Article citationsMore>>

Vermorken, J.B., Remenar, E., van Herpen, C., Gorlia, T., Mesia, R., Degardin, M., Stewart, J.S., Jelic, S., Betka, J., Preiss, J.H., van den Weyngaert, D., Awada, A., Cupissol, D., Kienzer, H.R., Rey, A., Desaunois, I., Bernier, J. and Lefebvre, J.L. (2007) Cisplatin, Fluorouracil, and Docetaxel in Unresectable Head and Neck Cancer. The New England Journal of Medicine, 357, 1695-1704.
http://dx.doi.org/10.1056/NEJMoa071028

has been cited by the following article:

• TITLE: High Incidence of Null-Type Mutations of the TP53 Gene in Japanese Patients with Head and Neck Squamous Cell Carcinoma

  AUTHORS: Yasuhiro Ebihara, Miwako Iwai, Ken Akashi, Takeshi Ito, Go Omura, Yuki Saito, Masafumi Yoshida, Mizuo Ando, Takahiro Asakage, Tatsuya Yamasoba, Yoshinori Murakami

  KEYWORDS: Head and Neck Squamous Cell Carcinoma, TP53 Mutation, KRAS, EGFR, Molecular Marker

  JOURNAL NAME: Journal of Cancer Therapy, Vol.5 No.7, June 12, 2014

  ABSTRACT: Objective: Molecular targeting therapy has not been generally established in head and neck squamous cell carcinoma (HNSCC) except for cetuximab treatment for targeting epidermal growth factor receptor (EGFR). We analyzed alterations of the TP53, KRAS2, and EGFR genes in Japanese HNSCC to identify subpopulations of tumors potentially susceptible or not susceptible to specific therapy based on their genetic alterations. Materials and Methods: A total of 56 Japanese subjects were included in this study. Genomic DNA of exons 5 - 9 of the TP53, exons 1 and 2 of the KRAS2, exons 19 - 22 of the EGFR, and their flanking sequences were amplified by polymerase chain reaction (PCR) followed by direct sequencing. Splicing variants of EGFR were examined by reverse transcription (RT)-PCR. Results: Mutations of the TP53 and KRAS genes were detected in 25 (45%) and 2 (4%) of 56 HNSCC cases, respectively, while neither mutation nor splicing variant of EGFR was observed. The TP53 mutation did not correlate with clinical stages or primary sites of the tumors. The patterns of nucleotide substitutions specific to HNSCC were not observed. However, the incidence of null-type mutations of the TP53, which cannot be detected as abnormal by conventional immunohistochemical (IHC) studies, was significantly higher (10/25; 40%) than that of HNSCC reported in other countries. Conclusion: Frequent TP53 mutations, especially null-type mutations, but infrequent or no alterations of the KRAS and EGFR suggest that the sequencing analysis of theTP53 mutation rather than IHC analysis of p53 provides a potentially useful marker to predict the response of HNSCC to chemotherapy or radiotherapy.