Evidence map›Paper›PMID 19011599›Full record

ArticleCancer gene therapy2009

Potentiation of methoxymorpholinyl doxorubicin antitumor activity by P450 3A4 gene transfer.

H Lu, C-S Chen, D J Waxman

Open access · greenAbstract read
In one paragraph

Article in Cancer gene therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.2field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Enhancement of Tumor Cell Death by CombiningFrontiers in pharmacology · 2018
    Article
  5. Effects of traditional herbal formulae on human CYP450 isozymes.Chinese journal of integrative medicine · 2017
    Article
  6. Review
  7. EET signaling in cancer.Cancer metastasis reviews · 2011
    Review
  8. Review
  9. Review
  10. Article
  11. Targeting drug-metabolizing enzymes for effective chemoprevention and chemotherapy.Drug metabolism and disposition: the biological fate of chemicals · 2010
    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

3 authors at 1 institution in 1 country.

H LuDepartment of Biology, Division of Cell and Molecular Biology, Boston University, Boston, MA 02215, USA.
C-S Chen
D J Waxman
Boston University · US

Funding

HEPATIC METABOLISM OF ANTICANCER DRUGSR01CA049248 · NCI · DANA-FARBER CANCER INSTITUTE · PI WAXMAN, DAVID J · 1991 to 2014
$4.3M
NCI NIH HHS CA49248NCI NIH HHS R01 CA049248
6 · The paper itself

Abstract

Preclinical and clinical studies of CYP gene-directed enzyme prodrug therapy have been focused on anticancer prodrugs activated by CYP2B enzymes, which have low endogenous expression in human liver; however, the gene therapeutic potential of CYP3A enzymes, which are highly expressed in human liver, remains unknown. This study investigated methoxymorpholinyl doxorubicin (MMDX; nemorubicin), a novel CYP3A-activated anticancer prodrug. Retroviral transfer of CYP3A4 increased 9L gliosarcoma cell chemosensitivity to MMDX 120-fold (IC(50)=0.2 nM in 9L/3A4 cells). In CHO cells, overexpression of P450 reductase in combination with CYP3A4 enhanced chemosensitivity to MMDX, and to ifosfamide, another CYP3A4 prodrug, 11- to 23-fold compared with CYP3A4 expression alone. CYP3A4 expression and MMDX chemosensitivity were increased in human lung (A549) and brain (U251) tumor cells infected with replication-defective adenovirus encoding CYP3A4. Coinfection with Onyx-017, a replication-conditional adenovirus that coamplifies and coreplicates the Adeno-3A4 virus, led to large increases in CYP3A4 RNA but only modest increases in CYP3A4 protein and activity. MMDX induced remarkable growth delay of 9L/3A4 tumors, but not the P450-deficient parental 9L tumors, in immunodeficient mice administered low-dose MMDX either intravenous or by direct intratumoral (i.t.) injection (60 microg kg(-1), every 7 days x 3). Notably, the i.t. route was substantially less toxic to the mouse host. No antitumor activity was observed with intraperitoneal MMDX treatment, suggesting a substantial hepatic first pass effect, with activated MMDX metabolites formed in the liver having poor access to the tumor site. These studies demonstrate that human CYP3A4 has strong potential for MMDX prodrug-activation therapy and suggest that endogenous tumor cell expression of CYP3A4, and not hepatic CYP3A4 activity, is a key determinant of responsiveness to MMDX therapy in cancer patients in vivo.

Indexed as

AdenoviridaeAnimalsAntineoplastic AgentsCell Line, TumorCHO CellsCricetinaeCricetulusCytochrome P-450 CYP3ACytochrome P-450 Enzyme SystemDoxorubicinGenetic TherapyGenetic VectorsGene Transfer TechniquesHumansIfosfamideMiceAntineoplastic AgentsCYP3A4 protein, humanCytochrome P-450 CYP3ACytochrome P-450 Enzyme SystemDoxorubicinIfosfamidemethoxy-morpholinyl-doxorubicin

Identifiers

PMID19011599
PMCPMC2669851
OpenAlexW2113451457

What OpenQuestion holds

Textmetadata
LicenceTDM
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.