# RF-003 — More tumours in chemically initiated mice

Why this matters
In mice given a cancer-causing chemical, some RF-exposed groups developed more tumours. The study raises a health-protection question about combined exposures and susceptibility: could the response depend on an existing biological vulnerability? It cannot show what RF alone would do, and the pattern did not rise steadily with dose.

Id: RF-003

Author: Lerchl et al.

Full Authors: Alexander Lerchl; Melanie Klose; Karen Grote; Adalbert F.X. Wilhelm; Oliver Spathmann; Thomas Fiedler; Joachim Streckert; Volkert Hansen; Markus Clemens

Year: 2015

Title: Tumor promotion by exposure to radiofrequency electromagnetic fields below exposure limits for humans

Journal: biochemical and biophysical research communications

Citation: Lerchl A, Klose M, Grote K, Wilhelm AFX, Spathmann O, Fiedler T, Streckert J, Hansen V, Clemens M. Tumor promotion by exposure to radiofrequency electromagnetic fields below exposure limits for humans. Biochemical and Biophysical Research Communications. 2015; 459(4): 585-590. doi:10.1016/j.bbrc.2015.02.151.

Doi: 10.1016/j.bbrc.2015.02.151

Pmid: 25749340

Topic: Tumours

Verification Group: Original text reviewed

Record Role: Original text reviewed

Featured: True

Exposure: UMTS; nominal whole-body SAR 0/0.04/0.4/2 W/kg, gestational day 6 onward; maternal ENU 40 mg/kg injection on day 14; 23.5 h/day for 72 weeks. Freely moving three-mouse cages; reference 20 g/mouse.

Design: 96 female B6C3F1 offspring/group; four ENU groups plus 96 untreated cage controls. Examined organ denominators 91-96. Blinded exposure codes; 107 pathology slides cross-checked externally; Helicobacter PCR negative.

Finding: At 0.04 W/kg, lung adenomas 43/94 vs 22/96 sham (p<.001), liver carcinomas 28/93 vs 13/96 (p<.01). At 0.4 W/kg, lymphoma 23/96 vs 9/96 (p<.01), lung carcinoma 92/96 vs 81/96 (p<.01). One-tailed Fisher tests; no monotonic dose-response; survival unaffected by RF.

Boundary: ENU coexposure; no RF-only experimental group. SAR variability 36% in reference configuration, 30-91% within cages; local maxima 3-5 times whole-body SAR. High-dose amplifier problem for 20 days; terminal sacrifices differed 1-2 weeks. Not a human compliance test.

Related: Replication/extension of RF-004 in different biology laboratory, with shared engineering investigators Streckert/Hansen and similar waveguide programme. Klose 2015 dissertation is related reporting. Lerchl 2020 adduct follow-up is a distinct mechanistic experiment, not tumour replication.

Protection Question: Could RF exposure modify tumour development in an already initiated animal? The nonmonotonic findings and variable absorbed dose leave that question distinct from RF-alone cancer initiation or a human exposure threshold.

Access: Six-page original proof dated 10 March 2015 reviewed, including Table 1; final citation confirmed with Scite/PubMed. Supplements not independently retrieved.

Locator: Proof pp 2-3, sections 2.1-2.4/Table 1; p 4 results; p 5 limitations/funding.

Notice: No correction/retraction/concern located in Scite/PubMed checks 2026-10-20. Nesslany 2015 DOI 10.1016/j.bbrc.2015.09.114 is a comment.

Funding: German Federal Office for Radiation Protection (BfS), which defined principal design with author; authors declare no conflicts.

Conflicts: Authors declare no conflicts or competing interests, as documented in the retrieved source disclosure.

Source Url: https://doi.org/10.1016/j.bbrc.2015.02.151

Retrieval Links: https://doi.org/10.1016/j.bbrc.2015.02.151 | https://pubmed.ncbi.nlm.nih.gov/25749340/ | https://andybromberg.com/assets/pdf/lerchl-2015.pdf

Verification Date: 2026-10-20