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Record W2497554238 · doi:10.1017/cbo9781107337459.020

Signaling network analysis of genomic alterations predicts breast cancer drug targets

2015· book-chapter· en· W2497554238 on OpenAlexaff
Naif Zaman, Edwin Wang

Bibliographic record

VenueCambridge University Press eBooks · 2015
Typebook-chapter
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicBioinformatics and Genomic Networks
Canadian institutionsMcGill University
Fundersnot available
KeywordsBreast cancerBiologyCancerGenomeComputational biologyGenomicsGenome instabilityGeneticsGeneDNADNA damage

Abstract

fetched live from OpenAlex

Introduction Thousands upon thousands of tumors have been sequenced so far, representing over 20 different cancer types. These efforts allowed scientists to take a closer look at the genomic alterations (i.e., mutations and copy number variations) within a tumor's genome, in order to be able to potentially explain the underlying mechanism that drives cancer cell survival and proliferation (Banerji et al ., 2012; Cancer Genome Atlas Network, 2012; Stephens et al ., 2012). However, extracting useful information from a vast source of various data types to establish a link between genomic alterations and the driving force behind cancer cells remains a challenge (Chin et al ., 2011). Over the past decades of cancer research, scientists have learned that during the evolution of normal cells to cancer cells, different genomic alterations are compiled. These alterations can impact gene expression and protein function to modulate certain fundamental characteristics (i.e., cancer hallmarks) of a cancer cell. Cell survival, proliferation, and apoptosis are among the most primitive cancer hallmarks (Hanahan and Weinberg, 2011). The accumulation of genomic alterations allows cancer cells to reach a neoplastic state that enables them to proliferate indefinitely and become nearly immortal. However, these changes appear to be random, with no patterns that can be used for classifications of patients or identifying drug targets for treatment. Recent studies (Schlabach et al ., 2008; Silva et al ., 2008) have gone on to identify genes that are required for cancer cell survival and proliferation (i.e., essential genes). They accomplished this by performing a genome-wide RNAi knockdown screening for different cancer cell lines from three different cancer types, whereupon a gene was considered to be an essential gene if the knockdown of that gene reduced the cell's survival and proliferation based on p -values. A key observation to note in these RNAi knockdown studies is that different cancer cell lines had different sets of essential genes, implying that the cancer hallmark traits, such as survival and proliferation, can be affected by different sets of genes. This was true for cell lines that belong to the same cancer type. Therefore, no two lung cancer cell lines, for example, had identical sets of essential genes, although there was some overlap. In addition, there was no one gene that appeared to be essential across all the different lung cancer cell lines.

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)0.001
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Simulation or modeling · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.004
Threshold uncertainty score0.014

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.001
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0000.001
Bibliometrics0.0020.002
Science and technology studies0.0000.000
Scholarly communication0.0010.001
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0040.001

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 head0.013
GPT teacher head0.201
Teacher spread0.188 · 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 designSimulation or modeling
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".

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Citations0
Published2015
Admission routes1
Has abstractyes

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