Evidence map›Paper›PMID 20412787›Full record

ReviewBiochemical pharmacology2010

Using genetics and genomics strategies to personalize therapy for cancer: focus on melanoma.

Katherine L Nathanson

Abstract readReview
In one paragraph

Review in Biochemical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Genotyping of cutaneous melanoma.Chinese clinical oncology · 2014
    Article
  6. Article
  7. Has discovery-based cancer research been a bust?Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2013
    Article
  8. Review
  9. The role of CCND1 alterations during the progression of cutaneous malignant melanoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. 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

1 author at 1 institution in 1 country.

Katherine L Nathanson351 BRB 2/3, University of Pennsylvania School of Medicine, 421 Curie Blvd, Philadelphia, PA 19104, United States. knathans@mail.med.upenn.edu
University of Pennsylvania · US

Funding

Tissue &PathologyP50CA093372 · NCI · WISTAR INSTITUTE · PI HERLYN, MEENHARD F · 2001 to 2009
$15.4M
Inherited genetic variation and predisposition to testicular germ cell tumorR01CA114478 · NCI · UNIVERSITY OF PENNSYLVANIA · PI NATHANSON, KATHERINE L. · 2007 to 2011
$3.1M
Somatic genetic predictors of response to therapy in metastatic melanomaR01CA118871 · NCI · UNIVERSITY OF PENNSYLVANIA · PI NATHANSON, KATHERINE L. · 2007 to 2011
$1.5M
NCI NIH HHS P50 CA093372NCI NIH HHS R01 CA114478NCI NIH HHS R01 CA118871
6 · The paper itself

Abstract

Individualizing therapeutic selection for patients is a major goal in cancer treatment today. This goal is best facilitated by understanding both an individual's inherited genetic variation and the somatic genetic changes arising during cancer development. Clinical decision making based on inherited genetic variation is done for those patients with cancer susceptibility syndromes and more generally to personalize drug dosing. Personalized medicine based on genetic and genomic changes within tumors is being applied more widely, with increased use of therapies targeted to somatic mutations and amplifications. Somatic mutations associated with resistance also are being used to select against therapies. Somatic point mutation testing being used clinically includes direct sequencing, short sequencing and single nucleotide interrogation. Single amplifications are commonly assessed using FISH or CISH; high throughput assessment of amplifications and deletions is done mainly on a research basis. Melanomas contain complex mutational profiles that allow them to be sub-grouped by their genetic and genomic profile, each of which then can be evaluated pre-clinically to determine their response to targeted therapies. BRAF V600E mutations are the most common found in melanoma; specific inhibitors of mutant BRAF have been developed and are currently in clinical trials. In addition, other melanoma sub-groups have been identified genetically, which respond to other inhibitors. These studies focus on somatic genetic changes in cancer, which can be targeted directly by therapies. However in the future, personalized medicine will use a combination of inherited and somatic genetics to select the optimal tailored therapy for each patient.

Indexed as

Genome, HumanPrecision MedicineHumansMelanomaMutationNucleic Acid Hybridization

Identifiers

PMID20412787
PMCPMC2897934
OpenAlexW2065775098

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.