Andrew Aw
Ottawa Hospital
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Featured researches published by Andrew Aw.
Thrombosis Research | 2012
Andrew Aw; Marc Carrier; Joshua Koczerginski; Sheryl McDiarmid; Jason Tay
INTRODUCTION The incidence of symptomatic catheter-related deep vein thrombosis (DVT) in cancer patients remains unclear and there is a lack of reliable data on the risk factors of PICC-related DVT. MATERIALS AND METHODS We performed a retrospective cohort study of consecutive cancer patients who received an ultrasound guided PICC line for the administration of chemotherapy. Univariable and multivariable logistic regression analyses were performed to identify risk factors for symptomatic PICC-related DVT. RESULTS In total, 340 cancer patients obtained PICC lines for the administration of chemotherapy. Of these patients, 19 (5.6%; 95% CI: 3.6-8.6) developed symptomatic PICC-related DVT. Factors previously associated with catheter-related DVT, including side of catheter placement, lumen size, tip location, need for repositioning, and number of insertion attempts, were not significant determinants in our analysis. Patients with diabetes were three times more likely to develop PICC-related DVT (OR 3.0, p=0.039), while the presence of COPD and metastatic cancer also increased the odds (OR 3.3, p=0.078 and OR 2.3, p=0.083 respectively). Diabetes remained a significant risk factor after adjustment for effect of metastases and COPD (OR 3.175, p=0.039). Further, the presence of metastases was a significant predictor (OR 3.34, p=0.024) in our multivariable model. CONCLUSIONS Symptomatic PICC-related DVT are frequent in cancer patients receiving chemotherapy. Previously described factors associated with catheter-related thrombosis were not predictive of PICC-related DVT in our study. Diabetes, advanced disease and COPD appear to increase the risk of developing PICC-related DVT in chemotherapy patients.
Clinical Cancer Research | 2017
Lijian Yu; Haesook T. Kim; Siddha Kasar; Parul Benien; Wei Du; Kevin Hoang; Andrew Aw; Bethany Tesar; Reina Improgo; Stacey M. Fernandes; Saranya Radhakrishnan; Josephine L. Klitgaard; Charles Lee; Gad Getz; Sunita R. Setlur; Jennifer R. Brown
Purpose: Chronic lymphocytic leukemia (CLL) with 17p deletion typically progresses quickly and is refractory to most conventional therapies. However, some del(17p) patients do not progress for years, suggesting that del(17p) is not the only driving event in CLL progression. We hypothesize that other concomitant genetic abnormalities underlie the clinical heterogeneity of del(17p) CLL. Experimental Design: We profiled the somatic mutations and copy number alterations (CNA) in a large group of del(17p) CLLs as well as wild-type CLL and analyzed the genetic basis of their clinical heterogeneity. Results: We found that increased somatic mutation number associates with poor overall survival independent of 17p deletion (P = 0.003). TP53 mutation was present in 81% of del(17p) CLL, mostly clonal (82%), and clonal mutations with del(17p) exhibit shorter overall survival than subclonal mutations with del(17p) (P = 0.019). Del(17p) CLL has a unique driver mutation profile, including NOTCH1 (15%), RPS15 (12%), DDX3X (8%), and GPS2 (6%). We found that about half of del(17p) CLL cases have recurrent deletions at 3p, 4p, or 9p and that any of these deletions significantly predicts shorter overall survival. In addition, the number of CNAs, but not somatic mutations, predicts shorter time to treatment among patients untreated at sampling. Indolent del(17p) CLLs were characterized by absent or subclonal TP53 mutation and few CNAs, with no difference in somatic mutation number. Conclusions: We conclude that del(17p) has a unique genomic profile and that clonal TP53 mutations, 3p, 4p, or 9p deletions, and genomic complexity are associated with shorter overall survival. Clin Cancer Res; 23(3); 735–45. ©2016 AACR.
Drugs & Aging | 2017
Andrew Aw; Jennifer R. Brown
The B-cell receptor (BCR) pathway plays an important role in the survival, proliferation and trafficking of cancer cells in a variety of B-cell malignancies. Recently, a number of agents have been developed to target various components of the BCR pathway. One such target is Bruton’s tyrosine kinase (BTK), a Tec family kinase member found near the cell membrane that is involved in upstream BCR signaling. The biological function of BTK in several B-cell lymphoid malignancies has led to the development of the oral BTK inhibitor ibrutinib. In chronic lymphocytic leukemia (CLL), ibrutinib has demonstrated durable clinical responses in relapsed/refractory (R/R) patients, including those with the high-risk del(17p) cytogenetic abnormality. These findings have paved the way for trials evaluating ibrutinib in previously untreated CLL patients, and also in combination with chemoimmunotherapy or other novel agents. Durable clinical responses have also been demonstrated in mantle cell lymphoma (MCL) and Waldenström’s macroglobulinemia (WM) patients treated with ibrutinib. Ibrutinib is generally well tolerated, although current follow-up remains short and patients of advanced age are more likely to discontinue treatment for toxicity. Treatment-specific side effects such as bleeding and atrial fibrillation may, at least partly, be related to off-target inhibition of non-BTK kinases. Studies evaluating other potential indications for BTK inhibition are ongoing, including in post-allogeneic hematopoietic stem cell transplant patients for whom ibrutinib may be effective in modulating graft-versus-host disease. Combination trials of ibrutinib with venetoclax, a Bcl-2 inhibitor, are underway and are supported by sound preclinical rationale. Several next-generation BTK inhibitors are under development with the goal of decreasing treatment-related toxicity and resistance.
Leukemia & Lymphoma | 2017
Andrew Aw; Jennifer R. Brown
Abstract The recent development of small molecule inhibitors targeted at the B-cell receptor (BCR) pathway and the anti-apoptotic protein BCL-2 has revolutionized the care of patients with chronic lymphocytic leukemia (CLL). While durable responses to the BCR inhibitor ibrutinib have been observed in both previously untreated and relapsed/refractory CLL patients, residual disease is common in patients treated with single-agent ibrutinib. Interest remains high in therapeutic combinations that may lead to better quality remissions. A potential partner to ibrutinib with a distinct mechanism of action that is likely to lead to deeper responses is the BCL-2 inhibitor venetoclax. Preclinical studies have suggested synergism between inhibitors of BCR and BCL-2 and have paved the way to the development of ongoing clinical trials aimed at evaluating the combination of ibrutinib with venetoclax in CLL patients.
Thrombosis Research | 2017
Leslie Skeith; Andrew Aw; Julia Hews-Girard; Natalia Rydz
Using an illustrative case of a patient with antithrombin (AT) deficiency who developed a recurrent venous thromboembolism (VTE) in pregnancy despite therapeutic low-molecular-weight heparin (LMWH), we highlight what is known in the literature and address areas of controversy through a series of questions around the case. The questions we address include the role of anti-Xa monitoring for patients with past VTE on antepartum LMWH, what treatment regimen is recommended for pregnant patients who develop a recurrent VTE while on therapeutic anticoagulation, the role of antepartum AT concentrate prophylaxis, and the management of labor/delivery, epidural anesthesia and postpartum anticoagulation. We also describe practical considerations for use of AT concentrate, including teaching our patient to self-infuse AT concentrate at home with support of a hemophilia treatment center (HTC), and the direct and indirect costs of AT concentrate for secondary prophylaxis.
Leukemia & Lymphoma | 2018
Andrew Aw; Haesook T. Kim; Stacey M. Fernandes; Kevin Hoang; Siddha Kasar; Malek Faham; Jennifer R. Brown
Andrew Aw, Haesook T. Kim, Stacey M. Fernandes, Kevin Hoang, Siddha Kasar, Malek Faham and Jennifer R. Brown Division of Hematology, Department of Medicine, The Ottawa Hospital, University of Ottawa, Ottawa, Canada; Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, MA, USA; Dana-Farber Cancer Institute, Boston, MA, USA; Adaptive Biotechnologies Corp, South San Francisco, CA, USA; CLL Center and Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Journal of hematology | 2016
Andrew Aw; Mitchell Sabloff; Dawn Sheppard; David Allan; Harold Atkins; Isabelle Bence-Bruckler; Carolyn Faught; Lothar Huebsch; Jason Tay; Kate Duke; Timothy Ramsay; Chris Bredeson
Biology of Blood and Marrow Transplantation | 2017
Anthony Grieco; Maria Doubova; Adam Bryant; Ranjeeta Mallick; Andrew Aw; Christopher Bredeson; Lothar Huebsch; Natasha Kekre
Blood | 2016
Andrew Aw; Kathryn Coyle; Isabelle Bence-Bruckler; Christopher Bredeson; Doug Coyle
Blood | 2015
Andrew Aw; Lee Mozessohn; Isabelle Bence-Bruckler; Rena Buckstein; Matthew C. Cheung