Clinico‐pathological description of three paediatric medulloblastoma cases with <scp><i>MLL2/3</i></scp> gene mutations

López, Giselle Y.; Grant, Gerald A.; Fuchs, Herbert E.; Leithe, Linda Gray; Gururangan, Sridharan; Bigner, Darell D.; Yan, Hai; McLendon, Roger E.; He, Yiping

doi:10.1111/nan.12060

Cited by 4 publications

(2 citation statements)

References 12 publications

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“…Indeed, more than 50 different translocations or partial tandem duplications involving MLL on chromosome 11q23 have been described and are found to be associated with poor prognosis in acute lymphoblastic leukemia or normal-karyotype acute myeloid leukemia (AML) (reviewed in 94 ). Of interest, on the basis of genome-wide sequencing data, mutations of other MLLs, MLL2 (also called MLL4, KMT2D) and MLL3 (KMT2C), have been described in both GBM and medulloblastoma, 46,50,95,96,97,98,99 further increasing the interest for these MTs in cancer. Importantly, UTX (KDM6A) is part of the MLL3/4 complexes, while JMJD3 (KDM6B) associates with the common MLL complex proteins WDR5, ASH2L, and RBBP5.…”

Section: Mixed-lineage Leukemiamentioning

confidence: 99%

Epigenetic modification in chromatin machinery and its deregulation in pediatric brain tumors: Insight into epigenetic therapies

Maury

Hashizume

2017

Epigenetics

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Malignancies are characterized by the reprogramming of epigenetic patterns. This reprogramming includes gains or losses in DNA methylation and disruption of normal patterns of covalent histone modifications, which are associated with changes in chromatin remodeling processes. This review will focus on the mechanisms underlying this reprogramming and, specifically, on the role of histone modification in chromatin machinery and the modifications in epigenetic processes occurring in brain cancer, with a specific focus on epigenetic therapies for pediatric brain tumors.

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Section: Mixed-lineage Leukemiamentioning

confidence: 99%

Epigenetic modification in chromatin machinery and its deregulation in pediatric brain tumors: Insight into epigenetic therapies

Maury

Hashizume

2017

Epigenetics

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“…It has been elucidated that MB tumors have stark epigenetic changes, which can be reflective of their subgroup status and prognostic outcome . For example, mutations in MLL2 and MLL3, the catalytic component in trithorax proteins that is responsible for methylation of histone H3 at the fourth lysine position (H3K4me), are found across all groups in MB . Furthermore, inactivation of the KDM family of proteins, which are lysine demethylases that erase H3K27me3 marks on histones, is also seen in MB tumors.…”

Section: Challenges and Advances In Medulloblastoma Researchmentioning

confidence: 99%

Medulloblastoma: Challenges and advances in treatment and research

Martirosian

Neman

2018

Cancer Reports

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Background: Medulloblastoma (MB) is a pediatric brain tumor occurring in the posterior fossa. MB is a highly heterogeneous tumor, which can be grouped into four main subgroups: WNT, SHH, Group 3, and Group 4. Each subgroup is different both in its implicated pathways and pathology, as well as how they are treated in the clinic. Recent Findings: Standard protocol for MB treatment consists of maximal safe resection, followed by craniospinal radiation (in patients 3 years and older) and adjuvant chemotherapy. Advances in clinical stratification of this tumor have allowed establishment of treatment de-escalation trials aimed at reducing long-term side effects. However, there have been few advances in identifying novel therapeutic strategies for MB patients due to difficulties in creating chemotherapeutics that can bypass the blood-brain-barrier-among other factors. On the other hand, with the help of whole genome sequencing technologies, molecular pathways involved in MB pathogenesis have become clearer and have helped drive MB research. Regardless, this advance in research has yet to translate to the clinic, which may be due to the inability of current in vivo and in vitro models to accurately recapitulate this heterogeneous tumor in humans.Conclusions: There have been significant advances in knowledge and treatment of medulloblastoma over the last few decades. Whole genome sequencing has helped elucidate clear differences between the subgroups of MB, allowing physicians to better tailor treatments to each patient in an effort to reduce long-term sequelae. However, there are still many more obstacles to overcome, including less cytotoxic therapies in the clinic and better modeling systems to accurately replicate this disease in the laboratory. Scientists and physicians must work in a more cohesive manner to create translatable results from the laboratory to the clinic-helping improve therapies for medulloblastoma patients.

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Downregulation of KMT2D suppresses proliferation and induces apoptosis of gastric cancer

Xiong

Deng

Tang

et al. 2018

Biochemical and Biophysical Research Communications

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Clinico‐pathological description of three paediatric medulloblastoma cases with MLL2/3 gene mutations

Cited by 4 publications

References 12 publications

Epigenetic modification in chromatin machinery and its deregulation in pediatric brain tumors: Insight into epigenetic therapies

Epigenetic modification in chromatin machinery and its deregulation in pediatric brain tumors: Insight into epigenetic therapies

Medulloblastoma: Challenges and advances in treatment and research

Downregulation of KMT2D suppresses proliferation and induces apoptosis of gastric cancer

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