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Cancer-Research-UpdatesWEB

Short-Time Outcome of Intraoperative Radiotherapy (IORT): A Study on Side-Effects and Quality of Life in the Treatment of Early Breast Cancer
Pages 237-245
Caroline Page, Pierre-Alain Brioschi and Jacques Bernier

DOI: http://dx.doi.org/10.6000/1929-2279.2013.02.04.2

Published: 31 October 2013

 


Abstract: Early prospective studies recently demonstrated the non-inferiority of intraoperative radiotherapy compared to protracted external radiotherapy in selected patients. The present study aims at analyzing, in a cohort of 80 women, the distribution and incidence of short-time side-effects induced by intraoperative radiotherapy as well as its impact on patient’s quality of life in the months following the treatment. No side-effect was found in the majority of patients (n: 46; 58%). Out of those 32 patients experiencing side-effects after IORT, 26 cases (81%) were found to develop only mild effects. More than 94% of the patients declared to consider IORT as a clear advantage over external radiotherapy in the armamentarium of breast cancer treatment.

Keywords: Breast Cancer, Intraoperative radiation therapy, Radiation therapy, Side-effect, Cosmetics.
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Cancer-Research-UpdatesWEB

Is FLT3 Internal Tandem Duplication an Unfavorable Risk Factor for High Risk Children with Acute Myeloid Leukemia? – Polish Experience
Pages 246-2353
K. Pawinska-Wasikowska, T. Ksiazek, A. Wieczorek, M. Matysiak, B. Fic-Sikorska, E. Adamkiewicz-Drozynska, L. Maciejka-Kapuscinska, A. Chybicka, K. Potocka, J. Wachowiak, J. Skalska-Sadowska, J. Kowalczyk, B. Wojcik, M. Wysocki, S. Koltan, M. Krawczuk-Rybak, K. Muszynska-Roslan, W. Mlynarski, M. Stolarska, T. Urasinski, E. Kamienska, T. Szczepanski, R. Tomaszewska, G. Sobol-Milejska, A. Mizia-Malarz, G. Karolczyk, J. Pohorecka, M. Wieczorek, I. Karpinska-Derda and W. Balwierz

DOI: http://dx.doi.org/10.6000/1929-2279.2013.02.04.3

Published: 31 October 2013Open Access 


Abstract: According to the AML-BFM 2004 Interim, a treatment protocol used in Poland since 2005, presence of FLT3 internal tandem duplication (FLT3/ITD) qualifies a patient with acute myeloid leukemia (AML) to a high-risk group (HRG).

The present study was aimed to identify the prevalence of FLT3/ITD in children with AML in Poland and to evaluate its prognostic significance in the HRG patients.

Out of 291 children with de novo AML treated in 14 Polish centers between January 2006 and December 2012, samples from 174 patients were available for FLT3/ITD analysis. Among study patients 108 children (61.7%) were qualified to HRG.Genomic DNA samples from bone marrow were tested for identification of FLT3/ITD mutation by PCR amplification of exon 14 and 15 of FLT3 gene. Clinical features and treatment outcome in patients with and without FLT3/ITD were analyzed in the study.

The FLT3/ITD was found in 14 (12.9%) of 108 HRG children. There were no significant differences between children with and without FLT3/ITD in age and FAB distribution. The white blood cells count in peripheral blood at diagnosis was significantly higher (p <0.01) in the children with FLT3/ITD. Over 5-year overall survival rate for FLT3/ITD positive children was worse (42.4%) comparing to FLT3/ITD negative children (58.9%), but the statistical difference was not significant. However, over 5-year survivals free from treatment failures were similar.

The FLT3/ITD rate (12.9%) observed in the study corresponded to the published data. There was no significant impact of FLT3/ITD mutation on survival rates, although further studies are needed on this subject.

Keywords: FLT3/ITD mutation, acute myeloid leukemia, children, treatment result, high risk group.
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Cancer-Research-UpdatesWEB

Disease–Free Remission Exceeding 37 Years in Patients Treated as Children for Acute Leukemia (AL) with Immunotherapy Using Viable (Cryopreserved) Allogeneic Leukemic Cells
Pages 254-264
Tatiana I. Bulycheva, Svetlana A. Mayakova and Simon V. Skurkovich

DOI: http://dx.doi.org/10.6000/1929-2279.2013.02.04.4

Published: 31 October 2013

Open Access 


Abstract: At present time in spite of great achievements in modern chemotherapy of acute leukemia (AL) the issue of eradication of residual leukemic cells (MRD) is still relevant. Since 1971 we included specific immunotherapy in the treatment of children with acute lymphoblastic leukemia in remission using viable cryopreserved allogeneic leukemic cells. 67 children in remission were divided into 2 groups: 27 constituted the control group (only continued standard-for-that-time chemotherapy) and 40 children – the treatment which received immunotherapy in addition to standard chemotherapy. In 3 years all children in the control group relapsed. The median length of remission was 15 months. In the treatment group we observed stabilization of remission only in children over 7 years of age when immunization was initiated after 6 or more months of remission and in children younger than 7 if it was initiated after 1-1,5 years of remission. The median length of remission was 60 months which significantly exceeded (4 times) that parameter in the control group of children. Cytotoxic antibodies against leukemic cells appeared in the serum of effectively immunized children at a higher titer than against donor lymphocytes. Intrathecal administration of this hyperimmune serum to patients with neuroleukemia resistant to chemotherapy led to a sharp decrease in the amount of leukemic cells in the spinal fluid. After 5 years of remission (and 3-5 years of immunotherapy) all treatment in these patients was stopped. Out of 19 patients who received immunotherapy on time, 8 patients (42%) have been in event-free remission for 37 to 41 years (median – 38 years) through the present time and enjoy high quality of life. Our results indicate that immunotherapy initiated during remission period of AL can lead to creation of anti-leukemic immunity with subsequent eradication of MRD and complete recovery.

Keywords: Acute leukemia, Immunotherapy, Cryopreserved leukemic cells, Prolongation of remission, Immunological indices.
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Cancer-Research-UpdatesWEB

Drug Resistance Mechanisms in Non-Small Cell Lung Carcinoma
Pages 265-282
Janet Wangari-Talbot and Elizabeth Hopper-Borge

DOI: http://dx.doi.org/10.6000/1929-2279.2013.02.04.5

Published: 31 October 2013

Open Access 


Abstract: Lung cancer is the most commonly diagnosed cancer in the world. “Driver” and “passenger” mutations identified in lung cancer indicate that genetics play a major role in the development of the disease, progression, metastasis and response to therapy. Survival rates for lung cancer treatment have remained stagnant at ~15% over the past 40 years in patients with disseminated disease despite advances in surgical techniques, radiotherapy and chemotherapy. Resistance to therapy; either intrinsic or acquired has been a major hindrance to treatment leading to great interest in studies seeking to understand and overcome resistance. Genetic information gained from molecular analyses has been critical in identifying druggable targets and tumor profiles that may be predictors of therapeutic response and mediators of resistance. Mutated or overexpressed epidermal growth factor receptor (EGFR) and translocations in the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) genes (EML4-ALK) are examples of genetic aberrations resulting in targeted therapies for both localized and metastatic disease. Positive clinical responses have been noted in patients harboring these genetic mutations when treated with targeted therapies compared to patients lacking these mutations. Resistance is nonetheless a major factor contributing to the failure of targeted agents and standard cytotoxic agents. In this review, we examine molecular mechanisms that are potential drivers of resistance in non-small cell lung carcinoma, the most frequently diagnosed form of lung cancer. The mechanisms addressed include resistance to molecular targeted therapies as well as conventional chemotherapeutics through the activity of multidrug resistance proteins.

Keywords: Non-small cell lung cancer, EGFR, EML4-ALK, tyrosine kinase inhibitors, drug resistance, ABC transporters, ABCB1, ABCC1, ABCC10, ABCG2.
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