Zhong et al., pp. 2125–2131 It is thought that only a minority of cells within any tumor have the ability to self-renew. In the context of retinoblastoma (RB), the consensus view is that RB cells originate from retinal stem cells (RSC) or multipotent primitive retinoblasts. There is, however, no direct evidence that tumorigenic RSCs actually exist within RBs. Previously, Zhong et al. had successfully cultivated stem-like cells from human RBs. In this report they have taken the results a step further by investigating whether these retinal stem-like cells (RSLCs) have the potential to reproduce the parental tumor in vivo. Using tumor tissues from eight patients with either differentiated or nondifferentiated RB, primary cell cultures were generated under conditions that favored stem cell growth. All tumor-derived cultures developed nonadherent neurospheres that could be passaged many times. These cells were found to be capable of self-renewal and expressed neural stem cell markers such as pax6, nestin and Bmi-1. RSLCs also exhibited an impressive degree of multipotentiality, forming neurons and glial cells – among others – though they fell short of the full cellular repertoire of RSCs. After intraocular (I.O.) injection of four of the RB primary cultures into NOD/SCID mice, the mice developed tumors within 2–12 weeks. Interestingly, these xenograft tumors were very similar to their parental tumor cells. To further confirm that these xenografts contain RSLCs, single tumor cells were isolated from the xenograft tumors and reinjected I.O. into new animals, which in turn developed RB-like tumors. These findings strongly suggest that RB derives from RSLCs. In addition to furthering our understanding of RB tumorigenesis, this model could be useful in developing new therapeutic approaches for the disease. Vickers et al., pp. 2212–2217 Total prostate specific antigen (tPSA) levels can be raised in benign prostate disease, particularly in older patients, complicating its usefulness as a predictor of prostate cancer. Previous studies have shown that levels of human kallikrein-2 (hK2) and the ratio of free to total PSA (%fPSA) may also reflect underlying prostate malignancy. In this study, Vickers et al., wanted to determine whether the combination of these biomarkers could offer a better means of detecting prostate cancer and whether the biomarkers vary as a function of age. Using blood samples from a very large (13,600) cohort of men between the ages of 44 and 50 and 59 and 61 and data from the Swedish Cancer Registry, the authors determined odds ratios and the predictive probability of the various biomarkers in over 500 prostate cancer patients. They found that the predictive value of tPSA is inversely associated with age but not with time of diagnosis. The predictive value of %fPSA combined with hK2 was inversely related to the time of diagnosis but not modified by age. Using tPSA, %fPSA and hK2 compared to tPSA alone enhanced prediction levels in older patients but not younger ones. The results from this study importantly show the value of screening younger men (<50) for PSA and that combined biomarker testing may be needed to detect prostate malignancy more accurately in older subjects. Inskip et al., pp. 2233–2240 Mortalities associated with childhood cancers have decreased over the last few decades. However, the aggressive nature of the treatments means that patients are subsequently at risk of developing new primary cancers. Setting up a large-scale follow-up of childhood cancer survivors is not an easy task. In this report, Inskip et al. use a US population-based cancer registry — SEER – which contains data on nearly 26,000 childhood cancer survivors from 1973–2002, to determine new malignancy risk in childhood cancer patients. Using observed to expected ratios and regression analysis, the cancer survivors were found to have an almost 6-fold increased risk of developing a new primary cancer compared to the general population. The degree of risk and nature of the second cancer was highly dependent on the first type of cancer the patient had suffered from. Hodgkin lymphoma (HL), retinoblastoma, primitive neuroectodermal tumor and Ewing sarcoma were the cancers associated with the highest risk of developing a second primary cancer. The most likely subsequent cancers were female breast, CNS, bone, thyroid, soft tissue, melanoma and acute nonlymphocytic leukemia (ANLL). The mode of original cancer treatment also had an influence on subsequent cancer development. Patients who had received radiotherapy were more likely to develop a solid tumor, whereas patients treated with chemotherapy were at higher risk of developing ANLL. This thorough study gives a comprehensive analysis of the new malignancy risks facing survivors of childhood cancer. This perspective and future follow-up studies will be important to help monitor patients and evaluate the risks associated with changing cancer treatments.
TUMOR FEATURES BEYOND TUMOR SIZE: A POPULATION-LEVEL ANALYSIS OF PATIENTS WITH SURGICALLY RESECTED NON-SMALL CELL LUNG CANCER (NSCLC) IN THE SEER MEDICARE DATABASE
TUMOR FEATURES BEYOND TUMOR SIZE: A POPULATION-LEVEL ANALYSIS OF PATIENTS WITH SURGICALLY RESECTED NON-SMALL CELL LUNG CANCER (NSCLC) IN THE SEER MEDICARE DATABASE
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102Association of surgical resection and survival in patients with malignant primary osseous spinal neoplasms from the Surveillance, Epidemiology, and End Results (SEER) database
Malignant osseous spinal neoplasms are aggressive tumors associated with poor outcomes despite aggressive multidisciplinary measures. While surgical resection has been shown to improve short-term local disease control, it remains debated whether surgical resection is associated with improved overall survival in patients with malignant primary osseous spinal neoplasms. The aim of this manuscript is to review survival data from a US cancer registry spanning 30 years to determine if surgical resection was independently associated with overall survival. The SEER registry (1973-2003) was queried to identify cases of histologically confirmed primary spinal chordoma, chondrosarcoma, osteosarcoma, or Ewing's sarcoma of the mobile spine and pelvis. Patients with systemic metastasis were excluded. Age, gender, race, tumor location, and primary treatments were identified. Extent of local tumor invasion was classified as confined within periosteum versus extension beyond periosteum to surrounding tissues. The association of surgical resection with overall survival was assessed via Cox analysis adjusting for age, radiotherapy, and tumor invasiveness. 827 patients were identified with non-metastatic primary osseous spinal neoplasms (215 chordoma, 282 chondrosarcoma, 158 osteosarcoma, 172 Ewing's sarcoma). Overall, median survival was histology specific (chordoma, 96 months; Ewing's sarcoma, 90 months; chondrosarcoma, 88 months; osteosarcoma, 18 months). Adjusting for age, radiation therapy, and extent of local tumor invasion in patients with isolated (non-metastatic) spine tumors, surgical resection was independently associated with significantly improved survival for chordoma [hazard ratio (95 % confidence interval; 0.617 (0.25-0.98)], chondrosarcoma [HR (95 %CI); 0.153 (0.07-0.36)], osteosarcoma [HR (95 %CI); 0.382 (0.21-0.69)], and Ewing's sarcoma [HR (95 %CI); 0.494 (0.26-0.96)]. In our analysis of a 30-year US population-based cancer registry (SEER), patients undergoing surgical resection of primary spinal chordoma, chondrosarcoma, Ewing's sarcoma, or osteosarcoma demonstrated prolonged overall survival independent of patient age, extent of local invasion, or location. Surgical resection may play a role in prolonging survival in the multi-modality treatment of patients with these malignant primary osseous spinal neoplasms.
Read more234Evolving risk of therapy-related acute myeloid leukemia following cancer chemotherapy among adults in the United States, 1975-2008
Evolving risk of therapy-related acute myeloid leukemia following cancer chemotherapy among adults in the United States, 1975-2008
Read more1Emerging Risks of AML/MDS and Other Myeloid Neoplasms Following Chemotherapy for First Primary Malignancy, 2000-2012
Emerging Risks of AML/MDS and Other Myeloid Neoplasms Following Chemotherapy for First Primary Malignancy, 2000-2012
3Risks of therapy-related hematologic neoplasms beyond myelodysplastic syndromes and acute myeloid leukemia
Risks of therapy-related hematologic neoplasms beyond myelodysplastic syndromes and acute myeloid leukemia
27P18Ink4c and p53 Act as tumor suppressors in cyclin D1-driven primitive neuroectodermal tumor.
The retinoblastoma (RB) tumor suppressor pathway is likely important in primitive neuroectodermal tumors (PNET) of the brain. In fact, 10% to 15% of children born with RB mutations develop brain PNETs, commonly in the pineal gland. Cyclin D1, which in association with cyclin-dependent kinase (Cdk) 4 and Cdk6 phosphorylates and inactivates the RB protein, is expressed in 40% of sporadic medulloblastoma, a PNET of the cerebellum. To understand tumorigenic events cooperating with RB pathway disruption in brain PNET, we generated a transgenic mouse where cyclin D1 was expressed in pineal cells. Cyclin D1 enhanced pinealocyte proliferation, causing pineal gland enlargement. However, proliferation ceased beyond 2 weeks of age with reversal of Cdk4-mediated Rb phosphorylation despite continued expression of the transgene, and the pineal cells showed heterochromatin foci suggestive of a senescent-like state. In the absence of the p53 tumor suppressor, cell proliferation continued, resulting in pineal PNET that limited mouse survival to approximately 4 months. Interestingly, the Cdk inhibitor p18(Ink4c) was induced in the transgenic pineal glands independently of p53, and transgenic mice that lacked Ink4c developed invasive PNET, although at an older age than those lacking p53. Analogous to our mouse model, we found that children with heritable RB often had asymptomatic pineal gland enlargement that only rarely progressed to PNET. Our finding that the Cdk4 inhibitor p18(Ink4c) is a tumor suppressor in cyclin D1-driven PNET suggests that pharmacologic interventions to inhibit Cdk4 activity may be a useful chemoprevention or therapeutic strategy in cancer driven by primary RB pathway disruption.
Read more1Life years lost by childhood cancer treatment and health related late effects among childhood cancer survivors
BackgroundIdentifying risk factors contributing the most to mortality of childhood cancer survivors is essential to guide harm reduction efforts in childhood cancer treatments, and long-term follow-up of childhood cancer survivors. MethodsWe assessed Life Years Lost from childhood cancer treatments and their health-related late effects among the French Childhood Cancer Survivors Study, a cohort of 7670 5-year childhood cancer survivors. Using a landmark strategy, we also assessed time-varying effects of risk factors, and how the multi-morbidity affects life years lost. ResultsWe found subsequent malignant neoplasm (9.0 years [95 %CI: 4.3–13.7]), severe cardiac disease (8.0 years [95 %CI: 1.2–14.9]), and the use of radiotherapy (6.0 years [95 %CI: 4.7–7.3]) to be the highest contributors to Life Years Lost among childhood cancer survivors. We found no interaction impact on life years lost between health related late effects considered. ConclusionsThose findings suggest that radiotherapy is the root cause of early mortality among childhood cancer survivors. Moreover patients experiencing a subsequent malignant neoplasm or a cardiac disease should be monitored closely after the event, as comorbidity is common and causes premature deaths.
Read more151Acute nonlymphocytic leukemia and residential exposure to power frequency magnetic fields.
Recent research has suggested that nonionizing radiation in the form of power-frequency magnetic fields may play some role in carcinogenesis in general and in acute nonlymphocytic leukemia in particular. Much of the epidemiologic evidence is preliminary in nature and the methods of previous studies have been criticized. In order to further evaluate this hypothesis, a population-based case-control study of adult acute nonlymphocytic leukemia and residential exposure to power-frequency magnetic fields was carried out in western Washington state. Analyses were based on 114 cases who were newly diagnosed from 1981 to 1984 and identified from a population-based cancer registry, and 133 controls who were chosen from the study area by random digit dialing. Magnetic field exposure was estimated from external electrical wiring configurations within 140 ft (42.7 m) of each subject's residence. In addition, magnetic fields were measured inside the subject's residence at the time of interview. Neither the directly measured magnetic fields nor the surrogate values based on the wiring configurations were associated with acute nonlymphocytic leukemia.
Read more144Childhood cancers in Chennai, India, 1990–2001: Incidence and survival
Childhood cancers (age at diagnosis: 0-14 years) comprise a variety of malignancies, with incidence varying worldwide by age, sex, ethnicity and geography, that provide insights into cancer etiology. A total of 1,334 childhood cancers registered in population-based cancer registry, Chennai, India, during 1990-2001 and categorized by International Classification of Childhood Cancer norms formed the study material. Cases included for survival analysis were 1,274 (95.5%). Absolute survival was calculated by actuarial method. Cox proportional hazard model was used to elicit the prognostic factors for survival. The age-standardized rates for all childhood cancers together were 127 per million boys and 88 per million girls. A decreasing trend in incidence rates with increasing 5-year age groups was observed in both sexes. The top 5 childhood cancers were the same among boys and girls: leukemias, lymphomas, central nervous system neoplasms, retinoblastomas and renal tumors. The highest 5-year absolute survival was observed in Hodgkin's disease (65%) followed by Wilm's tumor (64%), retinoblastomas (48%), non-Hodgkin's lymphomas (47%), osteosarcomas (44%), acute lymphoid leukemia and astrocytoma (39%). Multifactorial analysis of age at diagnosis and sex showed no differences in the risk of dying for all childhood cancers. Completeness of treatment and type of hospital combination emerged as a prognostic factor for survival for all childhood cancers together (p < 0.001), acute lymphoid leukemia (p < 0.001) and non-Hodgkin's lymphoma (p = 0.04). A Childhood Cancer Registry with high-resolution data collection is advocated for in-depth analysis of variation in incidence and survival.
Read moreAbstract A19: Transformation of primary neural crest cells to model pediatric cancers
Neural crest cells (NCCs) are a multipotent, highly migratory cell population specified from the neural tube during embryonic development. NCCs undergo EMT (epithelial to mesenchymal transition) then migrate throughout the body forming diverse lineages including neurons, Schwann cells, melanocytes, and osteoblasts. Precursor cells from NCC lineages are thought to be the cell of origin for several pediatric and adult cancers including neuroblastoma, peripheral primitive neuroectodermal tumors (pPNET), malignant peripheral nerve sheath tumors (MPNST), cranial-facial osteosarcoma, and melanoma. The most common pediatric cancer in infants is neuroblastoma, which arises from the sypathoadrenal lineage of trunk NCCs. To study early events in neuroblastoma oncogenesis we established a system based on transformation of primary mouse NCCs. Trunk NCCs were isolated from day E9.5 embryos, and resulted in a population that was &gt;95% positive for the NCC markers Sox10, p75, and Ascl1 (MASH1) by immunofluorescence. Culturing primary NCCs in neurogenic differentiation media resulted in neurons positive for Tuj1, Map2, and tyrosine hydroxylase (TH). Since a prominent category of high-risk neuroblastoma involves amplification of MYCN, we next determined whether MYCN overexpression was sufficient to transform wild-type NCCs in our assay. NCCs were isolated from C57Black6 mice and infected with MYCN retrovirus within 48hr of isolation, and then 10,000 cells/mouse were injected subcutaneously. MYCN overexpression alone generated a single tumor in 1 out of 12 mice, and the resulting tumor expressed the neuronal markers synaptophysin and tyrosine hydroxylase (TH) by immunohistochemistry (IHC). To determine whether loss of p53 could increase the transformation efficiency, NCCs from p53-compromised mice were infected with MYCN. These tumors had increased penetrance with 19 out of 19 mice developing tumors whether cells were injected into nude mice or into syngeneic C57Black6 mice with an intact immune system. Based on pathological analysis, these tumors were classified as primitive neuroectodermal tumors with divergent differentiation. Tumor regions which were diffusely positive for neuronal markers appeared neuroblastoma-like or PNET-like. Osteosarcoma was also a prominent feature in tumors with loss of p53. We also observed an additional tumor type which was negative by IHC for neuronal, Schwannian, and melanoma markers, and is not yet fully characterized. In general, mice with the fastest onset of tumor growth displayed micrometastases to the lung and liver, while mice with slower tumor growth had macrometastases to these organs. Injection of cell lines derived from the primary tumors also lead to aggressive metastasis to the lung and liver. Although metastasis from subcutaneous tumors is generally rare, it was a recurrent feature in our model which recapitulates the highly metastatic nature of human cancers derived from NCCs like neuroblastoma and melanoma. Lastly, we determined whether NCCs were sensitive to the BET bromodomain inhibitor JQ1. JQ1 treatment significantly inhibited growth of both primary NCCs and cell lines derived from NCC tumors, while having minimal effect on NIH-3T3 fibroblasts. Furthermore, our results imply that JQ1 sensitivity in these cells is independent of MYCN expression levels. Using primary mouse NCCs, we found that MYCN overexpression is capable of initiating cell transformation and formed a single tumor with characteristics of neuroblastoma. Additional loss of p53 resulted in a more diverse panel of tumor types, which emphasizes the ability of NCCs to contribute to multiple lineages. Our results suggest that studies utilizing primary NCCs may be beneficial to identify initiating oncogenic events in neuroblastoma and perhaps other pediatric cancers. Citation Format: Rachelle R. Olsen, Joel H. Otero, Jesus Garcia-Lopez, Kirby A. Wallace, Zhirong Yin, Kevin W. Freeman. Transformation of primary neural crest cells to model pediatric cancers. [abstract]. In: Proceedings of the AACR Special Conference: Developmental Biology and Cancer; Nov 30-Dec 3, 2015; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Res 2016;14(4_Suppl):Abstract nr A19.
Read moreIRANCANSURV: A comprehensive analysis of childhood cancer survival in Iran.
We aimed to assess the 5-year survival probability of childhood cancer in Iran, utilizing data from eight population-based cancer registries across the country. The study employed data from 1809 childhood cancer patients aged 0-14 years, diagnosed between 2014 and 2016. Patients underwent active and passive follow-up procedures, and cases with uncertain vital status were excluded. We used the relative survival method to estimate age-standardized net survival probability for childhood cancer in Iran. The 5-year net survival for leukemia was 67.85% (95% confidence interval [CI] = 64.57, 70.90), while for central nervous system (CNS) cancers, it was 48.63% (95% CI = 43.21, 53.82). An analysis of regional disparities revealed a significant discrepancy of 14.56% in the 5-year survival of childhood leukemia, from 56.96 % in West Azerbaijan to 71.52% in Fars province. The geographical disparity in the 5-year survival of childhood CNS cancer became more pronounced, with a staggering 57.33% difference ranging from 73.50% in Khuzestan to 16.17% in Isfahan provinces. The study highlights low childhood cancer survival rates in Iran and calls for a robust surveillance system, public awareness campaigns, implementing national clinical practice guidelines, and financial support from government and NGOs to improve patient outcomes.
Read moreEndocrine Late Effects in Young Cancer Patients: Adrenal Gland
Secondary adrenal insufficiency (SAI) is a rare endocrine late effect of childhood cancer treatment and occurs by injury of the hypothalamic-pituitary (HP) axis due to CNS tumors and surgery, and particularly after cranial radiation. SAI can also occur transiently after unilateral adrenalectomy for adrenal hypercortisolism, or after chronic glucocorticoid therapy. Primary adrenal insufficiency plays no role in childhood cancer survivors and occurs as an acute consequence of cancer treatment (e.g., bilateral adrenalectomy or by inhibition of adrenal steroid biosynthesis). There are many different tests assessing the function of the HP-adrenal axis, but the optimal evaluation for ACTH deficiency is still controversial. The clinical diagnosis of SAI can be challenging due to unspecific symptoms which can develop over a long period. Thus, all childhood cancer survivors should have a regular endocrinology examination of the HPA axis. All physicians involved in the long-term follow-up of childhood cancer survivors must be aware of individuals at risk of developing HPA dysfunction. Implementation of an appropriate treatment together with a detailed instruction regarding stress dose and emergency glucocorticoid administration is necessary to prevent life-threatening adrenal crises in SAI patients.
Read more83Quality of life in long-term childhood cancer survivors and the relation of late effects and subjective well-being
The purpose of the present study was the assessment of health-related quality of life in adult long-term survivors of childhood cancer and the detection of possible treatment- and cancer-related late effects. The relation of objective medical data and subjective appraisal was also examined by combining the doctor's and the patient's views of the perceived health status. Seventy-eight young adults at the age of at least 18 years who had been diagnosed with cancer in the years 1975-1995 and were off therapy at least 5 years with no evidence of disease participated. Cancer survivors completed self-rating instruments [SF-36 Health Survey, Nottingham Health Profile (NHP), Beck's Depression Inventory (BDI), State-Trait Anxiety Inventory (STAI) trait-anxiety scale]; the doctor assessed the patient's health by means of the Common Toxicity Criteria (CTCv2). The cancer survivors showed a mostly higher-than-average positive subjective rating of the various areas of quality of life. In comparison to the general population, the cancer survivors showed lower extents of depression. In 64.1% of the cancer survivors, medical rating and self-assessment regarding the perceived health status corresponded. Cancer survivors who felt severely impaired regarding their subjectively perceived well-being showed worse results in some dimensions of quality of life than persons who subjectively felt mildly impaired. The so-called "unfortunate" persons showed the worst assessment of quality of life and the highest extent of depression and anxiety. The results of the present study may be helpful in planning an appropriate multidisciplinary, long-term follow-up of childhood cancer survivors.
Read more2Collection and Reporting of National Cancer Stage at Diagnosis Data in Australia (STaR Project)
Background: Stage at diagnosis is an important prognostic factor for cancer, providing contextual information for interpreting population health indicators such as mortality from cancer and cancer survival. Australian population-based cancer registries (PBCRs) routinely collect information on cancer incidence and mortality. The need for high quality, comprehensive national data on stage at diagnosis to supplement these data are widely recognized in Australia. The collection and dissemination of quality national stage data will enhance the: • ability to better monitor cancer outcomes, inform cancer control policy; • understand variations across different populations; and • identify where further research and targeted strategies may be required to improve cancer outcomes. Linking data on cancer stage at diagnosis with other administrative cancer data will also allow for a better understanding of the relationship between stage at diagnosis, treatments received, patterns of cancer recurrence, and survival outcomes. Aim: To strengthen national data capacity by collecting and reporting cancer stage at diagnosis for Cancer Australia's Stage, Treatment and Recurrence (STaR) project. Methods: Working with state and territory population-based cancer registries (PBCRs) and the Australian Pediatric Cancer Registry, Cancer Australia supported the development and testing of Business Rules for the collection of national cancer stage at diagnosis for: • The top 5 incident cancers based on the Tumor, Node, and Metastasis (TNM) staging system. These rules were endorsed by the Australasian Association of Cancer Registries (AACR) as a national standard in May 2016; and • Childhood cancers, with a separate set of Business Rules for 16 childhood cancer types based on the Toronto Pediatric Cancer Stage Guidelines. These rules were supported by the AACR as a national standard. Results: Using the AACR-endorsed Business Rules, comprehensive national cancer stage at diagnosis data for the top 5 incident cancers (for 2011) have been collected in Australia for the first time. Over 90% of incidence cases were able to be assigned a value for registry-derived (RD) stage at diagnosis for melanoma (97%), prostate (97%), and female breast (94%) cancers. Lower staging completeness was found for colorectal cancers (88%), and for lung cancers (72%). Business Rules for the collection of stage at diagnosis data for pediatric cancers have also been developed; 93% of sample cases diagnosed in the period 2006-2010 were able to be staged, ranging from 84% for nonrhabdomyosarcoma to 100% for hepatoblastoma. Conclusion: The Business Rules enabled the uniform collection of cancer stage at diagnosis data for the first time in Australia. The collection of these data will allow for the linkage of stage at diagnosis to other sources of information, including patterns of treatments applied, and enable reporting of survival and recurrence outcomes by stage.
Read more26Adult leukemia risk and personal appliance use: a preliminary study.
The hypothesis that use of personal electric appliances may be associated with increased risk of acute nonlymphocytic leukemia in adults was tested using interview data from a previously completed case-control study of 114 cases and 133 controls conducted between 1981 and 1984. Cases were obtained from a population-based cancer registry in western Washington state, and controls were obtained from the same area by random digit dialing. Of 32 electrical home appliances for which data on use were available for adult acute nonlymphocytic leukemia cases and controls, three motor-driven personal appliances (electric razors, hair dryers, and massage units) were selected a priori because their use represents exposure to higher peak magnetic fields than that from most other home appliances. When compared on an "ever used" versus "never used" basis, use of one or more of these appliances was not associated with increased risk of leukemia in the population studied (odds ratio (OR) = 0.71, 95% confidence interval (CI) 0.41-1.24). When the appliances were considered individually, massage units were more likely to have been used by cases than by controls (OR = 3.00, 95% CI 1.43-6.32), while hair dryers were more likely to have been used by controls than cases (OR = 0.38, 95% CI 0.22-0.66). There was a nonsignificant tendency for electric razor use to differentiate the cases from controls (OR = 1.33, 95% CI 0.80-2.23). When reported daily time of use was stratified, there was no overall increased risk with increased time of use except for electric razors (p < 0.05). In addition to the analysis of appliance use data from the case-control study, the authors obtained several models of these motor-driven personal appliances and characterized the magnetic fields they produce. Magnetic field flux density, or the B-field, and spectral measurements showed that partial body exposure from such appliances may exceed 0.5 mTesla (root mean squared) at rates-of-change exceeding 10 Tesla/sec. These epidemiologic data must be interpreted cautiously because the number of cases is limited and because of proxy reporting of appliance use for deceased cases. Nevertheless, the authors believe these data indicate that peak magnetic field exposure from personal appliances warrants further investigation as a possible risk factor for acute nonlymphocytic leukemia in adults.
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