Evidence map›Paper›PMID 33842931›Full record

ArticleF1000 faculty reviews2015

Targeting metastatic breast cancer: problems and potential.

Sarah Deasy, Karol Szczepanek, Kent W Hunter

Open access · goldAbstract read
In one paragraph

Article in F1000 faculty reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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 2 institutions in 1 country.

Sarah DeasyMetastasis Susceptibility Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Karol SzczepanekMetastasis Susceptibility Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Kent W HunterMetastasis Susceptibility Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
National Cancer Institute · USGeorge Washington University · US

Funding

GENETIC MODIFIERS OF MAMMARY CANCER INITIATION/ PROGRESSZ01CP010146 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI HUNTER, KENT WILLIAM · 2000 to 2008
$3.3M
Intramural NIH HHS Z01 CP010146Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

Breast cancer is one of the leading causes of cancer-related mortality of women in the United States. Since the majority of cancer deaths are due to metastases rather than the primary tumor, a better understanding of the biological mechanisms that lead to metastatic disease is critical to reduce breast cancer associated mortality. Current adjuvant therapies use the same broadly cytotoxic and targeted strategies against metastases as are used against the primary tumor. However, resistance to chemotherapy due to the cellular dormancy, high genotypic and phenotypic heterogeneity between primary tumor and metastases as well as among individual metastases, and the limitations in detection of disseminated tumor cells and micrometastases significantly hinder the efficiency of currently available therapies. While it is crucial to directly address the issue of metastatic dormancy and evaluate for anti-metastatic therapy the relevance of molecular targets chosen based on primary tumor profiling, it is also imperative to address metastasis-specific mechanisms of growth and survival that are likely to be distinct from those of the primary tumor. We believe that a three-pronged approach to therapy will be necessary to deal with progressive disease: blocking of further dissemination after diagnosis; eradication of disseminated tumor cells and prevention of the dormant-to-proliferative switch of those remaining; and elimination of established metastatic tumors. The implementation of this strategy requires a greater depth of knowledge of metastasis driver and maintenance genes and suggests the need for a "Metastasis Genome Atlas" project to complement the current investigations into cancer genomic landscapes.

Identifiers

PMID33842931
PMCPMC8034283
OpenAlexW2112761094

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.