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Background  The mechanisms of chemoresistance in ovarian cancer patients remain largely to be elucidated. Paclitaxel/cisplatin combination is the standard chemotherapeutic treatment for this disease, although some patients do not respond to therapy. Our goals were to investigate whether  TUBB  mutations and mismatch repair defects underlie paclitaxel and cisplatin resistance.    Methods  Thirty-four patients with primary ovarian carcinomas (26 serous and eight clear cell carcinomas) treated with paclitaxel/cisplatin were analysed.  TUBB  exon 4 was analysed by nested PCR after a first round PCR using intronic primers. Microsatellite analysis was performed with the quasimonomorphic markers BAT 26 and BAT 34.    Results  Twenty-two of the 34 ovarian cancers (64.7%) presented residual tumour after surgery, seven of which (7/22; 31.8%) were shown to be chemoresistant (five serous and two clear cell tumours). Sequence analysis did not find any mutation in  TUBB  exon 4. Microsatellite instability was not detected in any of the ovarian carcinomas.    Conclusion  We conclude that  TUBB  exon 4 mutations and mismatch repair defects do not play a significant role in paclitaxel/cisplatin resistance.

No significant role for beta tubulin mutations and mismatch repair defects in ovarian cancer resistance to paclitaxel/cisplatin