70P Combination of EGFR-TKI and chemotherapy versus EGFR-TKI monotherapy as neoadjuvant treatment of stage III-N2 EGFR-mutant non-small cell lung cancer
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This study explored the potential benefits of combining first-generation EGFR-TKI with chemotherapy as a neoadjuvant treatment of stage Ⅲ-N2 EGFR-mutant NSCLC patients. The medical records of patients with Ⅲ-N2 EGFR-mutant NSCLC who received neoadjuvant therapy with EGFR-TKI at Shanghai Chest Hospital from October 2011 to October 2022 were retrospectively reviewed. Patients with stage III-N2 EGFR-mutant NSCLC who received first-generation TKI combined with chemotherapy as neoadjuvant treatment were included in the observation group, and those who received EGFR-TKI monotherapy were included in the control group. A total of 74631 EGFR-mutant NSCLC patients were screened, and 60 patients were included, 7 of whom did not undergo surgery after neoadjuvant targeted therapy. Of the remaining 53 patients, 15 received first-generation EGFR-TKI combined with chemotherapy as neoadjuvant treatment, and 38 received EGFR-TKI monotherapy. The median follow-up time was 44.12 months. The ORR was 50.0% (9/18) in the combination group and 40.5% (17/42) in the monotherapy group (p =0.495). MPR was observed in 20.0% (3/15) and 10.5% (4/38) of patients in the combination and monotherapy groups, respectively (p =0.359). No patients achieved PCR in the combination group, while three attained PCR in the monotherapy group. The two groups did not differ in N2 downstaging rate (p =0.459). The median DFS was not reached in the combination group, while it was 23.6 months (95% CI: 8.16-39.02) in the monotherapy group (p = 0.832). Adverse events observed were consistent with those commonly associated with the two treatments. Combination therapy with first-generation EGFR-TKI and chemotherapy could be considered a neoadjuvant treatment option for NSCLC patients of EGFR-mutant stage III-N2, exhibiting acceptable toxicity. However, regarding short-term efficacy, combination therapy did not demonstrate superiority over EGFR-TKI monotherapy. Long-term follow-up is warranted for a more accurate assessment of the DFS and OS.We have isolated a novel enhanced-nodulating mutant astray (Ljsym77) from Lotus japonicus. The name astray derives from the non-symbiotic phenotype of this mutant, agravitropic lateral roots that go “astray” against gravity. In this report we evaluated the symbiotic aspects of this mutant in detail. The astray mutant developed approximately twice the number of nodules on a wider area of roots compared with the wild type. Furthermore, the astray mutant demonstrated early initiation of nodule development, which is an unprecedented symbiotic phenotype. The astray seedlings showed normal sensitivity to the general inhibitors of nodulation such as ethylene and nitrate. These results indicate that the astray mutant is distinct from the hypernodulating mutants reported previously, and that the ASTRAY gene acts as an early and negative regulator in the cascade of nodule development.
Lotus japonicus
Nodule (geology)
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The p53 family of proteins has grown substantially over the last 40 years. It started with p53, then p63, p73, isoforms and mutants of these proteins. The function of p53 as a tumour suppressor has been thoroughly investigated, but the functions of all isoforms and mutants and the interplay between them are still poorly understood. Mutant p53 proteins lose p53 function, display dominant-negative (DN) activity and display gain-of-function (GOF) to varying degrees. GOF was originally attributed to mutant p53′s inhibitory function over the p53 family members p63 and p73. It has become apparent that this is not the only way in which mutant p53 operates as a large number of transcription factors that are not related to p53 are activated on mutant p53 binding. This raises the question to what extent mutant p53 binding to p63 and p73 plays a role in mutant p53 GOF. In this review, we discuss the literature around the interaction between mutant p53 and family members, including other binding partners, the functional consequences and potential therapeutics.
P53 protein
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To investigate the architecture of the rolled leaf morphology in rice,the features of phenotype and histological level in 2 reverse rolled leaf mutants derived from rice Ac/Ds transposons insertional mutant library were investingated. The results showed that the number of bulliform cells was reduced in 2 reverse rolled leaf mutants(Ad-mutant:adaxial rolled mutant;Ab-mutant:abaxial rolled mutant) compared with the normal flat leaf in wild type,which may be an important cause of the rolled leaf in rice. And the number of parenchyma also was reduced and dehisced to 2 large air cavities in Abmutant. The cellulose content of leaf and culm in 2 rolled leaf mutant and wild type was measured,and the result showed that the cellulose content of leaf and culm in Ab-mutant was significant reduced compared with Ad-mutant and wild type.But the cellulose content of leaf and culm in Ad-mutant was not significantly different from that of wild type. This result suggested that Ab-mutant and Ad-mutant may be different in mutation of gene loci. In addition,the genetic rule of Abmutant and Ad-mutant was analyzed,and the result showed that both of them were controlled by single recessive gene.
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Genetic Analysis
Parenchyma
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Nonsense
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Lysogenic cycle
Strain (injury)
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Surgical oncology
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Guanidine
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(1) Three temperature-sensitive mutants were obtained from a microconidial wild type strain of Neurospora crassa. One of them is irreparable at 34°C; that is, it grows as well as the wild type at 23°C, but does not grow on any (including omplete) medium so far tested at 34°C. This mutant was the major subject of this report.(2) The temperature-sensitive irreparable mutant b39 differs from the parent strain by a single gene mutation. The gene responsible for the irreparable character is located on the first linkage group (mating type chromosome), about 30cM left of the centromere.(3) This mutant does not inhibit the growth of the other temperature-sensitive strains in the heterocaryotic condition.(4) The possibility of the accumulation of inhibitory substances by the mutant is unlikely, because the culture filtrate of the mutant did not inhibit the growth of the mutant at an intermediate temperature.(5) The growth characteristics of the mutant when the culture was transfered from 23°C to 34°C, and from 34°C to 23°C were determined.(6) The nature of the defect in an irreparable mutant was discussed.
Neurospora
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Crassa
Strain (injury)
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SUMMARY: An investigation was undertaken to determine to what extent the properties of oligosporogenous (Osp) mutants allow them to be considered as a separate class of sporulation mutant, distinct from asporogenous (Sp-) mutants. Of thirty Osp mutants examined, seventeen at least had a phenotype which had previously been identified with a Sp- mutant. The majority of cells in an Osp culture either reached a particular stage in the sporulation process and then stopped, or in some cases went on to produce aberrant forms. Some of these aberrant forms have their counterparts in Sp- mutants described by other authors, but some present new features. The morphological and biochemical sequences were linked so that if the majority of cells were blocked at a certain stage, then the biochemical sequence stopped accordingly. The general similarity in behaviour between the two types of mutant is consistent with the assumption that at least some of the Osp mutants have leaky mutations in genes where mutation can also give rise to Sp- phenotypes. Evidence is presented to suggest that the ability of a cell of an Osp mutant to overcome its block, and so go on to form a spore, is a chance event when that stage in the process is reached. A mutant has been obtained in which the spores are octanol-resistant yet contain no measurable dipicolinate. In several other mutants the spores contained well-developed coat layers, but the cortex was poorly formed or completely missing.
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