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Article ; Online: Spontaneous regression of neuroblastoma.

Brodeur, Garrett M

2018 Volume 372, Issue 2, Page(s) 277–286

Abstract: Neuroblastomas are characterized by heterogeneous clinical behavior, from spontaneous regression or differentiation into a benign ganglioneuroma, to relentless progression despite aggressive, multimodality therapy. Indeed, neuroblastoma is unique among ... ...

Abstract	Neuroblastomas are characterized by heterogeneous clinical behavior, from spontaneous regression or differentiation into a benign ganglioneuroma, to relentless progression despite aggressive, multimodality therapy. Indeed, neuroblastoma is unique among human cancers in terms of its propensity to undergo spontaneous regression. The strongest evidence for this comes from the mass screening studies conducted in Japan, North America and Europe and it is most evident in infants with stage 4S disease. This propensity is associated with a pattern of genomic change characterized by whole chromosome gains rather than segmental chromosome changes but the mechanism(s) underlying spontaneous regression are currently a matter of speculation. There is evidence to support several possible mechanisms of spontaneous regression in neuroblastomas: (1) neurotrophin deprivation, (2) loss of telomerase activity, (3) humoral or cellular immunity and (4) alterations in epigenetic regulation and possibly other mechanisms. It is likely that a better understanding of the mechanisms of spontaneous regression will help to identify targeted therapeutic approaches for these tumors. The most easily targeted mechanism is the delayed activation of developmentally programmed cell death regulated by the tropomyosin receptor kinase A (TrkA) pathway. Pan-Trk inhibitors are currently in clinical trials and so Trk inhibition might be used as the first line of therapy in infants with biologically favorable tumors that require treatment. Alternative approaches consist of breaking immune tolerance to tumor antigens but approaches to telomere shortening or epigenetic regulation are not easily druggable. The different mechanisms of spontaneous neuroblastoma regression are reviewed here, along with possible therapeutic approaches.
MeSH term(s)	Early Detection of Cancer ; Genomics ; Humans ; Immunotherapy ; Neuroblastoma/diagnosis ; Neuroblastoma/genetics ; Neuroblastoma/pathology ; Neuroblastoma/therapy ; Remission Induction
Language	English
Publishing date	2018-01-05
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	125067-x
ISSN	1432-0878 ; 0302-766X
ISSN (online)	1432-0878
ISSN	0302-766X
DOI	10.1007/s00441-017-2761-2
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Article: Spontaneous regression of neuroblastoma

Brodeur, GarrettM

Cell and tissue research. 2018 May, v. 372, no. 2

2018

Abstract	Neuroblastomas are characterized by heterogeneous clinical behavior, from spontaneous regression or differentiation into a benign ganglioneuroma, to relentless progression despite aggressive, multimodality therapy. Indeed, neuroblastoma is unique among human cancers in terms of its propensity to undergo spontaneous regression. The strongest evidence for this comes from the mass screening studies conducted in Japan, North America and Europe and it is most evident in infants with stage 4S disease. This propensity is associated with a pattern of genomic change characterized by whole chromosome gains rather than segmental chromosome changes but the mechanism(s) underlying spontaneous regression are currently a matter of speculation. There is evidence to support several possible mechanisms of spontaneous regression in neuroblastomas: (1) neurotrophin deprivation, (2) loss of telomerase activity, (3) humoral or cellular immunity and (4) alterations in epigenetic regulation and possibly other mechanisms. It is likely that a better understanding of the mechanisms of spontaneous regression will help to identify targeted therapeutic approaches for these tumors. The most easily targeted mechanism is the delayed activation of developmentally programmed cell death regulated by the tropomyosin receptor kinase A (TrkA) pathway. Pan-Trk inhibitors are currently in clinical trials and so Trk inhibition might be used as the first line of therapy in infants with biologically favorable tumors that require treatment. Alternative approaches consist of breaking immune tolerance to tumor antigens but approaches to telomere shortening or epigenetic regulation are not easily druggable. The different mechanisms of spontaneous neuroblastoma regression are reviewed here, along with possible therapeutic approaches.
Keywords	antigens ; cell-mediated immunity ; clinical trials ; enzyme activity ; epigenetics ; genomics ; humans ; immunosuppression ; infants ; neoplasms ; programmed cell death ; screening ; telomerase ; telomeres ; therapeutics ; tropomyosins ; Europe ; Japan ; North America
Language	English
Dates of publication	2018-05
Size	p. 277-286.
Publishing place	Springer Berlin Heidelberg
Document type	Article
Note	Review
ZDB-ID	125067-x
ISSN	1432-0878 ; 0302-766X
ISSN (online)	1432-0878
ISSN	0302-766X
DOI	10.1007/s00441-017-2761-2
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Article ; Online: Adult-Onset Cancer Predisposition Syndromes in Children and Adolescents-To Test or not to Test?

Kratz, Christian P / Lupo, Philip J / Zelley, Kristin / Schienda, Jaclyn / Nichols, Kim E / Stewart, Douglas R / Malkin, David / Brodeur, Garrett M / Maxwell, Kara / Plon, Sharon E / Walsh, Michael F

Clinical cancer research : an official journal of the American Association for Cancer Research

2024 Volume 30, Issue 9, Page(s) 1733–1738

Abstract: With the increasing use of comprehensive germline genetic testing of children and adolescents with cancer, it has become evident that pathogenic variants (PV) in adult-onset cancer predisposition genes (aoCPG) underlying adult-onset cancer predisposition ...

Abstract	With the increasing use of comprehensive germline genetic testing of children and adolescents with cancer, it has become evident that pathogenic variants (PV) in adult-onset cancer predisposition genes (aoCPG) underlying adult-onset cancer predisposition syndromes, such as Lynch syndrome or hereditary breast and ovarian cancer, are enriched and reported in 1% to 2% of children and adolescents with cancer. However, the causal relationship between PVs in aoCPGs and childhood cancer is still under investigation. The best-studied examples include heterozygous PVs in mismatch repair genes associated with Lynch syndrome in children with mismatch repair deficient high-grade glioma, heterozygous PVs in BARD1 in childhood neuroblastoma, and heterozygous PVs in BRCA2 in children with rhabdomyosarcoma. The low penetrance for pediatric cancers is considered to result from a combination of the low baseline risk of cancer in childhood and the report of only a modest relative risk of disease in childhood. Therefore, we do not advise that healthy children empirically be tested for PVs in an aoCPG before adulthood outside a research study. However, germline panel testing is increasingly being performed in children and adolescents with cancer, and exome and genome sequencing may be offered more commonly in this population in the future. The precise pediatric cancer risks and spectra associated with PVs in aoCPGs, underlying cellular mechanisms and somatic mutational signatures, as well as treatment response, second neoplasm risks, and psycho-oncological aspects require further research.
MeSH term(s)	Humans ; Genetic Predisposition to Disease ; Adolescent ; Genetic Testing/methods ; Child ; Germ-Line Mutation ; Age of Onset ; Neoplastic Syndromes, Hereditary/genetics ; Neoplastic Syndromes, Hereditary/diagnosis ; Adult ; Neoplasms/genetics ; Neoplasms/diagnosis ; Female
Language	English
Publishing date	2024-02-27
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-23-3683
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Article ; Online: Developmental and behavioral phenotypes of pediatric patients with PTEN hamartoma tumor syndrome.

MacFarland, Suzanne P / Duvall, Melani / Kemajou, Raissa Tchetcho / Baldino, Sarah E / Zelley, Kristin / Black, Chelsea / Thomas, Allison / Thomas, Nina H / Ruffner, Melanie / Li, Yimei / Miller, Judith S / Brodeur, Garrett M / Shabason, Emily

American journal of medical genetics. Part A

2024 , Page(s) e63608

Abstract: Our study characterized the neurodevelopmental spectrum of individuals with PTEN Hamartoma Tumor Syndrome (PHTS), a syndrome that predisposes to both neurodevelopmental phenotypes and cancer risk. We aim to better understand life-impacting ... ...

Abstract	Our study characterized the neurodevelopmental spectrum of individuals with PTEN Hamartoma Tumor Syndrome (PHTS), a syndrome that predisposes to both neurodevelopmental phenotypes and cancer risk. We aim to better understand life-impacting neurodevelopmental features of PHTS. Our study recruited 20 children/adolescents with PHTS, who were then administered assessments for autism spectrum disorder (ASD) and other neurocognitive measures, including assessment of IQ, executive and adaptive functioning, and health-related quality of life. Thirteen individuals (65%) were identified as having ASD, of which five were newly diagnosed during the study. Of those, ASD symptom severity was in the mild-moderate range for 77%. Overall, IQ was in the average range, with a mean of 92.61 (SD 24.45, p = 0.5), though there was a non-statistically significant trend toward individuals without ASD having a higher mean IQ (102.7 vs 82.3; p = 0.1). Subjects had significant impairment in processing speed (mean 75.38, SD 24.75, p < 0.05), decreased adaptive functioning skills across all domains, and a trend toward having more executive functioning problems. Individuals with PHTS are at increased risk of neurodevelopmental disorders, including ASD and impaired executive and adaptive functioning. Although clear guidelines exist for cancer surveillance for individuals with PHTS, additional guidelines and screening for neurodevelopmental disorders are warranted.
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2108614-X
ISSN	1552-4833 ; 0148-7299 ; 1552-4825
ISSN (online)	1552-4833
ISSN	0148-7299 ; 1552-4825
DOI	10.1002/ajmg.a.63608
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Article ; Online: B-cell acute lymphoblastic leukemia and juvenile xanthogranuloma in a patient with

Newman, Haley / MacFarland, Suzanne P / Brodeur, Garrett M / Olson, Timothy / Bhojwani, Deepa / Stokke, Jamie / Kovach, Alexandra E / Clark, Mary Egan / Luo, Minjie / Li, Marilyn / Shah, Amish / Hunger, Stephen P

Haematologica

2024 Volume 109, Issue 5, Page(s) 1624–1627

MeSH term(s)	Humans ; ETS Translocation Variant 6 Protein ; Proto-Oncogene Proteins c-ets/genetics ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/diagnosis ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/complications ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Xanthogranuloma, Juvenile/genetics ; Xanthogranuloma, Juvenile/diagnosis ; Xanthogranuloma, Juvenile/complications ; Xanthogranuloma, Juvenile/pathology ; Thrombocytopenia/genetics ; Thrombocytopenia/diagnosis ; Thrombocytopenia/etiology ; Thrombocytopenia/pathology ; Repressor Proteins/genetics ; Male ; Female ; Genetic Predisposition to Disease
Chemical Substances	ETS Translocation Variant 6 Protein ; Proto-Oncogene Proteins c-ets ; Repressor Proteins
Language	English
Publishing date	2024-05-01
Publishing country	Italy
Document type	Case Reports ; Letter ; Research Support, Non-U.S. Gov't ; Journal Article
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2023.284151
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Article ; Online: Knowing your ABCCs: novel functions of ABCC transporters.

Brodeur, Garrett M

Journal of the National Cancer Institute

2011 Volume 103, Issue 16, Page(s) 1207–1208

MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Female ; Humans ; Male ; Multidrug Resistance-Associated Proteins/metabolism ; Neuroblastoma/drug therapy ; Neuroblastoma/metabolism ; Pyrazoles/pharmacology ; Pyrimidines/pharmacology
Chemical Substances	Antineoplastic Agents ; Multidrug Resistance-Associated Proteins ; Pyrazoles ; Pyrimidines ; reversan
Language	English
Publishing date	2011-07-28
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2992-0
ISSN	1460-2105 ; 0027-8874 ; 0198-0157
ISSN (online)	1460-2105
ISSN	0027-8874 ; 0198-0157
DOI	10.1093/jnci/djr277
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Article ; Online: Getting into the AKT.

Brodeur, Garrett M

Journal of the National Cancer Institute

2010 Volume 102, Issue 11, Page(s) 747–749

MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Apoptosis/drug effects ; Cell Survival/drug effects ; Clinical Trials as Topic ; Disease Models, Animal ; Growth Inhibitors/pharmacology ; Growth Inhibitors/therapeutic use ; Humans ; Mice ; Neuroblastoma/drug therapy ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Phosphorylcholine/analogs & derivatives ; Phosphorylcholine/pharmacology ; Phosphorylcholine/therapeutic use ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; Proto-Oncogene Proteins c-akt/metabolism ; Receptor Protein-Tyrosine Kinases/drug effects ; Transplantation, Heterologous
Chemical Substances	Antineoplastic Agents ; Growth Inhibitors ; Phosphorylcholine (107-73-3) ; perifosine (2GWV496552) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2010-05-12
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	2992-0
ISSN	1460-2105 ; 0027-8874 ; 0198-0157
ISSN (online)	1460-2105
ISSN	0027-8874 ; 0198-0157
DOI	10.1093/jnci/djq171
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Article ; Online: FOCAD Indel in a Family With Juvenile Polyposis Syndrome.

MacFarland, Suzanne P / Xie, Hongbo / Dent, Maiah H / Greed, Bridgid / Plon, Sharon E / Scollon, Sarah R / Brodeur, Garrett M / Howe, James R

Journal of pediatric gastroenterology and nutrition

2022 Volume 75, Issue 1, Page(s) 56–58

Abstract: Juvenile polyposis syndrome (JPS) is a childhood polyposis syndrome with up to a 50% lifetime risk of gastrointestinal cancer. Germline pathogenic variants in BMPR1A and SMAD4 are responsible for around 40% of cases of JPS, but for the majority of ... ...

Abstract	Juvenile polyposis syndrome (JPS) is a childhood polyposis syndrome with up to a 50% lifetime risk of gastrointestinal cancer. Germline pathogenic variants in BMPR1A and SMAD4 are responsible for around 40% of cases of JPS, but for the majority of individuals, the underlying genetic cause is unknown. We identified a family for which polyposis spanned four generations, and the proband had a clinical diagnosis of JPS. Next-generation sequencing was conducted, followed by Sanger sequencing confirmation. We identified an internal deletion of the FOCAD gene in all family members tested that altered the reading frame and is predicted to be pathogenic. We conclude that inactivation of the FOCAD gene is likely to cause JPS in this family.
MeSH term(s)	Child ; Gastrointestinal Neoplasms ; Germ-Line Mutation ; Humans ; Intestinal Polyposis/congenital ; Intestinal Polyposis/genetics ; Neoplastic Syndromes, Hereditary/genetics
Chemical Substances	FOCAD protein, human
Language	English
Publishing date	2022-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603201-1
ISSN	1536-4801 ; 0277-2116
ISSN (online)	1536-4801
ISSN	0277-2116
DOI	10.1097/MPG.0000000000003470
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Article ; Online: Mechanisms of neuroblastoma regression.

Brodeur, Garrett M / Bagatell, Rochelle

Nature reviews. Clinical oncology

2014 Volume 11, Issue 12, Page(s) 704–713

Abstract: Recent genomic and biological studies of neuroblastoma have shed light on the dramatic heterogeneity in the clinical behaviour of this disease, which spans from spontaneous regression or differentiation in some patients, to relentless disease progression ...

Abstract	Recent genomic and biological studies of neuroblastoma have shed light on the dramatic heterogeneity in the clinical behaviour of this disease, which spans from spontaneous regression or differentiation in some patients, to relentless disease progression in others, despite intensive multimodality therapy. This evidence also suggests several possible mechanisms to explain the phenomena of spontaneous regression in neuroblastomas, including neurotrophin deprivation, humoral or cellular immunity, loss of telomerase activity and alterations in epigenetic regulation. A better understanding of the mechanisms of spontaneous regression might help to identify optimal therapeutic approaches for patients with these tumours. Currently, the most druggable mechanism is the delayed activation of developmentally programmed cell death regulated by the tropomyosin receptor kinase A pathway. Indeed, targeted therapy aimed at inhibiting neurotrophin receptors might be used in lieu of conventional chemotherapy or radiation in infants with biologically favourable tumours that require treatment. Alternative approaches consist of breaking immune tolerance to tumour antigens or activating neurotrophin receptor pathways to induce neuronal differentiation. These approaches are likely to be most effective against biologically favourable tumours, but they might also provide insights into treatment of biologically unfavourable tumours. We describe the different mechanisms of spontaneous neuroblastoma regression and the consequent therapeutic approaches.
MeSH term(s)	Epigenesis, Genetic/genetics ; Genomics ; Humans ; Neuroblastoma/genetics ; Signal Transduction
Language	English
Publishing date	2014-10-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/nrclinonc.2014.168
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Article ; Online: Environment-Sensitive Polymeric Micelles Encapsulating SN-38 Potently Suppress Growth of Neuroblastoma Cells Exhibiting Intrinsic and Acquired Drug Resistance.

Polunin, Yehor / Alferiev, Ivan S / Brodeur, Garrett M / Voronov, Andriy / Chorny, Michael

ACS pharmacology & translational science

2020 Volume 4, Issue 1, Page(s) 240–247

Abstract: Conventional treatment approaches fail to provide durable control over aggressive malignancies due to intrinsic or acquired drug resistance characteristic of high-risk disease. SN-38, a potent camptothecin analog specifically targeting DNA topoisomerase ... ...

Abstract	Conventional treatment approaches fail to provide durable control over aggressive malignancies due to intrinsic or acquired drug resistance characteristic of high-risk disease. SN-38, a potent camptothecin analog specifically targeting DNA topoisomerase I cleavage complexes, has shown promise in preclinical studies against aggressive solid tumors. However, its clinical utility is limited by inadequate solubility in pharmaceutically acceptable vehicles and by poor chemical and metabolic stability. Micelles formulated from amphiphilic invertible polymers (AIPs) can address these issues by concomitantly enabling solubilization of water-insoluble molecular cargoes and by protecting chemically labile agents from inactivation. Furthermore, the inversion of the AIP and disruption of the carrier-drug complexes triggered by contact with cell membranes makes it possible to deliver the therapeutic payload into the cell interior without compromising its biological activity. In the present study, we characterized a novel AIP-based micellar formulation of SN-38 and evaluated its growth inhibitory effect on neuroblastoma (NB) cells derived either at diagnosis or at relapse after intensive chemoradiotherapy. Colloidally stable, drug-loaded micellar assemblies with a uniform <100 nm size were prepared using an AIP consisting of alternating blocks of poly(ethylene glycol) and polytetrahydrofuran (PEG
Language	English
Publishing date	2020-12-04
Publishing country	United States
Document type	Journal Article
ISSN	2575-9108
ISSN (online)	2575-9108
DOI	10.1021/acsptsci.0c00182
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