ライフサイエンスコーパス: ADCA

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1 cancer in 181 tissue samples (31 MPM and 150 ADCA).

2 A training set of 32 samples (16 MPM and 16 ADCA) was used to identify pairs of genes with highly si

3 leural mesothelioma (MPM)and adenocarcinoma (ADCA) of the lung can be cumbersome using established me

4 lung cancer (SCLC) and lung adenocarcinoma (ADCA) exhibit unique immune cell composition of the tumo

5 Ms, from a control pulmonary adenocarcinoma (ADCA), and from normal lung tissue.

6 CAs) constituted one group, adenocarcinomas (ADCAs) clustered separately, and one signet-ring carcino

7 e SCA2 mutation is the most frequent amongst ADCA I patients, accounting for 40%, compared with SCA1

8 hese neurological signs were also seen in an ADCA I family in which the SCA2 mutation was not identif

9 HSAN IE and ADCA-DN are two extreme phenotypic manifestations of a D

10 ype of autosomal dominant cerebellar ataxia (ADCA) in which pure cerebellar ataxia is often accompani

11 s with autosomal dominant cerebellar ataxia (ADCA) types I, II and III, and 47 isolated cases with id

12 ly of autosomal dominant cerebellar ataxias (ADCA), a genetically heterogeneous group of neurodegener

13 The autosomal dominant cerebellar ataxias (ADCAs) are a clinically and genetically heterogeneous gr

14 The dominant cerebellar ataxias (ADCAs) represent a clinically and genetically heterogene

15 henotype, but in none of those with ADCA II, ADCA III or ILOCA confirms the specificity of this mutat

16 t the differential diagnoses of MPM and lung ADCA were 95% and 99% accurate, respectively.

17 ding of reduced CD8(+) content in human lung ADCA.

18 wledge of the immune cell contexture of lung ADCA and SCLC and suggest that molecular and histologica

19 mune cell content using three models of lung ADCA driven by mutations in Kras, p53, and Egfr Although

20 markedly reduced in SCLC compared with lung ADCA, which was validated in human lung cancer specimens

21 cerebellar ataxia, deafness and narcolepsy (ADCA-DN).

22 Phenotypic characterization pinpoints that ADCA-DN and HSAN IE represent two discrete clinical enti

23 ma was in its own cluster, distinct from the ADCA cluster.

24 A clinical comparison of the ADCA I patients with the three known mutations (SCA1, -2

25 2 mutation in 31 out of 38 families with the ADCA I phenotype, but in none of those with ADCA II, ADC

26 The utility of genetic classification of the ADCAs has been highlighted by the striking variability i

27 constitute >40% of the mutations leading to ADCA I in our population.

28 SCA2 accounts for 13% of patients with ADCA (without retinal degeneration), intermediate betwee

29 cting exon 21 of DNMT1 gene in patients with ADCA-DN, a novel heterozygous point mutation in exon 20

30 ADCA I phenotype, but in none of those with ADCA II, ADCA III or ILOCA confirms the specificity of t

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