BGPT: estimate how many peer-reviewed publications exist for direct cellular reprogramming in human cells

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Evidence Gap: Supplied Records Do Not Address Cellular Repprogramming

The provided claim-level evidence records cover EGFR trafficking (LDOC1/clathrin adaptors) in NSCLC, EGFR gene copy number screening, EGFR-TKI sensitivity, EGFR core fucosylation in antiviral immunity, and EGFR-targeted nanoparticles — none report data on direct cellular reprogramming in human cells or publication counts for that field (, ). I cannot estimate a publication count from these sources without confabulating.

What is missing: bibliometric data (PubMed/Europe PMC/Scopus query counts), terminology boundaries (direct/transdifferentiation vs. iPSC-mediated reprogramming), and human-cell inclusion criteria.

Viable query strategy once appropriate sources are available: run MeSH/keyword searches (e.g., "transdifferentiation" + "human"), count results by year, apply inclusion/exclusion screening, and report a range with uncertainty rather than a point estimate — then triangulate across PubMed, Scopus, and Web of Science to bound database-dependent bias.

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Updated: September 23, 2026

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1. LDOC1 interacts with clathrin adaptors AP1M1 and AP2M1 to regulate EGFR internalization and recycling, modulating EGFR signaling and gefitinib response in EGFR-mutant NSCLC, with LDOC1 loss promoting RTK activation and gefitinib resistance while associating with poorer patient outcomes. [2024]

9QualityResults Limitations Context Blindspots Methods Sample Conflict Data

↗ Paper Review ↗ Full Paper

2. This study demonstrates that pSTAT3 transactivates EGFR to maintain EGFR protein homeostasis and contributes to resistance against EGFR tyrosine kinase inhibitors in non-small cell lung cancer cells. [2024]

8QualityResults Limitations Context Blindspots Methods Sample Conflict

↗ Paper Review ↗ Full Paper

3. This study investigates the relationship between EGFR gene copy number alterations and EGFR mutation status in lung adenocarcinoma, concluding that EGFR gene copy number as detected by SISH is not a reliable screening tool for selecting patients for EGFR mutation testing. [2014]

7QualityResults Limitations Context Blindspots Methods Sample Data

↗ Paper Review ↗ Full Paper

4. A comprehensive review of EGFR pathway alterations in NSCLC, detailing activating EGFR mutations, copy-number changes, downstream signaling, predictive biomarkers for EGFR-targeted therapies, and mechanisms of resistance, with emphasis on the need for integrated molecular stratification for personalized treatment. [2011]

8QualityResults Limitations Context Blindspots Methods Sample Conflict

↗ Paper Review ↗ Full Paper

5. The study shows that hepatitis C virus (and other enveloped viruses) upregulates host FUT8 to increase EGFR core fucosylation, activating EGFR-JAK1-STAT3 signaling that recruits Trim40 to promote RIG-I degradation and suppresses type I interferon responses, with FUT8 inhibition or hepatic Fut8 silencing reducing RNA viral replication in vitro and in vivo, revealing a viral immune evasion mechanism and potential antiviral target. [2024]

9QualityResults Limitations Context Blindspots Methods Sample Conflict Data

↗ Paper Review ↗ Full Paper

Key Insight

Publication-count questions are bibliometric, not mechanistic; the supplied evidence layer (EGFR-focused extracts) cannot substitute for database query data, and any precise count would be false precision given terminology ambiguity.

Keep Exploring

How should 'direct cellular reprogramming' be operationally bounded to distinguish it from iPSC-mediated reprogramming in bibliometric searches?

What is the annual growth curve of transdifferentiation publications in human cells since 2008?

Hypothesis Graveyard

Assuming any citation-format record implies topical coverage — records here are EGFR/NSCLC-specific, none touch reprogramming.

Science Art

Science Movie

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Discussion

BGPT Bias

I may over-privilege citation-only sources, leading me to refuse estimates even when general biomedical knowledge could provide a cautious range.

Stay current without chasing every paper.

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Traceable Claims in Bioinformatics

See what computational analyses actually reported, with provenance for every claim.Know what the science actually supports before you trust the answer.

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Long Analysis Plan Copied

Evidence Gap: Supplied Records Do Not Address Cellular Repprogramming

Top Data Sources Export MCP

1. LDOC1 interacts with clathrin adaptors AP1M1 and AP2M1 to regulate EGFR internalization and recycling, modulating EGFR signaling and gefitinib response in EGFR-mutant NSCLC, with LDOC1 loss promoting RTK activation and gefitinib resistance while associating with poorer patient outcomes. [2024]

2. This study demonstrates that pSTAT3 transactivates EGFR to maintain EGFR protein homeostasis and contributes to resistance against EGFR tyrosine kinase inhibitors in non-small cell lung cancer cells. [2024]

3. This study investigates the relationship between EGFR gene copy number alterations and EGFR mutation status in lung adenocarcinoma, concluding that EGFR gene copy number as detected by SISH is not a reliable screening tool for selecting patients for EGFR mutation testing. [2014]

11. Src-mediated phosphorylation of CIN85 after EGF stimulation promotes CIN85 binding to the E3 ligase c-Cbl, enhancing EGFR ubiquitination and sorting into multivesicular bodies for degradation, whereas preventing CIN85 phosphorylation traps EGFR in early endosomes and delays degradation. [2012]

Ask a Follow-Up

Key Insight

Publication-count questions are bibliometric, not mechanistic; the supplied evidence layer (EGFR-focused extracts) cannot substitute for database query data, and any precise count would be false precision given terminology ambiguity.

Keep Exploring

How should 'direct cellular reprogramming' be operationally bounded to distinguish it from iPSC-mediated reprogramming in bibliometric searches?

What is the annual growth curve of transdifferentiation publications in human cells since 2008?

Hypothesis Graveyard

Assuming any citation-format record implies topical coverage — records here are EGFR/NSCLC-specific, none touch reprogramming.

Science Art

Science Movie

Make a narrated HD Science movie for this answer ($32 per minute)

Discussion

BGPT Bias

I may over-privilege citation-only sources, leading me to refuse estimates even when general biomedical knowledge could provide a cautious range.

Stay current without chasing every paper.

My BGPT

Trending

Traceable Claims in Bioinformatics

See what computational analyses actually reported, with provenance for every claim.Know what the science actually supports before you trust the answer.

Explore by Goal

Long Analysis Plan Copied

Evidence Gap: Supplied Records Do Not Address Cellular Repprogramming

Top Data Sources ExportMCP

1. LDOC1 interacts with clathrin adaptors AP1M1 and AP2M1 to regulate EGFR internalization and recycling, modulating EGFR signaling and gefitinib response in EGFR-mutant NSCLC, with LDOC1 loss promoting RTK activation and gefitinib resistance while associating with poorer patient outcomes. [2024]

2. This study demonstrates that pSTAT3 transactivates EGFR to maintain EGFR protein homeostasis and contributes to resistance against EGFR tyrosine kinase inhibitors in non-small cell lung cancer cells. [2024]

3. This study investigates the relationship between EGFR gene copy number alterations and EGFR mutation status in lung adenocarcinoma, concluding that EGFR gene copy number as detected by SISH is not a reliable screening tool for selecting patients for EGFR mutation testing. [2014]

11. Src-mediated phosphorylation of CIN85 after EGF stimulation promotes CIN85 binding to the E3 ligase c-Cbl, enhancing EGFR ubiquitination and sorting into multivesicular bodies for degradation, whereas preventing CIN85 phosphorylation traps EGFR in early endosomes and delays degradation. [2012]

Ask a Follow-Up

Key Insight

Publication-count questions are bibliometric, not mechanistic; the supplied evidence layer (EGFR-focused extracts) cannot substitute for database query data, and any precise count would be false precision given terminology ambiguity.

Keep Exploring

How should 'direct cellular reprogramming' be operationally bounded to distinguish it from iPSC-mediated reprogramming in bibliometric searches?

What is the annual growth curve of transdifferentiation publications in human cells since 2008?

Hypothesis Graveyard

Assuming any citation-format record implies topical coverage — records here are EGFR/NSCLC-specific, none touch reprogramming.

Science Art

Science Movie

Make a narrated HD Science movie for this answer ($32 per minute)

Discussion

BGPT Bias

I may over-privilege citation-only sources, leading me to refuse estimates even when general biomedical knowledge could provide a cautious range.

Stay current without chasing every paper.

My BGPT

Trending

Top Data Sources Export MCP