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The Fred Hutchinson Cancer Research Center , is one of the world’s leading cancer research institutes. Its interdisciplinary scientists research the prevention, early detection, and treatment of cancer and other diseases in the laboratory and at patient bedside in the United States and other countries.Fred Hutch's mission statement is "the elimination of cancer and related diseases as causes of human suffering and death". Wikipedia.

The association between cytomegalovirus (CMV) reactivation and relapse was evaluated in a large cohort of patients with acute myeloid leukemia (AML) (n = 761), acute lymphoblastic leukemia (ALL) (n = 322), chronic myeloid leukemia (CML) (n = 646), lymphoma (n = 254), and myelodysplastic syndrome (MDS) (n = 371) who underwent allogeneic hematopoietic cell transplantation (HCT) between 1995 and 2005. In multivariable models, CMV pp65 antigenemia was associated with a decreased risk of relapse by day 100 among patients with AML (hazard ratio [HR] = 0.56; 95% confidence interval [CI], 0.3-0.9) but not in patients with ALL, lymphoma, CML, or MDS. The effect appeared to be independent of CMV viral load, acute graft-versus-host disease, or ganciclovir-associated neutropenia. At 1 year after HCT, early CMV reactivation was associated with reduced risk of relapse in all patients, but this did not reach significance for any disease subgroup. Furthermore, CMV reactivation was associated with increased nonrelapse mortality (HR = 1.31; 95% CI, 1.1-1.6) and no difference in overall mortality (HR = 1.05; 95% CI, 0.9-1.3). This report demonstrates a modest reduction in early relapse risk after HCT associated with CMV reactivation in a large cohort of patients without a benefit in overall survival. Source

Houghton A.M.,Fred Hutchinson Cancer Research Center
Nature Reviews Cancer | Year: 2013

Numerous epidemiological studies have consistently linked the presence of chronic obstructive pulmonary disease (COPD) to the development of lung cancer, independently of cigarette smoking dosage. The mechanistic explanation for this remains poorly understood. Progress towards uncovering this link has been hampered by the heterogeneous nature of the two disorders: each is characterized by multiple sub-phenotypes of disease. In this Review, I discuss the nature of the link between the two diseases and consider specific mechanisms that operate in both COPD and lung cancer, some of which might represent either chemopreventive or chemotherapeutic targets. © 2013 Macmillan Publishers Limited. All rights reserved. Source

Ghajar C.M.,Fred Hutchinson Cancer Research Center
Nature Reviews Cancer | Year: 2015

Despite considerable advancements that shattered previously held dogmas about the metastatic cascade, the evolution of therapies to treat metastatic disease has not kept up. In this Opinion article, I argue that, rather than waiting for metastases to emerge before initiating treatment, it would be more effective to target metastatic seeds before they sprout. Specifically, I advocate directing therapies towards the niches that harbour dormant disseminated tumour cells to sensitize them to cytotoxic agents. Treatment sensitization, achieved by disrupting reservoirs of leukaemic stem cells and latent HIV, argues that this approach, although unconventional, could succeed in improving patient survival by delaying or even preventing metastasis. © 2015 Macmillan Publishers Limited. All rights reserved. Source

Maloney D.G.,Fred Hutchinson Cancer Research Center
New England Journal of Medicine | Year: 2012

A 62-year-old man is evaluated for abdominal pain. Computed tomography (CT) shows a 7-cm mesenteric mass. An incisional biopsy reveals a diffuse large B-cell lymphoma, and immunohistochemical staining is positive for the B-cell antigen CD20. The patient is referred to an oncologist. A positron-emission tomographic-CT (PET-CT) scan reveals involvement of additional nodes in the lower chest and abdomen. The serum level of lactate dehydrogenase is twice the upper limit of the normal range. The results of bone marrow biopsy and aspiration are normal on pathological analysis and flow cytometry. The patient reports an unintentional weight loss of 111/2 kg (25 lb) during the previous 6 months but no unexplained fevers or night sweats. He has no history of cardiac disease, and an echocardiogram shows a normal left ventricular ejection fraction. The oncologist recommends treatment with the anti-CD20 monoclonal antibody rituximab in combination with a chemotherapy regimen of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP). Copyright © 2012 Massachusetts Medical Society. Source

This randomized phase 3 clinical trial evaluated the potential benefit of the addition of gemtuzumab ozogamicin (GO) to standard induction and postconsolidation therapy in patients with acute myeloid leukemia. Patients were randomly assigned to receive daunorubicin (45 mg/m(2) per day on days 1, 2, and 3), cytarabine (100 mg/m(2) per day by continuous infusion on days 1-7), and GO (6 mg/m(2) on day 4; DA+GO) vs standard induction therapy with daunorubicin (60 mg/m(2) per day on days 1, 2, and 3) and cytarabine alone (DA). Patients who achieved complete remission (CR) received 3 courses of high-dose cytarabine. Those remaining in CR after consolidation were randomly assigned to receive either no additional therapy or 3 doses of GO (5 mg/m(2) every 28 days). From August 2004 until August 2009, 637 patients were registered for induction. The CR rate was 69% for DA+GO and 70% for DA (P = .59). Among those who achieved a CR, the 5-year relapse-free survival rate was 43% in the DA+GO group and 42% in the DA group (P = .40). The 5-year overall survival rate was 46% in the DA+GO group and 50% in the DA group (P = .85). One hundred seventy-four patients in CR after consolidation underwent the postconsolidation randomization. Disease-free survival was not improved with postconsolidation GO (HR, 1.48; P = .97). In this study, the addition of GO to induction or postconsolidation therapy failed to show improvement in CR rate, disease-free survival, or overall survival. Source

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