Last update 01 Nov 2024

Ferritin x MDM2

Last update 01 Nov 2024

Basic Info

Related Targets

FerritinMDM2

Drugs associated with Ferritin x MDM2

CN116554351

Patent Mining

Target

Ferritin x MDM2

Mechanism-

Active Org.

University of Science & Technology of China

Originator Org.

University of Science & Technology of China

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with Ferritin x MDM2

100 Translational Medicine associated with Ferritin x MDM2

0 Patents (Medical) associated with Ferritin x MDM2

Literatures (Medical) associated with Ferritin x MDM2

01 Aug 2010·Pediatric Blood & CancerQ3 · MEDICINE

MDM2 SNP309 genotype is associated with ferritin and LDH serum levels in children with stage 4 neuroblastoma

Q3 · MEDICINE

Article

Author: Raffaella Defferrari ; Chiara Perfumo ; Gian Paolo Tonini ; Stefano Parodi ; Gilberto Fronza ; Katia Mazzocco ; Riccardo Haupt ; Alberto Garaventa ; Alberto Inga

AbstractBackgroundMDM2 SNP309, characterised by a T‐to‐G substitution in the MDM2 promoter, is associated with higher gene expression compared to wild type and was recently found to be a negative prognostic factor for patients with stage 4 neuroblastoma (NB), but not for children with localised disease. This polymorphism was not associated with any clinical or genetic tumour characteristics, including MYCN amplification and 1p chromosome deletion.ProcedureTo better define the involvement of MDM2 SNP309 in NB, we explored its association with the main biochemical tumour markers, namely urinary concentrations of vanillyl mandelic acid (VMA) and homovanillic acid (HVA) and blood concentrations of ferritin and lactate dehydrogenase (LDH). A cohort of 497 NB children, enrolled in the Italian Neuroblastoma Registry between January 1985 and December 2005 and previously investigated for the prognostic role of MDM2 SNP309, was considered for this study.ResultsVMA and HVA concentrations as well as HVA/VMA ratio were not affected by the MDM2 SNP309 genotype. Ferritin and LDH concentrations were significantly lower in TT than in TG/GG only in patients with stage 4 disease (P = 0.007 and 0.015, respectively). No association emerged in patients with localised disease. These findings were not affected by confounding from clinical or biological characteristics.ConclusionsThe association between MDM2 SNP309 and both ferritin and LDH in patients with stage 4 disease confirms the prognostic role of this polymorphism. The results suggest that the MDM2 SNP309 genotype can impact on tumour responses to hypoxia and might play an important role in the alteration of energetic metabolism in NB cells. Pediatr Blood Cancer. 2010;55:267–272. © 2010 Wiley–Liss, Inc.

01 Jun 2002·Expert Opinion on Therapeutic TargetsQ2 · MEDICINE

Gene targets of antisense therapies in breast cancer

Q2 · MEDICINE

Review

Author: Yang, Ding Cheng ; Elliott, Robert L. ; Head, Jonathan F.

Advances in molecular and cell biology have led to further understanding of the mechanisms of malignant growth and metastasis in human breast cancer cells. Initiation and progression of breast cancer results from mutations and the abnormal expression of many genes that control cellular proliferation, differentiation, invasion, metastasis and sensitivity to therapy (chemotherapy and radiation therapy). Inhibition of host immunity also plays a role in breast cancer progression. Many genes have been selected as targets for antisense therapy, including HER-2/neu, PKA, TGF-alpha, EGFR, TGF-beta, IGFIR, P12, MDM2, BRCA, Bcl-2, ER, VEGF, MDR, ferritin, transferrin receptor, IRE, C-fos, HSP27, C-myc, C-raf and metallothionein genes. The strategy behind antisense therapy is the development of specific therapeutic agents that aim to correct the mutations and abnormal expression of cellular genes in breast tumour cells by decreasing gene expression, inducing degradation of target mRNA and causing premature termination of transcription. Many in vitro and in vivo studies have investigated the therapeutic efficacy of oligonucleotides and antisense RNAs. These studies have demonstrated specific inhibition of tumour cell growth by antisense therapy and have shown synergistic inhibitory effects between antisense oligonucleotides or antisense RNA and conventional chemotherapeutic drugs used in the treatment of breast cancer. Antisense oligonucleotides have been modified to improve their ability to penetrate cells, bind to gene sequences and downregulate target gene function. Many delivery systems for antisense RNA and antisense oligonucleotides have been developed, including virus vectors (retrovirus, adenovirus and adeno-associate virus) and liposomes, to carry the antisense RNA or oligonucleotides through the cell membrane into the cytoplasm and nucleus of the tumour cells. However, in order to determine their feasibility antisense therapies need to be further investigated to determine their antitumour activity, pharmacokinetics and toxicity in breast cancer patients.

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