Clinicopathological significance and potential drug target of p15INK4B in multiple myeloma

Li, Jun; Bi, Lintao; Lin, Yumei; Lu, Zhenxia; Hou, Gang

doi:10.2147/dddt.s71088

Cited by 11 publications

(10 citation statements)

References 31 publications

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“…Alterations in both p16 and p15 are reported in respectively more than 50% and 67% of the myeloma patients [ 49 ]. However, neither p16 nor p15 methylation is associated with survival in myeloma patients [ 49 , 50 ]. In addition, p18 deletions are found infrequent in myeloma [ 51 – 53 ].…”

Section: Deregulation Of the Cell Cycle In Multiple Myelomamentioning

confidence: 99%

The therapeutic potential of cell cycle targeting in multiple myeloma

Maes

Veirman

et al. 2017

Oncotarget

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Proper cell cycle progression through the interphase and mitosis is regulated by coordinated activation of important cell cycle proteins (including cyclin-dependent kinases and mitotic kinases) and several checkpoint pathways. Aberrant activity of these cell cycle proteins and checkpoint pathways results in deregulation of cell cycle progression, which is one of the key hallmarks of cancer. Consequently, intensive research on targeting these cell cycle regulatory proteins identified several candidate small molecule inhibitors that are able to induce cell cycle arrest and even apoptosis in cancer cells. Importantly, several of these cell cycle regulatory proteins have also been proposed as therapeutic targets in the plasma cell malignancy multiple myeloma (MM). Despite the enormous progress in the treatment of MM the past 5 years, MM still remains most often incurable due to the development of drug resistance. Deregulated expression of the cyclins D is observed in virtually all myeloma patients, emphasizing the potential therapeutic interest of cyclin-dependent kinase inhibitors in MM. Furthermore, other targets have also been identified in MM, such as microtubules, kinesin motor proteins, aurora kinases, polo-like kinases and the anaphase promoting complex/cyclosome. This review will provide an overview of the cell cycle proteins and checkpoint pathways deregulated in MM and discuss the therapeutic potential of targeting proteins or protein complexes involved in cell cycle control in MM.

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Section: Deregulation Of the Cell Cycle In Multiple Myelomamentioning

confidence: 99%

The therapeutic potential of cell cycle targeting in multiple myeloma

Maes

Veirman

et al. 2017

Oncotarget

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“…The other 29 publications were excluded due to lack of full text, for being vitro/ex vivo studies, using cell lines or human xenografts, or being irrelevant studies. 6 , 8 , 25 , 32 – 57 …”

Section: Resultsmentioning

confidence: 99%

“…The data extraction followed the procedure as described by the published literature. 25 Two investigators independently extracted data from eligible studies. Disagreements were resolved by discussion and consensus.…”

Section: Methodsmentioning

confidence: 99%

Clinical significance of DAPK promoter hypermethylation in lung cancer: a meta-analysis

Li¹,

Zhu²,

Cheng³

et al. 2015

DDDT

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Death-associated protein kinase 1 (DAPK) is an important serine/threonine kinase involved in various cellular processes, including apoptosis, autophagy, and inflammation. DAPK expression and activity are deregulated in a variety of diseases including cancer. Methylation of the DAPK gene is common in many types of cancer and can lead to loss of DAPK expression. However, the association between DAPK promoter hypermethylation and the clinicopathological significance of lung cancer remains unclear. In this study, we searched the MEDLINE, PubMed, Web of Science, and Scopus databases, systematically investigated the studies of DAPK promoter hypermethylation in lung cancer and quantified the association between DAPK promoter hypermethylation and its clinicopathological significance by meta-analysis. We observed that the frequency of DAPK methylation was significantly higher in lung cancer than in non-malignant lung tissues (odds ratio 6.02, 95% confidence interval 3.17–11.42, P<0.00001). The pooled results also showed the presence of a prognostic impact of DAPK gene methylation in lung cancer patients (odds ratio 3.63, 95% confidence interval 1.09–12.06, P=0.04). In addition, we summarized these findings and discuss tumor suppressor function, clinicopathological significance, and potential drug targeting of DAPK in lung cancer.

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“…23 Both genes are members of the INK4 family of cyclin-dependent kinase (CDK) inhibitors located at the same chromosomal region. Accumulation of methylation aberrancies at their promoter region, which is common mechanism for loss of tumor suppressor genes function, 24 represent potential step towards development of malignancies.…”

Section: Discussionmentioning

confidence: 99%