Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

lncRNA - Long Non-coding RNAs

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Time-to-progression ratio as a potential study endpoint in early-phase oncology trials: pooled analysis of phase II trials from the Australian MoST program.

Future oncology (London, England)·2026

Same author

BRAF-targeted therapy in non-melanomatous BRAF-mutant tumours: a systematic review of broad but histology-modulated efficacy.

International journal of clinical oncology·2026

Same author

Nivolumab and ipilimumab combination treatment in patients with advanced intrahepatic cholangiocarcinoma and gallbladder cancer: Results from the phase II MoST-CIRCUIT trial.

Clinical cancer research : an official journal of the American Association for Cancer Research·2026

Same author

Impact of Spiritual Wellbeing in Advanced Cancer Patients Receiving Genomic Test Results.

Psycho-oncology·2026

Same author

Challenging interpretation of low-level PTCH1 mosaicism in patients with clinically diagnosed Gorlin syndrome: a case series and review of the literature.

Hereditary cancer in clinical practice·2026

Same author

Genomic Therapy Matching in Rare and Refractory Cancers.

JAMA oncology·2026

Search research articles

Related Experiment Video

Updated: May 4, 2026

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos

Published on: December 13, 2018

Nutlin-3a efficacy in sarcoma predicted by transcriptomic and epigenetic profiling.

Kathleen I Pishas¹, Susan J Neuhaus, Mark T Clayer

¹Authors' Affiliations: Sarcoma Research Group, Discipline of Medicine, Centre for Personalised Cancer Medicine, Faculty of Health Sciences, School of Molecular and Biomedical Science, Departments of Orthopaedics and Trauma and Haematology, Cancer Clinical Trials Unit, Royal Adelaide Hospital; Department of Surgery, Royal Adelaide Hospital and University of Adelaide; ACRF Cancer Genomics Facility, Centre for Cancer Biology, Division of Tissue Pathology, SA Pathology; Centre for Neurological Diseases, Hanson Institute and SA Pathology; Department of Radiology, Queen Elizabeth Hospital; Department of Haematology and Oncology, Basil Hetzel Institute and Queen Elizabeth Hospital; University of Adelaide, Discipline of Surgery, Basil Hetzel Institute, Adelaide; Sarcoma Genomics and Genetics Laboratory, Peter MacCallum Cancer Centre, Melbourne, Australia; and Department of Medical Oncology, The Royal Melbourne Hospital, Parkville, Australia.

Cancer Research

|December 17, 2013

Summary

This summary is machine-generated.

Nutlin-3a efficacy in sarcoma treatment is not predicted by TP53 pathway alterations. Global gene expression and epigenetic status, not MDM2 amplification, determine sarcoma sensitivity to p53/MDM2 antagonists.

More Related Videos

Author Spotlight: Finding New Therapeutic Targets for Malignant Peripheral Nerve Sheath Tumor Through Genome-Scale shRNA Screens

Author Spotlight: Finding New Therapeutic Targets for Malignant Peripheral Nerve Sheath Tumor Through Genome-Scale shRNA Screens

Published on: August 25, 2023

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Related Experiment Videos

Last Updated: May 4, 2026

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos

Published on: December 13, 2018

Author Spotlight: Finding New Therapeutic Targets for Malignant Peripheral Nerve Sheath Tumor Through Genome-Scale shRNA Screens

Author Spotlight: Finding New Therapeutic Targets for Malignant Peripheral Nerve Sheath Tumor Through Genome-Scale shRNA Screens

Published on: August 25, 2023

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Nutlin-3a, a p53/MDM2 antagonist, is investigated for sarcoma treatment.
Understanding sarcoma sensitivity mechanisms to Nutlin-3a is crucial for therapeutic development.

Purpose of the Study:

To investigate the molecular mechanisms of sarcoma sensitivity to Nutlin-3a.
To identify reliable biomarkers for predicting Nutlin-3a response in sarcomas.

Main Methods:

Ex vivo tissue explant system with 24 sarcoma biopsies.
Analysis of TP53 pathway alterations (TP53 status, MDM2/MDM4 amplification/expression, MDM2 SNP309, TP53 SNP72).
RNA sequencing for global transcriptomic profiling and expression profiling of TP53 target genes.
DNA methylation analysis of the GADD45A promoter region.

Main Results:

TP53 pathway alterations did not correlate with apoptotic or cytostatic responses to Nutlin-3a.
MDM2 status was not a predictor of Nutlin-3a sensitivity.
Global transcriptomic profiles robustly predicted apoptotic responses.
Hypermethylation of the GADD45A promoter was observed in non-responsive wild-type TP53 sarcomas.

Conclusions:

Sarcoma sensitivity to Nutlin-3a is not determined by TP53 pathway alterations or MDM2 amplification.
Global gene expression profiles and epigenetic status are key determinants of sarcoma response to p53/MDM2 antagonists.
GADD45A promoter hypermethylation offers mechanistic insight into Nutlin-3a resistance in sarcomas.