scholarly journals Second tumor risk in children treated with proton therapy

2021 ◽  
Author(s):  
Daniel J. Indelicato ◽  
James E. Bates ◽  
Raymond B. Mailhot Vega ◽  
Ronny L. Rotondo ◽  
Bradford S. Hoppe ◽  
...  
Keyword(s):  
Proton Therapy ◽  
Tumor Risk ◽  
Second Tumor

Projected Second Tumor Risk and Dose to Neurocognitive Structures After Proton Versus Photon Radiotherapy for Benign Meningioma

2012 ◽  
Vol 83 (4) ◽  
pp. e495-e500 ◽  
Author(s):  
Nils D. Arvold ◽  
Andrzej Niemierko ◽  
George P. Broussard ◽  
Judith Adams ◽  
Barbara Fullerton ◽  
...  
Keyword(s):  
Benign Meningioma ◽  
Tumor Risk ◽  
Second Tumor ◽  
Photon Radiotherapy

Second non-ocular tumors among survivors of retinoblastoma treated with proton therapy.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 10018-10018
Author(s):  
Roshan V Sethi ◽  
Helen Alice Shih ◽  
David Kim ◽  
Beow Y. Yeap ◽  
Kent Mouw ◽  
...  
Keyword(s):  
Radiation Therapy ◽  
Proton Therapy ◽  
Massachusetts General Hospital ◽  
Secondary Malignancy ◽  
Target Tissue ◽  
Second Malignancy ◽  
Proton Radiation ◽  
Associated Malignancy ◽  
Second Tumor

10018 Background: The leading cause of death for patients with hereditary retinoblastoma is second malignancy. Proton radiation allows for significant sparing of non-target tissue. We sought to determine the risk of second malignancy for the largest and oldest cohort of retinoblastoma patients treated with proton therapy. Methods: We performed a retrospective review of patients treated at the Massachusetts General Hospital (MGH) between 1986 and 2011. Results: Fifty-two patients were identified (see Table). Forty-four patients (85%) were hereditary survivors. Patients were followed for a median of 6.9 years from the start of radiation therapy (range, 11.3 months to 24.4 years). The median age at follow-up was 9.0 years (range, 31.3 months to 24.5 years). Fifteen patients had more than 10 years of follow-up from the start of radiation therapy, and 20 patients were more than 10 years old at last follow-up. With 417.2 person-years of follow-up, we identified one secondary malignancy, an osteosarcoma of the distal femur. The cumulative incidence of second tumor was 5% at 10 years. No radiation-associated malignancies were reported. Conclusions: Retinoblastoma is highly responsive to radiation. The central objection to the use of radiation—the risk of second malignancy—is founded on studies of patients treated with relatively non-conformal techniques. We present the first series of patients treated with the most conformal of current available modalities. While longer follow up is necessary, our preliminary data suggest that the risk of radiation-associated malignancy is minimal with proton therapy. [Table: see text]

Second Tumor Risk With Modern Radiotherapy for Pituitary Adenomas

2007 ◽  
Vol 69 (3) ◽  
pp. S701 ◽  
Author(s):  
K.M. Winkfield ◽  
H.A. Shih ◽  
A. Niemierko ◽  
M.R. Bussiere ◽  
E.M. Crowley ◽  
...  
Keyword(s):  
Pituitary Adenomas ◽  
Tumor Risk ◽  
Second Tumor ◽  
Modern Radiotherapy

Modeling Intracranial Second Tumor Risk and Estimates of Clinical Toxicity with Various Radiation Therapy Techniques for Patients with Pituitary Adenoma

2011 ◽  
Vol 10 (3) ◽  
pp. 243-251 ◽  
Author(s):  
K. M. Winkfield ◽  
A. Niemierko ◽  
M. R. Bussière ◽  
E. M. Crowley ◽  
B. N. Napolitano ◽  
...  
Keyword(s):  
Radiation Therapy ◽  
Pituitary Adenoma ◽  
Clinical Toxicity ◽  
Tumor Risk ◽  
Second Tumor

Proton Therapy of Esthesioneuroblastoma: The UFPTI Experience

Skull Base ◽  
2011 ◽  
Vol 21 (S 01) ◽  
Author(s):  
Robert Malyapa ◽  
William Mendenhall ◽  
Craig McKenzie ◽  
Daniel Yeung ◽  
Zuofeng Li ◽  
...  
Keyword(s):  
Proton Therapy

Молекулярная биология менингиом головного мозга

2017 ◽  
pp. 82-91
Author(s):  
В.А. Бывальцев ◽  
И.А. Степанов ◽  
Е.Г. Белых ◽  
А.И. Яруллина
Keyword(s):  
Gene Therapy ◽  
Proton Therapy ◽  
Genetic Factors ◽  
Intracranial Tumor ◽  
Molecular Profile ◽  
Genetic Changes ◽  
Treatment Techniques ◽  
Downstream Effects ◽  
Si Rna ◽  
The Relationship

Цель обзора - анализ современных данных литературы о нарушении внутриклеточных сигнальных путей, играющих ведущую роль в развитии менингиом, генетических и молекулярных профилях данной группы опухолей. К настоящему времени изучено множество аберрантных сигнальных внутриклеточных путей, которые играют важнейшую роль в развитии менингиом головного мозга. Четкое понимание поврежденных внутриклеточных каскадов поможет изучить влияние генетических мутаций и их эффектов на менингиомогенез. Подробное исследование генетического и молекулярного профиля менингиом позволит сделать первый уверенный шаг в разработке более эффективных методов лечения данной группы интракраниальных опухолей. Хромосомы 1, 10, 14, 22 и связанные с ними генные мутации ответственны за рост и прогрессию менингиом. Предполагается, что только через понимание данных генетических повреждений будут реализованы новейшие эффективные методы лечения. Будущая терапия будет включать в себя комбинации таргетных молекулярных агентов, в том числе генную терапию, малые интерферирующие РНК, протонную терапию и другие методы воздействия, как результат дальнейшего изучения генетических и биологических изменений, характерных для менингеальных опухолей. Meningiomas are by far the most common tumors arising from the meninges. A myriad of aberrant signaling pathways involved with meningioma tumorigenesis, have been discovered. Understanding these disrupted pathways will aid in deciphering the relationship between various genetic changes and their downstream effects on meningioma pathogenesis. An understanding of the genetic and molecular profile of meningioma would provide a valuable first step towards developing more effective treatments for this intracranial tumor. Chromosomes 1, 10, 14, 22, their associated genes, have been linked to meningioma proliferation and progression. It is presumed that through an understanding of these genetic factors, more educated meningioma treatment techniques can be implemented. Future therapies will include combinations of targeted molecular agents including gene therapy, si-RNA mediation, proton therapy, and other approaches as a result of continued progress in the understanding of genetic and biological changes associated with meningiomas.

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