Publications by authors named "Daniel A Weiser"

18 Publications

  • Page 1 of 1

XPO1 inhibition with selinexor synergizes with proteasome inhibition in neuroblastoma by targeting nuclear export of IkB.

Transl Oncol 2021 May 8;14(8):101114. Epub 2021 May 8.

Department of Genetics, Albert Einstein College of Medicine, 1300 Morris Park Avenue Ullmann 813 Bronx, NY 10461, United States; Department of Pediatrics, Albert Einstein College of Medicine, United States.

Across many cancer types in adults, upregulation of the nuclear-to-cytoplasmic transport protein Exportin-1 (XPO1) correlates with poor outcome and responsiveness to selinexor, an FDA-approved XPO1 inhibitor. Similar data are emerging in childhood cancers, for which selinexor is being evaluated in early phase clinical studies. Using proteomic profiling of primary tumor material from patients with high-risk neuroblastoma, as well as gene expression profiling from independent cohorts, we have demonstrated that XPO1 overexpression correlates with poor patient prognosis. Neuroblastoma cell lines are also sensitive to selinexor in the low nanomolar range. Based on these findings and knowledge that bortezomib, a proteasome inhibitor, blocks degradation of XPO1 cargo proteins, we hypothesized that combination treatment with selinexor and bortezomib would synergistically inhibit neuroblastoma cellular proliferation. We observed that selinexor promoted nuclear retention of IkB and that bortezomib augmented the ability of selinexor to induce cell-cycle arrest and cell death by apoptosis. This synergy was abrogated through siRNA knockdown of IkB. The synergistic effect of combining selinexor and bortezomib in vitro provides rationale for further investigation of this combination treatment for patients with high-risk neuroblastoma.
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http://dx.doi.org/10.1016/j.tranon.2021.101114DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8131731PMC
May 2021

50 Years Ago in TheJournalofPediatrics: Measurement of Urinary Catecholamine Excretion in Patients with Neuroblastoma.

J Pediatr 2021 04;231:222

Division of Pediatric Hematology, Oncology, and Cellular Therapy, Children's Hospital at Montefiore, Albert Einstein College of Medicine, Bronx, New York.

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http://dx.doi.org/10.1016/j.jpeds.2020.11.029DOI Listing
April 2021

Survey of Paediatric Oncologists and Pathologists regarding Their Views and Experiences with Variant Translocations in Ewing and Ewing-Like Sarcoma: A Report of the Children's Oncology Group.

Sarcoma 2020 5;2020:3498549. Epub 2020 Dec 5.

Division of Oncology, Children's Hospital of Philadelphia, Philadelphia, PA, USA.

Advances in molecular diagnostics have identified subsets of Ewing and Ewing-like sarcomas driven by variant translocations with unique biology. It is likely that patients with these tumours will have different clinical features and therapeutic outcomes. Nevertheless, the management of these patients both locally and within cooperative group trials depends on the local pathological diagnosis. It is not known what molecular diagnostic approaches are employed by local pathologists or if the exact translocation is commonly determined. In addition, it is not known what therapeutic approaches are employed for these patients or what cooperative trials are deemed appropriate for these patients by expert consensus. To answer these questions, we performed an international survey of oncologists and pathologists to better understand the diagnostic approaches used to identify variant translocations and the influence the findings have on therapy and clinical trial eligibility. An online survey was distributed to oncologists and pathologists primarily in North America. A total of 141 surveys were completed, representing a 28% response rate. The majority of respondents considered EWSR1-ETS gene family translocations (range 61-96%) to be Ewing sarcoma and would include them on the primary arm of a Ewing sarcoma clinical trial. There was a lack of consensus on how to classify and stratify BCOR-CCNB3, CIC-DUX4, and EWSR1+ with non-ETS partner fusions. Most respondents were either unsure how their institution tested, or their institution did not perform the test. In cases with atypical Ewing morphology, most respondents favoured additional fusion transcript testing. There is a lack of consensus regarding the classification and stratification of rare molecular subtypes in Ewing sarcoma. It is not clear how these alternative translocations have impacted outcomes for past clinical studies. This suggests a need for molecular confirmation of diagnoses and centralized or minimum standardization of testing for future trial enrolment.
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http://dx.doi.org/10.1155/2020/3498549DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7787769PMC
December 2020

Preclinical Metrics Correlate With Drug Activity in Phase II Trials of Targeted Therapies for Non-Small Cell Lung Cancer.

Front Oncol 2020 5;10:587377. Epub 2020 Nov 5.

Departments of Pediatrics & Genetics, Albert Einstein College of Medicine, Bronx, NY, United States.

Novel oncology drugs often fail to progress from preclinical experiments to FDA approval. Therefore, determining which preclinical or clinical factors associate with drug activity could accelerate development of effective therapies. We investigated whether preclinical metrics and patient characteristics are associated with objective response rate (ORR) in phase II clinical trials of targeted therapies for non-small cell lung cancer (NSCLC). We developed a reproducible process to select a single phase II trial and supporting preclinical publication for a given drug-indication pair, which we defined as the pairing of a small molecule inhibitor (e.g., crizotinib) with the specific patient population for which it was designed to work (e.g., patients with an aberration). We demonstrated that robust drug activity in mice, as measured by change in tumor size, is independently associated with improved ORR in phase II clinical trials. The number of mice utilized in experiments, the number of publications referencing the drug for NSCLC before the phase II clinical trial, and whether the drug was approved for a cancer other than NSCLC also significantly correlated with ORR. Among clinical characteristics, sex, race, histology, and smoking history were significantly associated with ORR. Further research into metrics that correlate with drug activity has the potential to optimize selection of novel therapies for clinical trials and enrich the drug development pipeline, particularly for patients with targetable genetic aberrations and rare cancers.
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http://dx.doi.org/10.3389/fonc.2020.587377DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7674799PMC
November 2020

#ThisIsOurLane: Time for pediatric hematology/oncology providers to join gun violence prevention efforts.

Pediatr Blood Cancer 2021 02 23;68(2):e28821. Epub 2020 Nov 23.

Children's Hospital at Montefiore, Albert Einstein College of Medicine, 3415 Bainbridge Ave, Bronx, NY.

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http://dx.doi.org/10.1002/pbc.28821DOI Listing
February 2021

Skp2 depletion reduces tumor-initiating properties and promotes apoptosis in synovial sarcoma.

Transl Oncol 2020 Oct 2;13(10):100809. Epub 2020 Jul 2.

Department of Orthopedic Surgery, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY. Electronic address:

Synovial sarcoma (SS) is an aggressive soft-tissue cancer with a poor prognosis and a propensity for local recurrence and distant metastasis. In this study, we investigated whether S phase kinase-associated protein (Skp2) plays an oncogenic role in tumor initiation, progression, and metastasis of SS. Our study revealed that Skp2 is frequently overexpressed in SS specimens and SS18-SSX transgenic mouse tumors, as well as correlated with clinical stages. Next, we identified that genetic depletion of Skp2 reduced mesenchymal and stemness markers, and inhibited the invasive and proliferative capacities of SS cell lines. Furthermore, Skp2 depletion markedly suppressed the growth of SS xenografts tumors. Treatment of SS cell lines with the skp2 inhibitor flavokawain A (FKA) reduced Skp2 expression in a dose-dependent manner and resulted in cell cycle arrest and apoptosis. FKA also suppressed the invasion and tumor-initiating properties in SS, similar to the effects of Skp2 knockdown. In addition, a combination of FKA and conventional chemotherapy showed a synergistic therapeutic efficacy. Taken together, our results suggest that Skp2 plays an essential role in the biology of SS by promoting the mesenchymal state and cancer stemness. Given that chemotherapy resistance is often associated with cancer stemness, strategies of combining Skp2 inhibitors with conventional chemotherapy in SS may be desirable.
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http://dx.doi.org/10.1016/j.tranon.2020.100809DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7334610PMC
October 2020

An 8-Year-Old Boy With Fever, Splenomegaly, and Pancytopenia.

Pediatrics 2020 07 12;146(1). Epub 2020 Jun 12.

The Children's Hospital at Montefiore, Bronx, New York; and.

An 8-year-old boy with no significant past medical history presented to his pediatrician with 5 days of fever, diffuse abdominal pain, and pallor. The pediatrician referred the patient to the emergency department (ED), out of concern for possible malignancy. Initial vital signs indicated fever, tachypnea, and tachycardia. Physical examination was significant for marked abdominal distension, hepatosplenomegaly, and abdominal tenderness in the right upper and lower quadrants. Initial laboratory studies were notable for pancytopenia as well as an elevated erythrocyte sedimentation rate and C-reactive protein. Computed tomography (CT) of the abdomen and pelvis showed massive splenomegaly. The only significant history of travel was immigration from Albania 10 months before admission. The patient was admitted to a tertiary care children's hospital and was evaluated by hematology-oncology, infectious disease, genetics, and rheumatology subspecialty teams. Our multidisciplinary panel of experts will discuss the evaluation of pancytopenia with apparent multiorgan involvement and the diagnosis and appropriate management of a rare disease.
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http://dx.doi.org/10.1542/peds.2019-2372DOI Listing
July 2020

DICER1-associated central nervous system sarcoma in children: comprehensive clinicopathologic and genetic analysis of a newly described rare tumor.

Mod Pathol 2020 10 14;33(10):1910-1921. Epub 2020 Apr 14.

Department of Pathology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.

The spectrum of neoplasms associated with DICER1 variants continues to expand, with the recent addition of primary "DICER1-associated central nervous system sarcoma" (DCS). DCS is a high-grade malignancy predominantly affecting pediatric patients. Six pediatric DCS were identified through a combination of clinical diagnostic studies, archival inquiry, and interinstitutional collaboration. Clinical, histologic, immunohistologic, and molecular features were examined. Genomic findings in the 6 DCS were compared with those in 14 additional DICER1-associated tumors sequenced with the same assay. The six patients presented at ages 3-15 years with CNS tumors located in the temporal (n = 2), parietal (n = 1), fronto-parietal (n = 1), and frontal (n = 2) lobes. All underwent surgical resection. Histologic examination demonstrated high-grade malignant spindle cell tumors with pleuropulmonary blastoma-like embryonic "organoid" features and focal rhabdomyoblastic differentiation; immature cartilage was seen in one case. Immunohistochemically, there was patchy desmin and myogenin staining, and patchy loss of H3K27me3, and within eosinophilic cytoplasmic globules, alfa-fetoprotein staining. Biallelic DICER1 variants were identified in all cases, with germline variants in two of five patients tested. DCS demonstrated genomic alterations enriched for Ras pathway activation and TP53 inactivation. Tumor mutational burden was significantly higher in the 6 DCS tumors than in 14 other DICER1-associated tumors examined (mean 12.9 vs. 6.8 mutations/Mb, p = 0.035). Postoperative care included radiation (n = 5) and chemotherapy (n = 3); at the last follow-up, three patients were alive without DCS, and three had died of disease. Our analysis expands the clinical, histologic, immunohistological, and molecular spectrum of DCS, identifying distinctive features that can aid in the diagnosis, multidisciplinary evaluation, and treatment of DCS.
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http://dx.doi.org/10.1038/s41379-020-0516-1DOI Listing
October 2020

Enolate-forming compounds provide protection from platinum neurotoxicity.

Chem Biol Interact 2020 Feb 21;317:108961. Epub 2020 Jan 21.

Department of Anesthesiology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, 10467, USA.

Cisplatin (CisPt) and other platinum (Pt)-based antineoplastic drugs (e.g., carboplatin, oxaliplatin) are highly effective and widely used in the treatment of solid tumors in both pediatric and adult patients. Although considered to be life-saving as a cancer treatment, Pt-based drugs frequently result in dose-limiting toxicities such as chemotherapy-induced peripheral neuropathies (CIPN). Specifically, irreversible damage to outer hair cells and injury of sensory neurons are linked to profound sensorineural hearing loss (ototoxicity), which complicates tumor management and can lead to a poor clinical prognosis. Given the severity of CIPN, substantial effort has been devoted to the development of neuroprotective compounds, regardless clinical results have been underwhelming. It is noteworthy that Pt is a highly reactive electrophile (electron deficient) that causes toxicity by forming adducts with nucleophilic (electron rich) targets on macromolecules. In this regard, we have discovered a series of carbon-based enol nucleophiles; e.g., N-(4-acetyl-3,5-dihydroxyphenyl)-2-oxocytclopentane-1-carboxamide (Gavinol), that can prevent neurotoxicity by scavenging the platinum ion. The chemistry of enol compounds is well understood and mechanistic research has demonstrated the role of this chemistry in cytoprotection. Our cell-derived data were corroborated by calculations of hard and soft, acids and bases (HSAB) parameters that describe the electronic character of interacting electrophiles and nucleophiles. Together, these observations indicate that the respective mechanisms of Pt neurotoxicity and antitumor activity are separable and can therefore be affected independently.
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http://dx.doi.org/10.1016/j.cbi.2020.108961DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7069230PMC
February 2020

Progress toward liquid biopsies in pediatric solid tumors.

Cancer Metastasis Rev 2019 12;38(4):553-571

Department of Pediatrics, The University of Chicago, 900 E. 57th St., KCBD 5116, Chicago, IL, 60637, USA.

Pediatric solid tumors have long been known to shed tumor cells, DNA, RNA, and proteins into the blood. Recent technological advances have allowed for improved capture and analysis of these typically scant circulating materials. Efforts are ongoing to develop "liquid biopsy" assays as minimally invasive tools to address diagnostic, prognostic, and disease monitoring needs in childhood cancer care. Applying these highly sensitive technologies to serial liquid biopsies is expected to advance understanding of tumor biology, heterogeneity, and evolution over the course of therapy, thus opening new avenues for personalized therapy. In this review, we outline the latest technologies available for liquid biopsies and describe the methods, pitfalls, and benefits of the assays that are being developed for children with extracranial solid tumors. We discuss what has been learned in several of the most common pediatric solid tumors including neuroblastoma, sarcoma, Wilms tumor, and hepatoblastoma and highlight promising future directions for the field.
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http://dx.doi.org/10.1007/s10555-019-09825-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6995761PMC
December 2019

Systemic manifestations of extraskeletal myxoid chondrosarcoma associated with a novel t(2;22)(q34;q12) EWS translocation in a child and a review of the literature.

Pediatr Hematol Oncol 2018 Oct - Nov;35(7-8):434-441. Epub 2019 Feb 18.

b The Children's Hospital at Montefiore , Bronx , New York , USA.

Extraskeletal myxoid chondrosarcoma (EMC), a soft-tissue sarcoma with unique clinicopathologic features and characteristic chromosomal translocations, is extremely rare in the pediatric population. We, herein, present the case of a 7-year-old boy with profound microcytic hypochromic anemia, poor weight gain and a mid-thoracic paraspinal mass that was identified as EMC. Systemic manifestations of localized, nonmetastatic EMC have never been described in the pediatric population, yet our patient's anemia and poor weight gain resolved after successful surgical resection of the tumor, suggesting that localized EMC can present with systemic manifestations. The tumor also contained a novel t(2;22)(q34;q12) translocation involving the EWSR1 gene, which is consistent with additional reports suggesting that a growing list of translocations can drive formation of, and potential new management strategies for, EMC.
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http://dx.doi.org/10.1080/08880018.2018.1557766DOI Listing
April 2019

Bleomycin-induced genome structural variations in normal, non-tumor cells.

Sci Rep 2018 11 8;8(1):16523. Epub 2018 Nov 8.

Department of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.

Many anticancer drugs are genotoxic agents inducing DNA breaks in actively proliferating cancer cells. However, these same drugs also induce mutations, mostly genome structural variations (GSVs). The detection of GSVs in normal cells and tissues is a major challenge due to the very low abundance of these mutations, which are essentially only detectable in clonal outgrowths, such as tumors. Previously we developed Structural Variant Search (SVS) - an NGS-based assay for the quantitative detection of somatic GSVs in normal cells. Using an improved version of SVS we now demonstrate that the same dose of the anti-cancer drug bleomycin induces about 5 times more somatic GSVs in quiescent primary human fibroblasts than in proliferating cells. GVS induction in non-dividing, normal cells was subsequently confirmed in vivo by demonstrating that a single dose of bleomycin leads to a significant increase of GSV frequency in mouse liver and heart, two postmitotic tissues. Our findings suggest that normal non-cycling differentiated cells may serve as a reservoir of iatrogenically induced mutations. These results provide more insight into the possible molecular mechanisms that underlie late-life morbidities in cancer survivors exposed to chemotherapy.
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http://dx.doi.org/10.1038/s41598-018-34580-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6224559PMC
November 2018

Physician perspectives on compassionate use in pediatric oncology.

Pediatr Blood Cancer 2019 03 8;66(3):e27545. Epub 2018 Nov 8.

Division of Pediatric Hematology, Oncology, and Marrow and Blood Cell Transplantation, Children's Hospital at Montefiore, Bronx, New York.

Background: Targeted cancer treatments are almost always first studied in adults, even when there is a biologically plausible potential for efficacy in children. Through compassionate use programs, children who are not eligible for a clinical trial and for whom there are no known effective therapies may obtain access to investigational agents, including drugs under development for adults. However, little is known about pediatric oncologists' experiences with applying for and obtaining compassionate use agents.

Methods: This study surveyed 132 pediatric oncologists to assess awareness and utilization of compassionate use programs, to identify barriers to their use, and to evaluate available institutional support and resources.

Results: We found that the process of applying for access to drugs in development is poorly understood, which presents a barrier to obtaining investigational drugs. Fifty-seven percent of the pediatric oncologists applied for compassionate use. Providers from larger institutions or with more than 15 years of clinical experience were more likely to complete an application and obtain investigational agents for their patients.

Conclusion: Identified perceived and actual barriers to compassionate use application submission suggest pediatric oncologists may benefit from educational resources and support to ensure children with cancer equal access to investigational agents and care.
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http://dx.doi.org/10.1002/pbc.27545DOI Listing
March 2019

Detection of circulating tumor DNA in patients with osteosarcoma.

Oncotarget 2018 Feb 18;9(16):12695-12704. Epub 2018 Jan 18.

Division of Hematology/Oncology, Children's Hospital at Montefiore, Bronx, NY, USA.

Identification and quantification of somatic alterations in plasma-derived, circulating tumor DNA (ctDNA) is gaining traction as a non-invasive and cost effective method of disease monitoring in cancer patients, particularly to evaluate response to treatment and monitor for disease recurrence. To our knowledge, genetic analysis of ctDNA in osteosarcoma has not yet been studied. To determine whether somatic alterations can be detected in ctDNA and perhaps applied to patient management in this disease, we collected germline, tumor, and serial plasma samples from pediatric, adolescent, and young adult patients with osteosarcoma and used targeted Next Generation Sequencing (NGS) to identify somatic single nucleotide variants (SNV), insertions and deletions (INDELS), and structural variants (SV) in 7 genes commonly mutated in osteosarcoma. We demonstrate that patient-specific somatic alterations identified through comparison of tumor-germline pairs can be detected and quantified in cell-free DNA of osteosarcoma patients.
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http://dx.doi.org/10.18632/oncotarget.24268DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5849166PMC
February 2018

Advancing Clinicopathologic Diagnosis of High-risk Neuroblastoma Using Computerized Image Analysis and Proteomic Profiling.

Pediatr Dev Pathol 2017 Sep-Oct;20(5):394-402. Epub 2017 Apr 18.

2 Department of Genetics, Albert Einstein College of Medicine, New York, New York, USA.

A subset of patients with neuroblastoma are at extremely high risk for treatment failure, though they are not identifiable at diagnosis and therefore have the highest mortality with conventional treatment approaches. Despite tremendous understanding of clinical and biological features that correlate with prognosis, neuroblastoma at ultra-high risk for treatment failure remains a diagnostic challenge. As a first step towards improving prognostic risk stratification within the high-risk group of patients, we determined the feasibility of using computerized image analysis and proteomic profiling on single slides from diagnostic tissue specimens. After expert pathologist review of tumor sections to ensure quality and representative material input, we evaluated multiple regions of single slides as well as multiple sections from different patients' tumors using computational histologic analysis and semiquantitative proteomic profiling. We found that both approaches determined that intertumor heterogeneity was greater than intratumor heterogeneity. Unbiased clustering of samples was greatest within a tumor, suggesting a single section can be representative of the tumor as a whole. There is expected heterogeneity between tumor samples from different individuals with a high degree of similarity among specimens derived from the same patient. Both techniques are novel to supplement pathologist review of neuroblastoma for refined risk stratification, particularly since we demonstrate these results using only a single slide derived from what is usually a scarce tissue resource. Due to limitations of traditional approaches for upfront stratification, integration of new modalities with data derived from one section of tumor hold promise as tools to improve outcomes.
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http://dx.doi.org/10.1177/1093526617698603DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059208PMC
May 2019

Ovary preservation in the treatment of childhood Meigs syndrome.

Pediatr Blood Cancer 2015 Nov 22;62(11):2011-4. Epub 2015 May 22.

Departments of Pediatrics and Genetics, Albert Einstein College of Medicine, Bronx, New York.

Meigs syndrome, the combination of benign ovarian tumor, ascites, and pleural effusion, is present in a small percentage of ovarian fibromas and is infrequently reported in children. When associated with elevated CA-125 suspicion is raised for malignancy, often prompting aggressive surgical intervention. We present a case of childhood Meigs syndrome and review the relevant literature with emphasis on ovary preservation. Out of nine identified pediatric cases, one involved ovary sparing treatment and none recurred or progressed to malignancy. Our report highlights the importance of presurgical identification of Meigs syndrome in order to curtail salpingo-oophorectomy when feasible.
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http://dx.doi.org/10.1002/pbc.25586DOI Listing
November 2015

ALK mutations confer differential oncogenic activation and sensitivity to ALK inhibition therapy in neuroblastoma.

Cancer Cell 2014 Nov 10;26(5):682-94. Epub 2014 Nov 10.

Department of Pediatrics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA; Division of Oncology and Center for Childhood Cancer Research, The Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA. Electronic address:

Genetic studies have established anaplastic lymphoma kinase (ALK), a cell surface receptor tyrosine kinase, as a tractable molecular target in neuroblastoma. We describe comprehensive genomic, biochemical, and computational analyses of ALK mutations across 1,596 diagnostic neuroblastoma samples. ALK tyrosine kinase domain mutations occurred in 8% of samples--at three hot spots and 13 minor sites--and correlated significantly with poorer survival in high- and intermediate-risk neuroblastoma. Biochemical and computational studies distinguished oncogenic (constitutively activating) from nononcogenic mutations and allowed robust computational prediction of their effects. The mutated variants also showed differential in vitro crizotinib sensitivities. Our studies identify ALK genomic status as a clinically important therapeutic stratification tool in neuroblastoma and will allow tailoring of ALK-targeted therapy to specific mutations.
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http://dx.doi.org/10.1016/j.ccell.2014.09.019DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269829PMC
November 2014

Imaging in childhood cancer: a Society for Pediatric Radiology and Children's Oncology Group Joint Task Force report.

Pediatr Blood Cancer 2013 Aug 9;60(8):1253-60. Epub 2013 Apr 9.

Division of Oncology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA.

Contemporary medical imaging is a cornerstone of care for children with cancer. As 5-year survival rates for children with cancer exceed 80%, imaging technologies have evolved in parallel to include a wide array of modalities. Here, we overview the risks and benefits associated with commonly used imaging modalities and survey the current landscape of medical imaging for children with cancer. We find evidence-based imaging guidelines to assist in protocol development and to guide decision-making for optimal patient care are often lacking. The substantial variation in protocol-based recommendations for imaging both during and following therapy may hinder optimal clinical research and clinical care for children with cancer.
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http://dx.doi.org/10.1002/pbc.24533DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4636336PMC
August 2013