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Attribution caveat first

The supplied records contain full-text content but no author lists. Weidong Le is documented in the literature as an EGFR-endocytosis researcher, yet authorship cannot be confirmed from these records alone — a blind spot BGPT will not paper over. The two papers below are the best-supported candidates; the analysis critiques rigor from full text only.

1. LDOC1–clathrin adaptor paper (IJMS 2024): quantitatively rich, causally incomplete

Controls: Four cell lines spanning EGFR WT (A549, U2OS) and EGFR-mutant (PC9, HCC827) provide an internal isogenic contrast; co-IP, biotinylation endocytosis assays, and rescue-style overexpression (LDOC1-V5) are appropriately triangulated (LDOC1 clathrin adaptor methods).
Statistics: IC50 shifts are the weakest link — PC9 gefitinib IC50 "increased" with exact values unavailable in text; only HCC827 reports numbers (1.8 → 2.3 µM, a modest ~28% shift) and osimertinib shows no change (0.9 µM), a useful internal specificity control. The clinical association is strong (p < 0.001, n = 100 gefitinib-treated) but retrospective and univariate — no multivariable adjustment is reported (LDOC1 IC50 and survival data).
Reproducibility: Supplementary materials and software versions are documented; "no new data created" limits raw-data sharing. No independent shRNA validation or xenograft model — falsification therefore rests on untested shRNA off-targets.

Figure: Cytoplasmic EGFR frequency by LDOC1 status in the 200-patient IHC cohort — the paper's strongest quantitative clinical signal, reproduced directly from reported values.

2. CIN85 phosphorylation paper (MBoC 2012): the most rigorous of the set

Controls: The phospho-defective CIN85-4F mutant preserves Src binding (a critical structural-equivalence control), and SYF triple-kinase MEFs plus Src re-expression (3–4× degradation acceleration) form a genuine epistasis chain — kinase → phosphorylation → c-Cbl binding → ubiquitination → MVB sorting → degradation (CIN85-4F mutant quantitative controls).
Statistics: Reported p-values are specific (p < 0.0005, p < 0.0001) and ≥30 cells per condition were quantified — unusually transparent for trafficking microscopy. Gaps: Overexpression-only systems, four simultaneous Y→F substitutions (structure not checked), ~20–60 min observation windows, and no data-sharing statement (CIN85 paper methodological limitations).

The other three records are not rigor-testable

The SISH screening study (n = 96) has high reproducibility scores but only 10 patient-level rows were extracted; the JTO 2017 abstract has zero references and no numerical IC50 data; the EGFR-landscape review generates no primary evidence. None support a rigorous full-text verdict (EGFR SISH screening cohort study).

Verdict and what would change it

Confidence: moderate. The CIN85 study is the most rigorously controlled; the LDOC1 study is mechanistically detailed but underpowered on in vivo causality and statistical reporting. What would falsify or upgrade the verdict: (1) author-list confirmation that Weidong Le did or did not author these records; (2) raw IC50 dose-response curves from the LDOC1 study; (3) multi-shRNA rescue or CRISPR knockout reproducing the LDOC1 phenotype; (4) independent replication of CIN85-4F in a non-overexpression, genome-edited setting.