL cells...
March 9, 2015: Cancer Cell
https://www.readbyqxmd.com/read/25753524/identification-of-foxm1-as-a-therapeutic-target-in-b-cell-lineage-acute-lymphoblastic-leukaemia
#20
Maike Buchner, Eugene Park, Huimin Geng, Lars Klemm, Johanna Flach, Emmanuelle Passegué, Hilde Schjerven, Ari Melnick, Elisabeth Paietta, Dragana Kopanja, Pradip Raychaudhuri, Markus Müschen
Despite recent advances in the cure rate of acute lymphoblastic leukaemia (ALL), the prognosis for patients with relapsed ALL remains poor. Here we identify FOXM1 as a candidate responsible for an aggressive clinical course. We show that FOXM1 levels peak at the pre-B-cell receptor checkpoint but are dispensable for normal B-cell development. Compared with normal B-cell populations, FOXM1 levels are 2- to 60-fold higher in ALL cells and are predictive of poor outcome in ALL patients. FOXM1 is negatively regulated by FOXO3A, supports cell survival, drug resistance, colony formation and proliferation in vitro, and promotes leukemogenesis in vivo...
March 10, 2015: Nature Communications
keyword
keyword
24886
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"