Aberrant DNA methylation-induced gene inactivation is associated with the diagnosis and/or therapy of T-cell leukemias

Kim, Sun Young; Shin, Dong‐Yeop; Kim, Sang-Man; Lee, Minyoung; Kim, Sang Hyun

doi:10.1016/j.leukres.2016.05.020

Cited by 5 publications

(3 citation statements)

References 40 publications

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“…The role of LMX1B has not been thoroughly evaluated in any tumor type. Two studies have identified that this gene is methylated in prostate cancer [71] and leukemia [72]. However, there is no experimental evidence showing that this gene is downregulated and could function as a tumor suppressor gene in these tumor types.…”

Section: Lmx1b-lim Homeobox Transcription Factor 1 Beta (9q333)mentioning

confidence: 99%

Oncogenes in high grade serous adenocarcinoma of the ovary

et al. 2020

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High grade serous ovarian cancer is characterized by relatively few mutations occurring at low frequency, except in TP53. However other genetic aberrations such as copy number variation alter numerous oncogenes and tumor suppressor genes. Oncogenes are positive regulators of tumorigenesis and play a critical role in cancer cell growth, proliferation, and survival. Accumulating evidence suggests that they are crucial for the development and the progression of high grade serous ovarian carcinoma (HGSOC). Though many oncogenes have been identified, no successful inhibitors targeting these molecules and their associated pathways are available. This review discusses oncogenes that have been identified recently in HGSOC using different screening strategies. All the genes discussed in this review have been functionally characterized both in vitro and in vivo and some of them are able to transform immortalized ovarian surface epithelial and fallopian tube cells upon overexpression. However, it is necessary to delineate the molecular pathways affected by these oncogenes for the development of therapeutic strategies.

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Section: Lmx1b-lim Homeobox Transcription Factor 1 Beta (9q333)mentioning

confidence: 99%

Oncogenes in high grade serous adenocarcinoma of the ovary

et al. 2020

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“…In this context, the tumor microenvironment plays a fundamental role in which epigenetic components are associated with and contribute to tumorigenesis [ 44 – 47 ]. Epigenetic events, such as DNA methylation, are commonly identified in tumors, and these phenomena may aid in the understanding of the carcinogenic process since it is widely accepted that DNA methylation is related to cancer development and progression [ 48 – 51 ]. Moreover, these changes may be traced back and associated with disease staging and aggressiveness, allowing them to be employed as diagnostic and prognostic biomarkers.…”

Section: Dna Methylation As An Epigenetic Biomarkermentioning

confidence: 99%

“…Leukemias are a heterogeneous group of malignant neoplasms arising from the myeloid and/or lymphoid lineage, according to the dysplastic cell type, and which affects bone marrow, peripheral blood, and lymphoid tissues [ 54 ]. Aberrant epigenetic mutations have been demonstrated in different leukemia subtypes [ 48 , 49 , 55 ], and the number of identified changes is uprising, including genes involved in a plethora of signaling pathways and cellular processes [ 56 , 57 ]. Association between epigenetic changes, such as DNA methylation, and clinical outcome among leukemia types suggests that these modifications should be explored in order to develop a method that could improve patient stratification [ 55 ].…”

Section: Dna Methylation As An Epigenetic Biomarkermentioning

confidence: 99%

DNA Methylation Events as Markers for Diagnosis and Management of Acute Myeloid Leukemia and Myelodysplastic Syndrome

et al. 2017

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During the onset and progression of hematological malignancies, many changes occur in cellular epigenome, such as hypo- or hypermethylation of CpG islands in promoter regions. DNA methylation is an epigenetic modification that regulates gene expression and is a key event for tumorigenesis. The continuous search for biomarkers that signal early disease, indicate prognosis, and act as therapeutic targets has led to studies investigating the role of DNA in cancer onset and progression. This review focuses on DNA methylation changes as potential biomarkers for diagnosis, prognosis, response to treatment, and early toxicity in acute myeloid leukemia and myelodysplastic syndrome. Here, we report that distinct changes in DNA methylation may alter gene function and drive malignant cellular transformation during several stages of leukemogenesis. Most of these modifications occur at an early stage of disease and may predict myeloid/lymphoid transformation or response to therapy, which justifies its use as a biomarker for disease onset and progression. Methylation patterns, or its dynamic change during treatment, may also be used as markers for patient stratification, disease prognosis, and response to treatment. Further investigations of methylation modifications as therapeutic biomarkers, which may correlate with therapeutic response and/or predict treatment toxicity, are still warranted.

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