Evidence map›Paper›PMID 18347132›Full record

ReviewMolecular cancer therapeutics2008

Turning the gene tap off; implications of regulating gene expression for cancer therapeutics.

James F Curtin, Marianela Candolfi, Weidong Xiong, Pedro R Lowenstein, Maria G Castro

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular cancer therapeutics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Engineering theFrontiers in pharmacology · 2021
    Article
  3. A computational analysis of pro-angiogenic therapies for peripheral artery disease.Integrative biology : quantitative biosciences from nano to macro · 2018
    Article
  4. Article
  5. Article
  6. Review
  7. Recombinant adenovirus-p53 (Gendicine) sensitizes a pancreatic carcinoma cell line to radiation.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2013
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Release of HMGB1 in response to proapoptotic glioma killing strategies: efficacy and neurotoxicity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

James F CurtinUniversity of California-Los Angeles and Cedars Sinai Medical Center, Los Angeles, CA 90048, USA.
Marianela Candolfi
Weidong Xiong
Pedro R Lowenstein
Maria G Castro
University of California, Los Angeles · USUCLA Jonsson Comprehensive Cancer Center

Funding

Trophic gene transfer in MPTP animalsU54NS045309 · NINDS · UNIVERSITY OF ROCHESTER · PI FEDEROFF, HOWARD J. · 2002 to 2006
$9.7M
Gutless Adenovirus Mediated Gene Therapy for GliomaU01NS052465 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CASTRO, MARIA G · 2007 to 2011
$3.1M
Gene therapy for chronic neurodegenerative disordersR01NS044556 · NINDS · CEDARS-SINAI MEDICAL CENTER · PI CASTRO, MARIA G · 2002 to 2006
$2.0M
Gene Therapy for Neurological DiseasesR01NS042893 · NINDS · CEDARS-SINAI MEDICAL CENTER · PI LOWENSTEIN, PEDRO R · 2002 to 2006
$1.8M
Gene Therapy and the Brain: Neuroimmune InteractionsR01NS054193 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOWENSTEIN, PEDRO R. · 2007 to 2011
$1.6M
Targeted Toxin for Brain Cancer Gene TherapyR21NS054143 · NINDS · CEDARS-SINAI MEDICAL CENTER · PI CASTRO, MARIA G · 2007 to 2008
$383k
Gene Therapy for GliomaR21NS047298 · NINDS · CEDARS-SINAI MEDICAL CENTER · PI LOWENSTEIN, PEDRO R · 2003 to 2004
$354k
Gutless Adenovirus Mediated Targeted Therapeutics for GliomaF32NS058156 · NINDS · CEDARS-SINAI MEDICAL CENTER · PI CANDOLFI, MARIANELA · 2007 to 2009
$154k
APOPTOSIS OF ANTERIOR PITUITARY CELLSR03TW006273 · FIC · CEDARS-SINAI MEDICAL CENTER · PI CASTRO, MARIA G · 2004 to 2006
$102k
FIC NIH HHS 1 R03 TW 006273-01FIC NIH HHS R03 TW006273NINDS NIH HHS 1 F32 NS 058156-01NINDS NIH HHS 1 R01 NS 054193-01NINDS NIH HHS 1 R01 NS 44556-01NINDS NIH HHS 1 R21 NS 047298-01NINDS NIH HHS 1 R21 NS 054143-01NINDS NIH HHS 1 U01 NS 052465-01NINDS NIH HHS F32 NS058156NINDS NIH HHS NS 445561NINDS NIH HHS R01 NS042893NINDS NIH HHS R01 NS044556NINDS NIH HHS R01 NS054193NINDS NIH HHS R01 NS 42893-01NINDS NIH HHS R21 NS047298NINDS NIH HHS R21 NS054143NINDS NIH HHS U01 NS052465NINDS NIH HHS U54 NS045309NINDS NIH HHS U54 NS 045309-01
6 · The paper itself

Abstract

Cancer poses a tremendous therapeutic challenge worldwide, highlighting the critical need for developing novel therapeutics. A promising cancer treatment modality is gene therapy, which is a form of molecular medicine designed to introduce into target cells genetic material with therapeutic intent. Anticancer gene therapy strategies currently used in preclinical models, and in some cases in the clinic, include proapoptotic genes, oncolytic/replicative vectors, conditional cytotoxic approaches, inhibition of angiogenesis, inhibition of growth factor signaling, inactivation of oncogenes, inhibition of tumor invasion and stimulation of the immune system. The translation of these novel therapeutic modalities from the preclinical setting to the clinic has been driven by encouraging preclinical efficacy data and advances in gene delivery technologies. One area of intense research involves the ability to accurately regulate the levels of therapeutic gene expression to achieve enhanced efficacy and provide the capability to switch gene expression off completely if adverse side effects should arise. This feature could also be implemented to switch gene expression off when a successful therapeutic outcome ensues. Here, we will review recent developments related to the engineering of transcriptional switches within gene delivery systems, which could be implemented in clinical gene therapy applications directed at the treatment of cancer.

Indexed as

Gene Expression RegulationAnimalsAntineoplastic AgentsHumansNeoplasmsAntineoplastic Agents

Identifiers

PMID18347132
PMCPMC2593107
OpenAlexW2111225862

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.