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In two patients, there were concomitant mutations of KRAS codon 146 and PIK3CA exon 9 and NRAS codon 61and PIK3CA exon 9. Patients with genomic mutations achieved no response to anti-EGFR antibodies (SD: N=6, PD: N=12).
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Hormonal therapies as adjuvant treatment and/or for metastatic disease (⩽2) were also allowed provided there was a 4-week interval between the last hormonal treatment and study entry in patients who achieved a response (no time interval was required for patients with no response).
The primary efficacy end point was the proportion of subjects who achieved complete response (CR; no vomiting and no use of rescue medication) during the delayed phase (25 120 h following initiation of the first MEC dose).
In particular, for those patients who had achieved little or no response to preoperative chemotherapy, the use of alternative forms of adjuvant therapy could be considered to improve outcomes.
The 18 patientes evaluable for response achieved complete clinical response after EBRT.
No patient achieved a complete response, while six (7.0%) experienced a partial response (PR) (overall response rate=7.0%95%5% CI=1.59 12.36) and 40 (46.5%) stable disease (SD); the disease control rate (DCR; PR+SD) was 53.5% (95% CI=42.95 64.03%).
No patients with del(17p) achieved a response.
If the patient achieved complete response, incisional biopsy of previous lesion was performed to confirm no residual tumour.
By longer treatment, beyond the achieved response, we do not obtain higher response.
Optimization was achieved by response surface method.
Even after all the effort, that survey achieved a response rate of 22percentt.
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