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[en] Highlights: • The mutation frequency is unnormalized. • While the mean mutation frequency is infamously erratic, the median mutation frequency is not an effective remedy. • Nonmutant cell death can inflate mutation frequencies. • The mutation rate should be the only yardstick of microbial mutability. - Abstract: The mutation frequency, also known as the mutant frequency, is an unnormalized quantity, and its normalized counterpart is the mutation rate. Due to historical reasons, the mutation frequency has been a predominant yardstick of microbial mutability in the field of mutator identification. While the mean mutation frequency is infamously erratic, replacing it with the median mutation frequency is not an effective remedy. By encouraging investigators to substitute mutation rates for mutation frequencies in microbial research, this paper directs attention to substantial open problems such as false positive control and massive nonmutant cell death.

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[en] Conventional treatment for locally advanced rectal cancer usually combines neoadjuvant radiochemotherapy and surgery. Until recently, there have been limited predictive factors (clinical or biological) for rectal tumor response to conventional treatment. KRAS, BRAF and PIK3CA mutations are commonly found in colon cancers. In this study, we aimed to determine the mutation frequencies of KRAS, BRAF and PIK3CA and to establish whether such mutations may be used as prognostic and/or predictive factors in rectal cancer patients. We retrospectively reviewed the clinical and biological data of 98 consecutive operated patients between May 2006 and September 2009. We focused in patients who received surgery in our center after radiochemotherapy and in which tumor samples were available. In the 98 patients with a rectal cancer, the median follow-up time was 28.3 months (4–74). Eight out of ninety-eight patients experienced a local recurrence (8%) and 17/98 developed distant metastasis (17%). KRAS, BRAF and PIK3CA were identified respectively in 23 (23.5%), 2 (2%) and 4 (4%) patients. As described in previous studies, mutations in KRAS and BRAF were mutually exclusive. No patient with local recurrence exhibited KRAS or PIK3CA mutation and one harbored BRAF mutation (12.5%). Of the seventeen patients with distant metastasis (17%), 5 were presenting KRAS mutation (29%), one BRAF (5%) and one PIK3CA mutation (5%). No relationship was seen between PIK3CA, KRAS or BRAF mutation and local or distant recurrences. The frequencies of KRAS, BRAF and PIK3CA mutations in our study were lower than the average frequencies reported in colorectal cancers and no significant correlation was found between local/distant recurrences and KRAS, BRAF or PIK3CA mutations. Future studies with greater number of patients, longer follow-up time and greater power to predict associations are necessary to fully understand this relationship

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[en] A recent paper by Mothersill and Seymour (1987), and its precursor by Seymour et al. (1986), prompt several comments. The points the letter makes are: (1) the dose-dependence of lethal mutations, or lethal sectoring, in a developing colony can depend upon the cells in question and/or the cell culture conditions which may apply; (2) lethal mutation probably depends upon radiation quality; (3) damage which may give rise to lethal mutations is very likely reparable; and (4) the dose-dependence of the frequency of induction of the neoplastic transformation of C3H 10T1/2 mouse cells, normalized to surviving cells, is probably not influenced by lethal mutations. The reply discusses the distinction between initiation and expression of transformation. (author)

[en] The four indica restorers in the wild abortion hybrid rice system were treated with physical and chemical mutagens, and the mutation frequency in the M₂ generation and the correlation between the heading date of the mutants and other characters were investigated