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Point: Interferon-α for Adjuvant Therapy for Melanoma Patients

Michael S. Sabel and Vernon K. Sondak

trial E1690/S9111/C9190 . J Clin Oncol 2000 ; 18 : 2444 – 2458 . 21 Eggermont AMM Gore M . A critical appraisal of the role of interferon-α in the treatment of malignant melanoma . Principles and Practice of Biologic Therapy of Cancer

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Counterpoint: The Case Against Adjuvant High-Dose Interferon-α for Melanoma Patients

Paul B. Chapman

Oncol 2000 ; 18 : 2444 – 2458 . 8 Wheatley K Hancock B Gore M . Interferon-α as adjuvant therapy for melanoma: a Meta-analysis of the randomised trials . Proceedings of ASCO , San Francisco, CA , May 15, 2001 , Vol. 20 . 9

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Management of Metastatic Renal Cancer

Patricia Thompson and Mayer Fishman

(RCC) (Abstr #2430) . Proc Am Soc Clin Onc 2002 . 56 Gordon MS Manola J Fairclough D . Low dose interferon-α2b (IFN) + thalidomide (T) in patients (pts) with previously untreated renal cell cancer (RCC): Improvement in progression

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Contemporary Intravesical Treatment Options for Urothelial Carcinoma of the Bladder

Stephen A. Brassell and Ashish M. Kamat

. Perioperative single dose instillation of epirubicin or interferon-α after transurethral resection for the prophylaxis of primary superficial bladder cancer recurrence: a prospective randomized multicenter study-FinnBladder III long-term results . J Urol 2002

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Issues of Imatinib and Pregnancy Outcome

Jane Apperley

is not confirmed. Therapies other than TKIs include interferon-α (IFN-α), hydroxyurea, busulphan, and leukapheresis, although hydroxyurea and busulphan should be avoided if treatment is required in pregnancy ( Table 3 ). Busulphan is an alkylating

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New Agents in the Treatment of Chronic Myelogenous Leukemia

Javier Pinilla-Ibarz and Alfonso Quintás-Cardama

The discovery of molecularly targeted agents that selectively inhibit bcr-abl tyrosine kinase activity, such as imatinib, has revolutionized the treatment and natural history of chronic myelogenous leukemia (CML). Treatment of chronic-phase CML with imatinib showed complete cytogenetic response rates of more than 40% in patients after failure of interferon-α, and more than 80% in patients with newly diagnosed CML. Patients with CML can now expect excellent long-term survival, often without major side effects. In most patients, however, residual leukemic burden remains detectable using a sensitive reverse transcription-polymerase chain reaction method. In addition, many patients undergoing imatinib therapy will either not respond or lose their response over time because of resistance or intolerance. The introduction of second-generation tyrosine kinase inhibitors (TKIs) re-establishes response in approximately half of these patients. Several agents are being developed for treating patients who experience suboptimal response to second-generation TKIs and for those who develop resistance caused by the emergence of highly resistant BCR-ABL1 mutations. This article provides an overview of novel targeted agents available for CML.

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Non–Clear Cell Renal Cancer: Features and Medical Management

Daniel Y. C. Heng and Toni K. Choueiri

; 356 : 125 – 134 . 16 Escudier B Koralewski P Pluzanska A . A randomized, controlled, double-blind phase III study (AVOREN) of bevacizumab/interferon-α2a vs placebo/interferon- α2a as first-line therapy in metastatic renal cell carcinoma

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Focal Takotsubo Cardiomyopathy With High-Dose Interleukin-2 Therapy for Malignant Melanoma

Senthil Damodaran, Ewa Mrozek, David Liebner, and Kari Kendra

. Subsequently, the patient opted for adjuvant interferon α-2b therapy, and received intravenous high-dose interferon, 20 MU/m 2 daily 5 times a week for 20 total doses followed by maintenance subcutaneous interferon, 10 MU/m 2 3 times a week for a total

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Is Observation Dead in Follicular Lymphoma? Still Appropriate

Caron A. Jacobson and Arnold S. Freedman

Brice et al 4 in patients with low tumor burden. Moreover, when treatment was needed, delay in treatment did not adversely impact response to treatment, with response rates of 78% and 70% after initial treatment with prednimustine and interferon-α

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BRAF-Mutated Erdheim-Chester Disease: Profound Response to Vemurafenib Visualized With Serial Multimodality Imaging

Javaughn Corey R. Gray, Jongho Kim, Michael Digianvittorio, Nancy K. Feeley, Paul J. Scheel, Stanley S. Siegelman, Elliot K. Fishman, and Steven P. Rowe

main therapeutic approach to ECD was interferon-α–based regimens. Now, there is increasing evidence that almost all patients carrying the BRAF V600E mutation have excellent responses to the now FDA-approved BRAF inhibitor vemurafenib and other BRAF