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Angels Camp, CA, United States

Inghirami G.,University of Turin | Inghirami G.,New York University | Inghirami G.,New York Medical College | Chan W.C.,City of Hope Medical Center | Pileri S.,University of Bologna
Immunological Reviews | Year: 2015

Summary: T-cell lymphoproliferative disorders are a heterogeneous group of neoplasms with distinct clinical-biological properties. The normal cellular counterpart of these processes has been postulated based on functional and immunophenotypic analyses. However, T lymphocytes have been proven to be remarkably capable of modulating their properties, adapting their function in relationship with multiple stimuli and to the microenvironment. This impressive plasticity is determined by the equilibrium among a pool of transcription factors and by DNA chromatin regulators. It is now proven that the acquisition of specific genomic defects leads to the enforcement/activation of distinct pathways, which ultimately alter the preferential activation of defined regulators, forcing the neoplastic cells to acquire features and phenotypes distant from their original fate. Thus, dissecting the landscape of the genetic defects and their functional consequences in T-cell neoplasms is critical not only to pinpoint the origin of these tumors but also to define innovative mechanisms to re-adjust an unbalanced state to which the tumor cells have become addicted and make them vulnerable to therapies and targetable by the immune system. In our review, we briefly describe the pathological and clinical aspects of the T-cell lymphoma subtypes as well as NK-cell lymphomas and then focus on the current understanding of their pathogenesis and the implications on diagnosis and treatment. © 2015 John Wiley & Sons A/S. Source

Fenton J.J.,University of California | Xing G.,University of California | Elmore J.G.,University of Washington | Bang H.,University of California at Davis | And 3 more authors.
Annals of Internal Medicine | Year: 2013

Background: Computer-aided detection (CAD) has rapidly diffused into screening mammography practice despite limited and conflict-ing data on its clinical effect. Objective: To determine associations between CAD use during screening mammography and the incidence of ductal carcinoma in situ (DCIS) and invasive breast cancer, invasive cancer stage, and diagnostic testing. Design: Retrospective cohort study. Setting: Medicare program. Participants: Women aged 67 to 89 years having screening mam-mography between 2001 and 2006 in U.S. SEER (Surveillance, Epidemiology and End Results) regions (409 459 mammograms from 163 099 women). Measurements: Incident DCIS and invasive breast cancer within 1 year after mammography, invasive cancer stage, and diagnostic testing within 90 days after screening among women without breast cancer. Results: From 2001 to 2006, CAD prevalence increased from 3.6% to 60.5%. Use of CAD was associated with greater DCIS incidence (adjusted odds ratio [OR], 1.17 [95% CI, 1.11 to 1.23]) but no difference in invasive breast cancer incidence (adjusted OR, 1.00 [CI, 0.97 to 1.03]). Among women with invasive cancer, CAD was associated with greater likelihood of stage I to II versus III to IV cancer (adjusted OR, 1.27 [CI, 1.14 to 1.41]). In women without breast cancer, CAD was associated with increased odds of diagnos-tic mammography (adjusted OR, 1.28 [CI, 1.27 to 1.29]), breast ultrasonography (adjusted OR, 1.07 [CI, 1.06 to 1.09]), and breast biopsy (adjusted OR, 1.10 [CI, 1.08 to 1.12]). Limitation: Short follow-up for cancer stage, potential unmeasured confounding, and uncertain generalizability to younger women. Conclusion: Use of CAD during screening mammography among Medicare enrollees is associated with increased DCIS incidence, the diagnosis of invasive breast cancer at earlier stages, and increased diagnostic testing among women without breast cancer. © 2013 American College of Physicians. Source

Groot Koerkamp B.,Rotterdam University | Fong Y.,City of Hope Medical Center
Journal of Surgical Oncology | Year: 2014

The biliary malignancies that are reviewed here are gallbladder cancer (GBC), intrahepatic cholangiocarcinoma (IHC), and perihilar cholangiocarcinoma (PHC). The focus is on outcomes after potentially curative resection of biliary malignancies. Key outcomes are postoperative mortality, median and 5-year overall survival (OS), recurrence-free survival, and recurrence patterns. Poor prognostic factors for recurrence and survival as well as prognostic models are also discussed. The incidence of biliary malignancies in the United States is about 5 in 100,000. Postoperative mortality for resection of GBC and IHC is similar to that of liver resections for other indications. However, 90 day postoperative mortality after liver resection for PHC is about 10%. For GBC, median OS depends strongly on the T-stage and ranges from 8 months (pT3) to 79 months (pT1b). Median OS after resection for IHC is about 30 months, and for PHC about 38 months. The majority of patients with biliary malignancies develop a recurrence after resection. Patients with GBC recur early with a median time to recurrence of 12 months, versus about 20 months for IHC and PHC. In patients with resected IHC or PHC locoregional recurrence was the only site of recurrence in about 60% of patients, versus 15% in patients with GBC. Poor prognostic factors after resection of all biliary malignancies include the presence of lymph node metastasis, a positive surgical resection margin, and moderate or poor tumor differentiation. Several prognostic nomograms have been developed to predict long-term outcomes of biliary cancer resection. © 2014 Wiley Periodicals, Inc. Source

Ferrell B.,City of Hope Medical Center
Nursing Science Quarterly | Year: 2010

The focus of this column is to describe a body of research on palliative care and end-of-life that has been the focus of Dr. Betty Ferrell's career and her work at the City of Hope. The impact of this work on the nursing workforce is described and research resources for nurses are included. © The Author(s) 2010. Source

Pullarkat V.,City of Hope Medical Center
Advances in Hematology | Year: 2010

Recipients of hematopoietic stem cell transplantation (HSCT) frequently have iron overload resulting from chronic transfusion therapy for anemia. In some cases, for example, in patients with myelodysplastic syndromes and thalassemia, this can be further exacerbated by increased absorption of iron from the gut as a result of ineffective erythropoiesis. Accumulating evidence has established the negative impact of elevated pretransplantation serum ferritin, a surrogate marker of iron overload, on overall survival and nonrelapse mortality after HSCT. Complications of HSCT associated with iron overload include increased bacterial and fungal infections as well as sinusoidal obstruction syndrome and possibly other regimen-related toxicities. Based on current evidence, particular attention should be paid to prevention and management of iron overload in allogeneic HSCT candidates, especially in patients with thalassemia and myelodysplastic syndromes. The pathophysiology of iron overload in the HSCT patient and optimum strategies to deal with iron overload during and after HSCT require further study. © 2010 Vinod Pullarkat. Source

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