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ER+ PR- breast cancer defines a unique subtype of breast cancer that is driven by growth factor signaling and may be more likely to respond to EGFR targeted therapies

2006· article· en· W1797772724 on OpenAlexaff
Richard S. Finn, Judy Dering, Charles Ginther, Michael F. Press, J. Forbes, J. Mackey, Tim French, Michael S. South, Matthieu Rupin, DJ Slamon

Bibliographic record

VenueJournal of Clinical Oncology · 2006
Typearticle
Languageen
FieldMedicine
TopicHER2/EGFR in Cancer Research
Canadian institutionsAstraZeneca (Canada)
Fundersnot available
KeywordsMedicineBreast cancerGefitinibTissue microarrayCancerInternal medicineOncologyEstrogen receptorMicroarrayCancer researchImmunohistochemistryEpidermal growth factor receptorFulvestrantPathologyGene expressionBiologyGene

Abstract

fetched live from OpenAlex

514 Background: Hormonal based therapy has long been the mainstay for treatment of ER+ breast cancer. ER+ PR- disease is now known to exhibit different clinical behavior compared to ER+PR+ disease. Recent data indicate that ER+PR- disease is characterized by a lower response rate to estrogen deprivation, has a worse prognosis compared to ER+ PR+ disease, and may be dependent on other signaling pathways. To evaluate the role of the EGFR tyrosine kinase inhibitor gefitnib in the treatment of breast cancer, we conducted a pre-surgical study in women with operable disease. Methods: Frozen core biopsies were obtained at baseline. Patients then received a short-term exposure to gefitinib (at least 2 weeks) prior to definitive surgery when a frozen tumor specimen was obtained. Tissue integrity and composition was verified by H and E and RNA was isolated for microarray analysis. 59 women were enrolled in the study of which 43 were evaluable for molecular analysis. Baseline microarrays were performed on the initial biopsies to classify the ‘subtype‘ of breast cancer (e.g. basal, luminal, HER2 amplified). To analyze the genetic changes that occur in breast cancer tissue with exposure to gefitinib, a direct comparison of the baseline sample and post-treatment tumor was performed. In addition, ER and PR status were determined by immunohistochemistry and compared to the microarray findings. Changes in Ki67 and a set of cell cycle genes were used to define ‘molecular response” to gefitinib. Of the 43 samples evaluated by microarray, 11 patients were categorized as exhibiting molecular growth inhibition, 10 patients as molecular growth proliferation, and 22 did not have a significant change in Ki67 and the cell cycle gene set to assign a response. When grouped by subtype, ER+PR- and HER2 amplified tumors define a subgroup more likely to show molecular growth inhibition with gefitinib. Conversely, ER+PR+ tumors were more likely to show molecular growth proliferation. Conclusions: These results support the hypothesis that ER+PR- breast cancer is growth factor dependent and constitutes a unique subgroup of ER+ patients which may be more likely to benefit from EGFR inhibition. [Table: see text]

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: Observational
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.003
Threshold uncertainty score0.011

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0010.000
Bibliometrics0.0000.001
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0030.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.114
GPT teacher head0.475
Teacher spread0.361 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations15
Published2006
Admission routes1
Has abstractyes

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