Radiation-induced changes in long-term survivors of childhood cancer after treatment with radiation therapy

Ried, Hubert L.; Jaffe, Norman

doi:10.1016/s0037-198x(05)80068-9

Cited by 16 publications

(10 citation statements)

References 62 publications

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“…Accurate information regarding previous treatment exposures reflects an important factor for determining appropriate health screening and healthcare delivery (21). While little previous research has occurred on this topic, several studies have documented rates between 77–90% for accurate reporting of cancer history (22, 23).…”

Section: Survivors’ Knowledge Of Prior Radiation Exposurementioning

confidence: 99%

Long-Term Effects of Radiation Exposure among Adult Survivors of Childhood Cancer: Results from the Childhood Cancer Survivor Study

2010

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In the last four decades, advances in therapies for primary cancers have improved overall survival for childhood cancer. Currently, almost 80% of children will survive beyond 5 years from diagnosis of their primary malignancy. These improved outcomes have resulted in a growing population of childhood cancer survivors. Radiation therapy, while an essential component of primary treatment for many childhood malignancies, has been associated with risk of long-term adverse outcomes. The Childhood Cancer Survivor Study (CCSS), a retrospective cohort of over 14,000 survivors of childhood cancer diagnosed between 1970 and 1986, has been an important resource to quantify associations between radiation therapy and risk of long-term adverse health and quality of life outcomes. Radiation therapy has been associated with increased risk for late mortality, development of second neoplasms, obesity, and pulmonary, cardiac and thyroid dysfunction as well as an increased overall risk for chronic health conditions. Importantly, the CCSS has provided more precise estimates for a number of dose–response relationships, including those for radiation therapy and development of subsequent malignant neoplasms of the central nervous system, thyroid and breast. Ongoing study of childhood cancer survivors is needed to establish long-term risks and to evaluate the impact of newer techniques such as conformal radiation therapy or proton-beam therapy.

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Section: Survivors’ Knowledge Of Prior Radiation Exposurementioning

confidence: 99%

Long-Term Effects of Radiation Exposure among Adult Survivors of Childhood Cancer: Results from the Childhood Cancer Survivor Study

2010

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“…This heralds a major life change, with the abrupt loss of ovarian estrogens in aging women leading to increased risks for a number of debilitating health problems, including cardiovascular disease, osteoporosis, neurological dysfunction and macular degeneration in the eyes 6 . Furthermore, adjuvant cancer therapies greatly accelerate oocyte depletion, resulting in early ovarian failure, a loss of reproductive potential, and a premature onset of menopause-related health problems in young women 4,[7][8][9] .…”

Section: Articlesmentioning

confidence: 99%

Oocyte apoptosis is suppressed by disruption of the acid sphingomyelinase gene or by sphingosine -1-phosphate therapy

Morita

Perez

Pâris

et al. 2000

Nat Med

556

423

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The time at which ovarian failure (menopause) occurs in females is determined by the size of the oocyte reserve provided at birth, as well as by the rate at which this endowment is depleted throughout post-natal life. Here we show that disruption of the gene for acid sphingomyelinase in female mice suppressed the normal apoptotic deletion of fetal oocytes, leading to neonatal ovarian hyperplasia. Ex vivo, oocytes lacking the gene for acid sphingomyelinase or wild-type oocytes treated with sphingosine-1-phosphate resisted developmental apoptosis and apoptosis induced by anti-cancer therapy, confirming cell autonomy of the death defect. Moreover, radiation-induced oocyte loss in adult wild-type female mice, the event that drives premature ovarian failure and infertility in female cancer patients, was completely prevented by in vivo therapy with sphingosine-1-phosphate. Thus, the sphingomyelin pathway regulates developmental death of oocytes, and sphingosine-1-phosphate provides a new approach to preserve ovarian function in vivo.

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“…Indeed, infertility and premature menopause are well documented in young girls and reproductive-age women who have been treated for cancer 65,66 . Given that up to 1 in 52 human females between birth and age 39 (the pre-reproductive and reproductive years) are diagnosed with cancer 67 , many people are potentially affected.…”

Section: The Untimely Death Of Innocent Bystandersmentioning

confidence: 99%

Commuting the death sentence: how oocytes strive to survive

Tilly

2001

Nat Rev Mol Cell Biol

338

240

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Programmed cell death claims up to 99.9% of the cells in the mammalian female germ line, which eventually drives irreversible infertility and ovarian failure - the menopause in humans. New insights into the mechanisms that underlie germ-cell apoptosis have been provided by the study of oocyte death in lower organisms and in genetically manipulated mice that lack apoptosis-regulatory proteins. With new therapeutic tools to control fertility, oocyte quality and ovarian lifespan on the horizon, understanding how and why the female body creates, only to delete, so many germ cells is imperative.

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Radiation-induced changes in long-term survivors of childhood cancer after treatment with radiation therapy

Cited by 16 publications

References 62 publications

Long-Term Effects of Radiation Exposure among Adult Survivors of Childhood Cancer: Results from the Childhood Cancer Survivor Study

Long-Term Effects of Radiation Exposure among Adult Survivors of Childhood Cancer: Results from the Childhood Cancer Survivor Study

Oocyte apoptosis is suppressed by disruption of the acid sphingomyelinase gene or by sphingosine -1-phosphate therapy

Commuting the death sentence: how oocytes strive to survive

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