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Journal articles on the topic 'Childhood cancers'

Author: Grafiati

Published: 18 May 2024

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1

Smith, Helin, and Bob Phillips. "Childhood Cancer." InnovAiT: Education and inspiration for general practice 5, no. 10 (September 14, 2012): 595–603. http://dx.doi.org/10.1093/innovait/ins133.

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Childhood cancers are uncommon, accounting for only 0.5% of all cancers in the UK. Approximately, 1500 children are diagnosed with cancer in the UK every year. Despite it being a rare occurrence, cancer still remains the largest cause of death in the 1–14 year age group, amongst whom it counts for 20% of all deaths. Although most adult cancers affect the lung, breast, bowel and prostate, the majority of childhood cancers are haematological and central nervous system (CNS) tumours. The primary care physician's role is vital across the disease trajectory, requiring them to recognize the signs and symptoms of childhood cancer, understand treatment, provide support to children and families, and finally consider the issues affecting survivors of childhood cancer.

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Manirakiza, A. "The Role of Childhood Cancer Civil Society on Cancer Control on Low-Income Countries." Journal of Global Oncology 4, Supplement 2 (October 1, 2018): 136s. http://dx.doi.org/10.1200/jgo.18.71600.

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Background and context: Over 250,000 new pediatric cancer cases are diagnosed yearly worldwide. In the developing countries, the childhood cancer burden is estimated to increase even more. Rwanda Children's Cancer Relief (RCCR) is a nonprofit organization with a mission to ensure that children with cancers access high standards of treatment and support. After realizing that majority in our community lack information on childhood cancers, our efforts since 2014 has been concentrated on raising awareness of childhood cancers. Aim: Raise awareness on childhood cancer among community members. Strategy/Tactics: During a massive walk, trained volunteers with informative brochures, posters in both local and international languages comprising information on early symptoms of childhood cancers, ways to navigate referral system among others are used during community outreaches. These activities are aired on national radios and TVs, newspapers and social media are also used to spread information. Program/Policy process: Many activities are carried out in September during the RCCR Annual Childhood Cancers Awareness Month. We involve community health workers, private sectors and academic institutions. We focus on talks, community outreaches and childhood cancers awareness activities. Outcomes: 2017 campaign included the aforementioned activities and was concluded by a walk dubbed (#KidsCancerWalk2016) which attracted more than 600 participants. Two local TVs, 6 radios and 7 online diaries covered the campaign in its different phases. More than 1000 posters, 1100 brochures and 500 flyers were distributed followed by intensive online campaign with more than 100 Facebook posts, 350 Tweets, and 700 Retweets. Strong partnerships with private, public sectors were created and Ministry of Health approved September as the national childhood cancer awareness month following RCCR campaigns. What was learned: Childhood cancers are fatal when left untreated but treatable when they are detected at an early stage. Activities that RCCR carry out on annual basis increase the general population knowledge about childhood cancers. Civil societies like RCCR play a crucial role in addressing the growing burden of childhood cancers and the disparities in access to and quality of care. They can also influence policy changes and address the specific patients' and community needs.

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3

Brooks, G. A., J. E. Stopfer, J. Erlichman, R. Davidson, K. L. Nathanson, and S. M. Domchek. "Childhood cancer in families with and without germline BRCA1/2 mutations ascertained at a high-risk breast cancer clinic." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 10013. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.10013.

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10013 Background: Germline mutations in the BRCA1 and BRCA2 genes (BRCA1/2) are associated with breast cancer, ovarian cancer and other malignancies. Biallelic mutations of BRCA2 are a cause of Fanconi anemia and characteristic childhood cancers. We undertook this study to evaluate the contribution of familial heterozygous BRCA1/2 mutations to childhood cancer in hereditary breast cancer families. Methods: We conducted a retrospective cohort study to compare the prevalence of childhood cancers among 379 families with BRCA1/2 mutations and 426 families without known mutations. All families were ascertained at a high-risk breast cancer clinic. Our study and comparison cohorts included first- through fourth-degree relatives of cancer-affected mutation carriers and cancer-affected individuals with negative full sequencing for BRCA1/2 mutations. The primary endpoint was any case of childhood cancer (diagnosed <age 21) as recorded in the family history. Results were analyzed using Fisher’s exact test. Results: 20 cases of childhood cancer were observed in 379 families with BRCA1/2 mutations and 35 cases of childhood cancer were observed in 426 families with negative mutation testing (p = 0.12). Apart from two very early-onset breast cancers, the types of childhood cancers occurring in the BRCA1/2 mutation positive families were similar to those occurring in the mutation negative families and in the general population. Nine childhood cancers occurred in 240 families with BRCA1 mutations, and 11 childhood cancers occurred in 141 families with BRCA2 mutations (p=0.1). 13 of 18 BRCA1/2 mutation positive families with cases of childhood cancer (72%) and 13 of 31 families with childhood cancer cases and negative mutation testing (42%) met the Birch clinical criteria for Li-Fraumeni like syndrome (LFL); no individual has undergone testing for germline TP53 mutations. Conclusions: Heterozygous BRCA1/2 mutations do not appear to be a significant risk factor for childhood cancer in hereditary breast cancer families. This observation supports the current practice of delaying BRCA1/2 mutation testing until candidates reach adulthood. Although many families in both groups met criteria for LFL, the clinical significance of this finding is uncertain. No significant financial relationships to disclose.

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Cole, Catherine. "Registering childhood cancers." Lancet 364, no. 9451 (December 2004): 2074–76. http://dx.doi.org/10.1016/s0140-6736(04)17561-2.

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Herzog, Cynthia E., Richard J. Andrassy, and Farzin Eftekhari. "Childhood Cancers: Hepatoblastoma." Oncologist 5, no. 6 (December 2000): 445–53. http://dx.doi.org/10.1634/theoncologist.5-6-445.

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6

Houghton, Peter J. "Developing novel treatments for childhood solid cancers." Open Access Government 39, no. 1 (July 10, 2023): 112–13. http://dx.doi.org/10.56367/oag-039-10780.

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Developing novel treatments for childhood solid cancers With a particular focus on glioma, Dr Peter J Houghton from Greehey Children’s Cancer Research Institute outlines the barriers that have hindered the development of effective therapies for childhood solid cancers. Childhood cancer represents less than 1% of human cancers, thus, is not a priority for drug development in the pharmaceutical industry. However, the consequences of having a child diagnosed with a malignant disease can be devastating for families. Developing new therapies for childhood solid cancers presents certain constraints that are seldom encountered with neoplastic diseases diagnosed in adults. Childhood tumours are rare, which has therefore restricted large-scale drug evaluations or randomised clinical trials. For example, of the new Phase I agents evaluated in adult malignancies, less than 30% receive an adequate assessment in children.

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Robison, L. L. "Second primary cancers after childhood cancer." BMJ 312, no. 7035 (April 6, 1996): 861–62. http://dx.doi.org/10.1136/bmj.312.7035.861.

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Houghton, Peter J. "Developing novel therapies for childhood cancers." Open Access Government 40, no. 1 (October 25, 2023): 154–55. http://dx.doi.org/10.56367/oag-040-10780.

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Developing novel therapies for childhood cancers Dr Peter J Houghton from Greehey Children’s Cancer Research Institute discusses the obstacles in developing new treatments for childhood cancers and new approaches in preclinical testing. In my previous article for Open Access Government, I focused on the challenges of developing novel therapies for children with glioma, the most prevalent brain cancer in children. Here, I want to discuss the challenges at the preclinical stage of drug development, an area of research that will be altered significantly by the Research to Accelerate Cures and Equity for Children Act (RACE for Children Act). This U.S. law requires the Food and Drug Agency (FDA) to develop a list of molecular targets and molecular targets of new drugs and biologics in development that are determined to be relevant to pediatric cancers. The objective is to facilitate a more rapid introduction of new drugs into the pediatric cancer armamentarium. The FDA may now require pediatric assessments when molecular targets under FDA review are considered relevant to childhood cancer.

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MacDonald, Tamara. "Pediatric Cancer: A Comprehensive Review. Part I: Biology, Epidemiology, Common Tumours, Principles of Treatment and Late Effects." Canadian Pharmacists Journal / Revue des Pharmaciens du Canada 143, no. 4 (July 2010): 176–83. http://dx.doi.org/10.3821/1913-701x-143.4.176.

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The incidence rates of pediatric cancer, like adult cancer, are increasing, though to a lesser degree. Options for the treatment of childhood cancers are continually changing and improving and overall survival has increased dramatically over the last 60 years. This paper discusses the incidence and survival trends of childhood cancer. The biology and epidemiology of the most common cancers seen in children and the late effects of treatment for childhood cancer will also be discussed. A basic understanding of childhood cancer is important for both hospital and community pharmacists, since many young adults in North America are now survivors of childhood cancer and may experience long-term consequences of chemotherapy.

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Smith, Malcolm A., Nita L. Seibel, Sean F. Altekruse, Lynn A. G. Ries, Danielle L. Melbert, Maura O'Leary, Franklin O. Smith, and Gregory H. Reaman. "Outcomes for Children and Adolescents With Cancer: Challenges for the Twenty-First Century." Journal of Clinical Oncology 28, no. 15 (May 20, 2010): 2625–34. http://dx.doi.org/10.1200/jco.2009.27.0421.

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Purpose This report provides an overview of current childhood cancer statistics to facilitate analysis of the impact of past research discoveries on outcome and provide essential information for prioritizing future research directions. Methods Incidence and survival data for childhood cancers came from the Surveillance, Epidemiology, and End Results 9 (SEER 9) registries, and mortality data were based on deaths in the United States that were reported by states to the Centers for Disease Control and Prevention by underlying cause. Results Childhood cancer incidence rates increased significantly from 1975 through 2006, with increasing rates for acute lymphoblastic leukemia being most notable. Childhood cancer mortality rates declined by more than 50% between 1975 and 2006. For leukemias and lymphomas, significantly decreasing mortality rates were observed throughout the 32-year period, though the rate of decline slowed somewhat after 1998. For remaining childhood cancers, significantly decreasing mortality rates were observed from 1975 to 1996, with stable rates from 1996 through 2006. Increased survival rates were observed for all categories of childhood cancers studied, with the extent and temporal pace of the increases varying by diagnosis. Conclusion When 1975 age-specific death rates for children are used as a baseline, approximately 38,000 childhood malignant cancer deaths were averted in the United States from 1975 through 2006 as a result of more effective treatments identified and applied during this period. Continued success in reducing childhood cancer mortality will require new treatment paradigms building on an increased understanding of the molecular processes that promote growth and survival of specific childhood cancers.

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McNally, Richard JQ. "The Epidemiology of Childhood Cancers." European Oncology & Haematology 05, no. 01 (2009): 79. http://dx.doi.org/10.17925/eoh.2009.05.1.79.

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In this article, the recent epidemiological literature on childhood cancer is reviewed. This includes findings from descriptive, case-control and cohort studies. The aetiology of most childhood cancers is unclear. Both genetic and environmental factors are likely to contribute. Increasing incidence, findings of clustering and seasonality in the incidence of certain cancers support a role for environmental agents in aetiology. The evidence concerning putative risk factors is considered and suggests that the aetiology is likely to be multifactorial and involve a number of different agents. These include infections, ionising radiation, certain chemical exposures, parental smoking, parental alcohol consumption and hair dyes. Conversely, breastfeeding and certain dietary supplements may convey protection. Recent findings regarding electromagnetic fields suggest that this factor is not likely to have a major role in aetiology.

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Coorens, Tim H. H., and Sam Behjati. "Tracing and Targeting the Origins of Childhood Cancer." Annual Review of Cancer Biology 6, no. 1 (April 11, 2022): 35–47. http://dx.doi.org/10.1146/annurev-cancerbio-070620-091632.

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Despite the success of treating childhood cancers with cytotoxic agents, novel therapeutic strategies are required to achieve the next leap in cure rates. A promising avenue may be to target the origin of childhood cancers. Here, we review recent advances in tracing the origins of pediatric tumors. Cancer-to-normal cell comparisons by single-cell mRNA sequencing reveal the fetal state of cancer cells, as well as their cell of origin. Recent phylogenetic analyses have uncovered large tissue-resident precursor clones to childhood cancers, which already possess key genomic alterations leading to tumor formation. Both the transcriptional fetalness and genomic status of the premalignant tissue bed provide further avenues for targeted therapy. Overall, these advances begin to describe the precise origins of pediatric tumors and pave the way for novel methods in detecting, treating, and perhaps even preventing childhood cancers.

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T, Yasmin. "Physician Delay for Delayed Diagnosis of Acute Lymphoblastic Leukemia among Children in a Tertiary Care Hospital." Cytokines Their Relation with Mineral Dust Induced Diseases 4, no. 1 (July 28, 2020): 1–5. http://dx.doi.org/10.24966/ppp-5649/100018.

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Early diagnosis of cancer gives an opportunity for early treatment which is very important. Unfortunately, late presentation and delayed diagnosis of childhood cancers remain a problem in developing countries including Bangladesh. Few studies on delayed diagnosis of childhood cancers have been conducted in Bangladesh.

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Berendsen, A. J., A. Groot Nibbelink, R. Blaauwbroek, M. Y. Berger, and W. J. E. Tissing. "Second cancers after childhood cancer – GPs beware!" Scandinavian Journal of Primary Health Care 31, no. 3 (August 2, 2013): 147–52. http://dx.doi.org/10.3109/02813432.2013.824152.

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Bhatia, Smita, and Charles Sklar. "Second cancers in survivors of childhood cancer." Nature Reviews Cancer 2, no. 2 (February 2002): 124–32. http://dx.doi.org/10.1038/nrc722.

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Daniels, J. L., A. F. Olshan, and D. A. Savitz. "Pesticides and childhood cancers." Environmental Health Perspectives 105, no. 10 (October 1997): 1068–77. http://dx.doi.org/10.1289/ehp.971051068.

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Parker, Karen, and Mellisa A. Hall. "Childhood Cancers: Diagnostic Considerations." Journal for Nurse Practitioners 13, no. 8 (September 2017): e401-e402. http://dx.doi.org/10.1016/j.nurpra.2017.05.017.

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18

Cartwright, RA, JCH Miles, and GM Kendall. "Childhood cancers and radon." Lancet 361, no. 9369 (May 2003): 1658. http://dx.doi.org/10.1016/s0140-6736(03)13289-8.

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Parker, L., and A. W. Craft. "Radon and childhood cancers." European Journal of Cancer 32, no. 2 (February 1996): 201–4. http://dx.doi.org/10.1016/0959-8049(96)00021-4.

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20

Printz, Carrie. "Advances in childhood cancers." Cancer 118, no. 19 (September 19, 2012): 4639–40. http://dx.doi.org/10.1002/cncr.27827.

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Suzuki, Keiji, Vladimir Saenko, Shunichi Yamashita, and Norisato Mitsutake. "Radiation-Induced Thyroid Cancers: Overview of Molecular Signatures." Cancers 11, no. 9 (September 2, 2019): 1290. http://dx.doi.org/10.3390/cancers11091290.

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Enormous amounts of childhood thyroid cancers, mostly childhood papillary thyroid carcinomas (PTCs), after the Chernobyl nuclear power plant accident have revealed a mutual relationship between the radiation exposure and thyroid cancer development. While the internal exposure to radioactive 131I is involved in the childhood thyroid cancers after the Chernobyl accident, people exposed to the external radiation, such as atomic-bomb (A-bomb) survivors, and the patients who received radiation therapy, have also been epidemiologically demonstrated to develop thyroid cancers. In order to elucidate the mechanisms of radiation-induced carcinogenesis, studies have aimed at defining the molecular changes associated with the thyroid cancer development. Here, we overview the literatures towards the identification of oncogenic alterations, particularly gene rearrangements, and discuss the existence of radiation signatures associated with radiation-induced thyroid cancers.

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Ricci, Angela M., Rebecca T. Emeny, Pamela J. Bagley, Heather B. Blunt, Mary E. Butow, Alexandra Morgan, Jennifer A. Alford-Teaster, Linda Titus, Raymond R. Walston, and Judy R. Rees. "Causes of Childhood Cancer: A Review of the Recent Literature: Part I—Childhood Factors." Cancers 16, no. 7 (March 27, 2024): 1297. http://dx.doi.org/10.3390/cancers16071297.

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Purpose: To review the childhood risk factors for pediatric cancer (diagnosis before age 20). Methods: We conducted literature searches using Ovid Medline and Scopus to find primary research studies, review articles, and meta-analyses published from 2014 to 3 March 2021. Results: Strong evidence indicates that an array of genetic and epigenetic phenomena, structural birth defects, and chromosomal anomalies are associated with an increased risk of various childhood cancers. Increased risk is also associated with prior cancer, likely due to previous treatment agents and therapeutic ionizing radiation. Convincing evidence supports associations between several pediatric cancers and ionizing radiation, immunosuppression, and carcinogenic virus infection both in healthy children and in association with immune suppression following organ transplantation. Breastfeeding and a childhood diet rich in fruits and vegetables appears to reduce the risk of pediatric leukemia but the evidence is less strong. Childhood vaccination against carcinogenic viruses is associated with a lower risk of several cancers; there is less strong evidence that other childhood vaccinations more broadly may also lower risk. Ultraviolet (UV) radiation is associated with increased melanoma risk, although most melanomas following childhood UV exposure occur later, in adulthood. Evidence is weak or conflicting for the role of body mass index, other childhood infections, allergies, and certain treatments, including immunomodulator medications and human growth therapy.

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Teepen, Jop C., Flora E. van Leeuwen, Wim J. Tissing, Eline van Dulmen-den Broeder, Marry M. van den Heuvel-Eibrink, Helena J. van der Pal, Jacqueline J. Loonen, et al. "Long-Term Risk of Subsequent Malignant Neoplasms After Treatment of Childhood Cancer in the DCOG LATER Study Cohort: Role of Chemotherapy." Journal of Clinical Oncology 35, no. 20 (July 10, 2017): 2288–98. http://dx.doi.org/10.1200/jco.2016.71.6902.

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Purpose Childhood cancer survivors (CCSs) are at increased risk for subsequent malignant neoplasms (SMNs). We evaluated the long-term risk of SMNs in a well-characterized cohort of 5-year CCSs, with a particular focus on individual chemotherapeutic agents and solid cancer risk. Methods The Dutch Childhood Cancer Oncology Group–Long-Term Effects After Childhood Cancer cohort includes 6,165 5-year CCSs diagnosed between 1963 and 2001 in the Netherlands. SMNs were identified by linkages with the Netherlands Cancer Registry, the Dutch Pathology Registry, and medical chart review. We calculated standardized incidence ratios, excess absolute risks, and cumulative incidences. Multivariable Cox proportional hazard regression analyses were used to evaluate treatment-associated risks for breast cancer, sarcoma, and all solid cancers. Results After a median follow-up of 20.7 years (range, 5.0 to 49.8 years) since first diagnosis, 291 SMNs were ascertained in 261 CCSs (standardized incidence ratio, 5.2; 95% CI, 4.6 to 5.8; excess absolute risk, 20.3/10,000 person-years). Cumulative SMN incidence at 25 years after first diagnosis was 3.9% (95% CI, 3.4% to 4.6%) and did not change noticeably among CCSs treated in the 1990s compared with those treated earlier. We found dose-dependent doxorubicin-related increased risks of all solid cancers ( Ptrend < .001) and breast cancer ( Ptrend < .001). The doxorubicin-breast cancer dose response was stronger in survivors of Li-Fraumeni syndrome–associated childhood cancers (leukemia, CNS, and non-Ewing sarcoma) versus survivors of other cancers ( Pdifference = .008). In addition, cyclophosphamide was found to increase sarcoma risk in a dose-dependent manner ( Ptrend = .01). Conclusion The results strongly suggest that doxorubicin exposure in CCSs increases the risk of subsequent solid cancers and breast cancer, whereas cyclophosphamide exposure increases the risk of subsequent sarcomas. These results may inform future childhood cancer treatment protocols and SMN surveillance guidelines for CCSs.

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Yu, Chu-Ling, Emily S. Tonorezos, Chiung-Yu Huang, Brian C.-H. Chiu, Chun-Ju Chiang, Hui-Ju Ch'ang, Yen-Lin Liu, James S. Miser, Hung-Yi Chiou, and Yun Yen. "Second malignant neoplasms in a nationwide population-based cohort of childhood cancer survivors in Taiwan." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): 10569. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.10569.

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10569 Background: Childhood cancer survivors have excess risk of second malignant neoplasms, but data are limited in Asian populations. We established a nationwide retrospective cohort of childhood cancer survivors in Taiwan to study the risk of second malignant neoplasms in the population. Methods: Children and adolescents diagnosed with cancer before age 21 years between 1990 and 2011 were identified from the Taiwan Cancer Registry, the national cancer registry in Taiwan. One-year survivors of childhood cancer were ascertained through data linkage with the national death registry. Survivors were followed up through December 2012. Standardized incidence ratios (SIRs), absolute excess risks (AERs), and cumulative incidence of second malignant neoplasms were calculated. Results: A total of 186 second malignant neoplasms occurred among 15,263 1-year survivors of childhood cancer after a mean follow-up time of 8.0 years (SIR = 5.4, 95% confidence interval [CI] = 4.6-6.2; AER = 12.4 per 10,000 person-years). The most common types of second malignant neoplasms were gastrointestinal cancers (n = 37), leukemia (n = 28), endocrine cancers (n = 18), and brain cancer (n = 17). Cancers in the liver (n = 11, including 9 hepatocellular carcinoma) and colorectum (n = 16) accounted for 73% of second gastrointestinal malignant neoplasms in this population. The cumulative incidence of second malignant neoplasms at 10 and 20 years from follow-up was 1.0% (95% CI = 0.8-1.2%) and 3.0% (95% CI = 2.3-3.6%), respectively. Conclusions: Childhood cancer survivors in Taiwan experience excess risk of second malignant neoplasms, in particular gastrointestinal cancers, compared with the general population.

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Galinski, Basia, Thomas B. Alexander, Daniel A. Mitchell, Hannah V. Chatwin, Chidiebere Awah, Adam L. Green, and Daniel A. Weiser. "Therapeutic Targeting of Exportin-1 in Childhood Cancer." Cancers 13, no. 24 (December 7, 2021): 6161. http://dx.doi.org/10.3390/cancers13246161.

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Overexpression of Exportin-1 (XPO1), a key regulator of nuclear-to-cytoplasmic transport, is associated with inferior patient outcomes across a range of adult malignancies. Targeting XPO1 with selinexor has demonstrated promising results in clinical trials, leading to FDA approval of its use for multiple relapsed/refractory cancers. However, XPO1 biology and selinexor sensitivity in childhood cancer is only recently being explored. In this review, we will focus on the differential biology of childhood and adult cancers as it relates to XPO1 and key cargo proteins. We will further explore the current state of pre-clinical and clinical development of XPO1 inhibitors in childhood cancers. Finally, we will outline potentially promising future therapeutic strategies for, as well as potential challenges to, integrating XPO1 inhibition to improve outcomes for children with cancer.

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Mastrangelo, Stefano. "Special Issue: Childhood Brain Cancer Treatment." Cancers 15, no. 21 (November 3, 2023): 5278. http://dx.doi.org/10.3390/cancers15215278.

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Bashar, Md Abu, and Nazia Begam. "Trend of Childhood cancers in India: A review of Population based cancer registries data on Childhood cancers." European Journal of Cancer Prevention 31, Supplement 1 (December 2021): S7—S8. http://dx.doi.org/10.1097/01.cej.0000816672.18030.22.

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Bithell, JF, GJ Draper, T. Sorahan, and CA Stiller. "Childhood cancer research in Oxford I: the Oxford Survey of Childhood Cancers." British Journal of Cancer 119, no. 6 (August 21, 2018): 756–62. http://dx.doi.org/10.1038/s41416-018-0180-0.

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Spiotto, Michael T., Susan L. McGovern, G. Brandon Gunn, David Grosshans, Mary Frances McAleer, Steven J. Frank, and Arnold C. Paulino. "Proton Radiotherapy to Reduce Late Complications in Childhood Head and Neck Cancers." International Journal of Particle Therapy 8, no. 1 (June 1, 2021): 155–67. http://dx.doi.org/10.14338/ijpt-20-00069.1.

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Abstract In most childhood head and neck cancers, radiotherapy is an essential component of treatment; however, it can be associated with problematic long-term complications. Proton beam therapy is accepted as a preferred radiation modality in pediatric cancers to minimize the late radiation side effects. Given that childhood cancers are a rare and heterogeneous disease, the support for proton therapy comes from risk modeling and a limited number of cohort series. Here, we discuss the role of proton radiotherapy in pediatric head and neck cancers with a focus on reducing radiation toxicities. First, we compare the efficacy and expected toxicities in proton and photon radiotherapy for childhood cancers. Second, we review the benefit of proton radiotherapy in reducing acute and late radiation toxicities, including risks for secondary cancers, craniofacial development, vision, and cognition. Finally, we review the cost effectiveness for proton radiotherapy in pediatric head and neck cancers. This review highlights the benefits of particle radiotherapy for pediatric head and neck cancers to improve the quality of life in cancer survivors, to reduce radiation morbidities, and to maximize efficient health care use.

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Segbefia, C. I., L. A. Renner, Y. Dei-Adomakoh, and J. Welbeck. "Changing Pattern of Childhood Cancers at Korle Bu Teaching Hospital, Accra, Ghana." Postgraduate Medical Journal of Ghana 2, no. 2 (July 12, 2022): 65–67. http://dx.doi.org/10.60014/pmjg.v2i2.35.

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Background: Worldwide, the incidence of childhood cancers is increasing and majority of children with cancers live in developing countries. The main aim of the study was to determine the current pattern of childhood malignancies at Korle Bu Teaching Hospital(KBTH), Accra.Methods: A retrospective review of registry data from the KBTH paediatric oncology unit between January 1, 2008 and December 31, 2011 was conducted, and results analysed.Results: Out of 495 new cases of cancer, lymphomas (30.7%), leukaemias (18.8%) and retinoblastomas (15.8%) were the commonest cancers diagnosed. CNS tumours were rare (3.4%). Overall, the male: female ratio was 1.3:1. Most patients (232/495; 47%) were inthe 5-10 year age group and majority of embryonal tumours were diagnosed in the 0-4 year age group. The peak ages for Burkitt’s lymphoma and acute lymphoblastic leukaemia were similar, in contrast to reports from developed countries.Conclusion: The number of children diagnosed with cancers at KBTH has increased significantly. Concerted efforts and advocacy towards improving childhood cancer care are required.

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Eastman, Peggy. "Cancer Genome Project hones in on childhood cancers." Oncology Times UK 7, no. 3 (March 2010): 15. http://dx.doi.org/10.1097/01.otu.0000398559.53171.49.

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Oeffinger, Kevin C., and Smita Bhatia. "Second primary cancers in survivors of childhood cancer." Lancet 374, no. 9700 (October 2009): 1484–85. http://dx.doi.org/10.1016/s0140-6736(09)61885-7.

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Knapke, Sara, Kristin Zelley, Kim E. Nichols, Wendy Kohlmann, and Joshua D. Schiffman. "Identification, Management, and Evaluation of Children with Cancer-Predisposition Syndromes." American Society of Clinical Oncology Educational Book, no. 32 (June 2012): 576–84. http://dx.doi.org/10.14694/edbook_am.2012.32.8.

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Overview: A substantial proportion of childhood cancers are attributable to an underlying genetic syndrome or inherited susceptibility. Recognition of affected children allows for appropriate cancer risk assessment, genetic counseling, and testing. Identification of individuals who are at increased risk to develop cancers during childhood can guide cancer surveillance and clinical management, which may improve outcomes for both the patient and other at-risk relatives. The information provided through this article will focus on the current complexities involved in the evaluation and management of children with cancer-predisposing genetic conditions and highlight remaining questions for discussion.

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Ayhan, Ali, Mehmet Coskun Salman, Husnu Celik, Polat Dursun, Ozgur Ozyuncu, and Murat Gultekin. "Association between fertility drugs and gynecologic cancers, breast cancer, and childhood cancers." Acta Obstetricia et Gynecologica Scandinavica 83, no. 12 (November 16, 2004): 1104–11. http://dx.doi.org/10.1111/j.0001-6349.2004.00669.x.

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Norman, Rosana E. "Environmental Contributions to Childhood Cancers." Journal of Enviromental Immunology and Toxicology 2, no. 2 (2014): 86. http://dx.doi.org/10.7178/jeit.17.

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Muslu, Leyla, and Rahşan Kolutek. "Childhood Cancers and Health Literacy." Güncel Pediatri 16, no. 3 (December 1, 2018): 117–32. http://dx.doi.org/10.4274/jcp.2018.0049.

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Kerim, Yasser Abdel. "AKT question on childhood cancers." InnovAiT: Education and inspiration for general practice 10, no. 4 (March 21, 2017): e49-e49. http://dx.doi.org/10.1177/1755738017691912.

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Knox, E. G. "Roads, railways, and childhood cancers." Journal of Epidemiology & Community Health 60, no. 2 (February 1, 2006): 136–41. http://dx.doi.org/10.1136/jech.2005.042036.

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Josephson, Maureen B., and Samuel Brian Goldfarb. "Pulmonary complications of childhood cancers." Expert Review of Respiratory Medicine 8, no. 5 (May 28, 2014): 561–71. http://dx.doi.org/10.1586/17476348.2014.923311.

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Knox, E. G. "Childhood cancers and atmospheric carcinogens." Journal of Epidemiology & Community Health 59, no. 2 (February 1, 2005): 101–5. http://dx.doi.org/10.1136/jech.2004.021675.

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Knox, E. G. "Oil combustion and childhood cancers." Journal of Epidemiology & Community Health 59, no. 9 (September 1, 2005): 755–60. http://dx.doi.org/10.1136/jech.2004.031674.

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Lerner, Barron H. "Curing formerly fatal childhood cancers." Lancet 371, no. 9625 (May 2008): 1655–56. http://dx.doi.org/10.1016/s0140-6736(08)60711-4.

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Poole, C., and D. Ozonoff. "Magnetic fields and childhood cancers." IEEE Engineering in Medicine and Biology Magazine 15, no. 4 (1996): 41–49. http://dx.doi.org/10.1109/51.511981.

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Balis, Frank M. "Clinical Trials in Childhood Cancers." Oncologist 5, no. 3 (June 2000): 2–3. http://dx.doi.org/10.1634/theoncologist.5-3-2.

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Stone, William L. "Childhood cancers and systems medicine." Frontiers in Bioscience 22, no. 7 (2017): 1148–61. http://dx.doi.org/10.2741/4538.

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Knox, E. G., A. M. Stewart, E. A. Gilman, and G. W. Kneale. "Background radiation and childhood cancers." Journal of Radiological Protection 8, no. 1 (March 1, 1988): 9–18. http://dx.doi.org/10.1088/0952-4746/8/1/302.

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Kuehn, Bridget. "Global Effect of Childhood Cancers." JAMA 322, no. 11 (September 17, 2019): 1035. http://dx.doi.org/10.1001/jama.2019.13826.

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Omobuwa, O., RO Akande, CA Akinleye, SO Olarewaju, IO Faramade, O. Opakunle, SC Adeyemo, E. Asekun-Olarinmoye, G. Omisore, and OF Ariyo. "Knowledge of Childhood Cancer Case Detection among Primary Health Care Workers in Osun State." Journal of Community Medicine and Primary Health Care 35, no. 3 (December 13, 2023): 15–26. http://dx.doi.org/10.4314/jcmphc.v35i3.2.

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Abstract:

Background: Survival rates of childhood cancer in Nigeria is low because suspected cases of childhood cancer are usually diagnosed at an advanced stage. It is hoped that assessing the knowledge gaps in the identification of warning signs and symptoms of childhood cancer among healthcare workers in primaryhealthcare facilities would lead to an improvement in early diagnosis, detection, and referral, which will subsequently reduce mortality from childhood cancer.Objective: To assess the knowledge of childhood cancer case detection among primary health care workers in Osun state.Materials and Methods: A descriptive cross-sectional study was carried out among 210 primary health care workers recruited by multistage sampling technique. Data was collected using a pretested semi-structured questionnaire. Analysis was done using SPSS software version 23.0 and level of significance set at p<0.05.Results: About 55.7% and 44.3% of the respondents had good and poor knowledge of childhood cancer respectively. There was a statistically significant association between respondents’ knowledge, their marital status (p=0.00) and years of experience with case detection practices of childhood cancers (p=0.006). Married respondents were 6 times less likely to have poor knowledge (OR 0.398, 95% CI 0.213 - 0.745, p=0.004). Also, those with 6-10 years of experience were 7 times less likely to have poor knowledge (OR 0.349, 95% CI 0.13 - 0.939, p=0.037)Conclusion: Respondents had good level of knowledge on detection of childhood cancer however, there is a need for continuous training to further build their capacities on detection of signs and symptoms of childhood cancers

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Gröbner, Susanne N., Barbara C. Worst, Joachim Weischenfeldt, Ivo Buchhalter, Kortine Kleinheinz, Vasilisa A. Rudneva, Pascal D. Johann, et al. "The landscape of genomic alterations across childhood cancers." Nature 555, no. 7696 (February 28, 2018): 321–27. http://dx.doi.org/10.1038/nature25480.

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Abstract Pan-cancer analyses that examine commonalities and differences among various cancer types have emerged as a powerful way to obtain novel insights into cancer biology. Here we present a comprehensive analysis of genetic alterations in a pan-cancer cohort including 961 tumours from children, adolescents, and young adults, comprising 24 distinct molecular types of cancer. Using a standardized workflow, we identified marked differences in terms of mutation frequency and significantly mutated genes in comparison to previously analysed adult cancers. Genetic alterations in 149 putative cancer driver genes separate the tumours into two classes: small mutation and structural/copy-number variant (correlating with germline variants). Structural variants, hyperdiploidy, and chromothripsis are linked to TP53 mutation status and mutational signatures. Our data suggest that 7–8% of the children in this cohort carry an unambiguous predisposing germline variant and that nearly 50% of paediatric neoplasms harbour a potentially druggable event, which is highly relevant for the design of future clinical trials.

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Rahesh, Jasmin, Shazma Khan, Arham Siddiqui, and Roy Jacob. "Second primary cancer in the brain: a longitudinal case study from childhood into adulthood." Southwest Respiratory and Critical Care Chronicles 10, no. 45 (October 21, 2022): 63–66. http://dx.doi.org/10.12746/swrccc.v10i45.1065.

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Second cancers occur after the remission of a previous cancer in patients. Due to the increased successful treatment of childhood cancers, these second cancers are more likely to occur for these patients, later in life. Risk factors and causes for these second cancers include predisposing genetic factors, exposure to radiation and chemotherapy from initial cancer treatment, and environmental conditions. The most likely the reason second cancers occur is multifactorial and involves an interaction of both environmental and genetic factors. We present a longitudinal case study following a patient who was treated for an ependymoma at age three and twenty-two years later presenting with symptoms indicative of another cancer, at age 25.

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