Detection of Metastatic Tumor Cells in Bone Marrow
Adrian P. Gee in BONE MARROW PROCESSING and PURGING, 2020
This chapter provides a comprehensive review of methods for the sensitive detection of tumor cells in bone marrow that is to be used for transplantation. It discusses the clinical relevance of bone marrow disease in different malignancies, such as neuroblastoma, breast carcinoma, and small cell lung carcinoma. The new sensitive methods of tumor detection have demonstrated that the incidence of marrow disease is significantly higher than previously indicated by routine analysis. However, the sensitivity of tumor detection is low, because identification of metastatic disease is based solely on cellular morphology and single tumor cells, or small clumps of malignant cells may go unappreciated by the pathologist. Although this results in increased sensitivity of tumor detection, it is uncomfortable for the patient and is still inferior to more specific methods of detection. The gold standard for detection of bone marrow metastases has always been routine histology and cytology.
Wilms’ Tumor
Victor A. Bernstam in Pocket Guide to GENE LEVEL DIAGNOSTICS in Clinical Practice, 2019
Suppression of the tumorigenic phenotype of Wilms’ tumor (WT) by introduction of human chromosome 11 into the tumor cells strengthened the belief that Tumor Suppressor Genes may be located on chromosome 11. A role for genetic imprinting in the pathogenesis of WT is demonstrated by the preferential loss of heterozygosity of the maternal alleles from 11p. A candidate gene for the WT locus has been identified and sequences mapping in the WT area of band 11p13 have been isolated. It is possible that the WT-2–1 gene product acts as a transcriptional regulator during normal kidney development to switch off genes involved in maintaining cell proliferation. Abnormalities of chromosome 1 seem to be the most recently detected secondary structural change, with 80% of the breakpoints occurring in 1q and 20% in 1p34 regions. Extensive overexpression of the N-myc gene without amplification, similar to that in neuroblastoma, is characteristic of WT.
Adjuvant therapy in childhood cancer
Brice Antao, S Irish Michael, Anthony Lander, S Rothenberg MD Steven in Succeeding in Paediatric Surgery Examinations, 2017
The treatment of stage four neuroblastoma in those greater than one year of age is multimodal and includes maturation therapy with 13-cis-retinoic acid after myeloablative chemotherapy with stem cell rescue and radiotherapy. Systemic corticosteroids and local radiotherapy have been implicated in the development of avascular necrosis in cancer patients. Corticosteroids form an important part of acute lymphoblastic leukaemia treatment but radiotherapy does not. It is therefore most likely that the avascular necrosis is caused by the corticosteroid therapy. Increased use of dexamethasone has resulted in an increase in the numbers of paediatric leukaemia patients presenting with symptomatic avascular necrosis. Gabapentin is a gamma-aminobutyric acid analogue originally developed for epilepsy but is also effective against neuropathic pain. The history of previous radiotherapy to this area suggests that there would be limited scope for additional radiotherapy because of the risk of exceeding local tissue tolerance.
Overview and recent advances in the treatment of neuroblastoma
Published in Expert Review of Anticancer Therapy, 2017
Sarah B. Whittle, Valeria Smith, Erin Doherty, Sibo Zhao, Scott McCarty, Peter E. Zage
Introduction: Children with neuroblastoma have widely divergent outcomes, ranging from cure in >90% of patients with low risk disease to
The mTOR Signaling Pathway in Pediatric Neuroblastoma
Published in Pediatric Hematology and Oncology, 2013
Hong Mei, Ye Wang, Zhenyu Lin, Qiangsong Tong
Neuroblastoma (NB) is the most common extracranial malignant solid tumors of childhood, and the majority of these high-risk tumors is resistant to nearly all the treatments and has a significantly worse outcome. The mammalian target of rapamycin (mTOR) plays a critical role in oncogenesis and cancer progression of many tumors. This review will describe the function of mTOR, its genetic regulation in pediatric neuroblastoma, and its value as a target for inhibition by anticancer agents for patients with NB.
Advances in emerging drugs for the treatment of neuroblastoma
Published in Expert Opinion on Emerging Drugs, 2017
Pablo Berlanga, Adela Cañete, Victoria Castel
Introduction: Neuroblastoma is the most common solid extracranial tumor of childhood. Outcome for children with high-risk neuroblastoma remains suboptimal. More than half of children diagnosed with high-risk neuroblastoma either do not respond to conventional therapies or relapse after treatment with dismal prognosis. Areas covered: This paper presents a short review of the state of the art in the current treatment of high-risk neuroblastoma. An updated review of new targeted therapies in this group of patients is also presented. Expert opinion: In order to improve prognosis for high-risk patients there is an urgent need to better understand spatial and temporal heterogeneity and obtain new predictive preclinical models in neuroblastoma. Combination strategies with conventional chemotherapy and/or other targeted therapies may overcome current ALK inhibitors resistance. Improvement of international and transatlantic cooperation to speed clinical trials accrual is needed.
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