Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

[EX Q]: Context: DNA methylation at CpG dinucleotides is modified in tumorigenesis with potential impact on transcriptional activity.', 'We used the Illumina 450 K platform to evaluate DNA methylation patterns of 50 metastatic melanoma tumors, with matched gene expression data.', 'We identified three different methylation groups and validated the groups in independent data from The Cancer Genome Atlas. One group displayed hypermethylation of a developmental promoter set, genome-wide demethylation, increased proliferation and activity of the SWI/SNF complex. A second group had a methylation pattern resembling stromal and leukocyte cells, over-expressed an immune signature and had improved survival rates in metastatic tumors (p < 0.05). A third group had intermediate methylation levels and expressed both proliferative and immune signatures. The methylation groups corresponded to some degree with previously identified gene expression phenotypes.
Answer: Melanoma consists of divergent methylation groups that are distinguished by promoter methylation, proliferation and content of immunological cells.
[EX A]: Are dNA methylation subgroups in melanoma associated with proliferative and immunological processes?

[EX Q]: Context: Central core disease is a congenital myopathy, characterized by presence of central core-like areas in muscle fibers. Patients have mild or moderate weakness, hypotonia and motor developmental delay. The disease is caused by mutations in the human ryanodine receptor gene (RYR1), which encodes a calcium-release channel. Since the RYR1 gene is huge, containing 106 exons, mutation screening has been limited to three 'hot spots', with particular attention to the C-terminal region. Recent next-generation sequencing methods are now identifying multiple numbers of variants in patients, in which interpretation and phenotype prevision is difficult.", "In a Brazilian Caucasian family, clinical, histopathological and molecular analysis identified a new case of central core disease in a 48-year female. Sanger sequencing of the C-terminal region of the RYR1 gene identified two different missense mutations: c.14256 A >\u2009C polymorphism in exon 98 and c.14693 T >\u2009C in exon 102, which have already been described as pathogenic. Trans-position of the 2 mutations was confirmed because patient's daughter, mother and sister carried only the exon 98's mutation, a synonymous variant that was subsequently found in the frequency of 013-0,05 of alleles. Further next generation sequencing study of the whole RYR1 gene in the patient revealed the presence of additional 5 common silent polymorphisms in homozygosis and 8 polymorphisms in heterozygosis.
Answer: Considering that patient's relatives showed no pathologic phenotype, and the phenotype presented by the patient is within the range observed in other central core disease patients with the same mutation, it was concluded that the c.14256 A > C polymorphism alone is not responsible for disease, and the associated additional silent polymorphisms are not acting as modifiers of the primary pathogenic mutation in the affected patient. The case described above illustrates the present reality where new methods for wide genome screening are becoming more accessible and able to identify a great variety of mutations and polymorphisms of unknown function in patients and their families.
[EX A]: Do silent polymorphisms in the RYR1 gene modify the phenotype of the p.4898 I > T pathogenic mutation in central core disease : a case report?

[EX Q]: Context: To investigate cellular immune responses to streptococcal antigens in patients with psoriatic arthritis (PsA). To specifically examine responses of the gamma delta + T cell subset.', 'Proliferation of PsA synovial fluid lymphocytes (SFL) and peripheral blood lymphocytes (PBL) cultured with streptococcal antigen was measured using a 3H thymidine (3HTdr) uptake assay system. gamma delta + T cells from PsA PBL and SFL were phenotyped by flow cytometry. Following culture with streptococcal antigen, gamma delta + enriched SFL were sorted by automated flow cytometry and 3HTdr uptake measured.', 'Patients with PsA and the control group did not differ significantly in their PBL responses to 2 strains of streptococci, one of which was isolated from a patient with guttate psoriasis (Strep 1) and the other from a patient with rheumatic fever (Strep 2). There was also no difference in their responses to a cell wall preparation derived from the former strain. SFL from 8 of 9 patients with PsA responded to both streptococcal strains as did SFL from 3 patients with rheumatoid arthritis (RA). gamma delta + SFL from 7 patients with PsA 3 patients with RA responded only to the psoriasis associated strain.
Answer: PsA PBL and SFL responded to stimulation by streptococcal antigen but this reactivity was not disease specific. We have demonstrated that gamma delta + T cells from PsA SF proliferated when cultured with a psoriasis associated strain of streptococcus (Strep 1). However, RA gamma delta + SFL responded similarly suggesting that gamma delta + T cell reactivity to streptococcal antigen may be a feature of inflammatory arthritis.
[EX A]:
Do gamma delta + T cells from patients with psoriatic and rheumatoid arthritis respond to streptococcal antigen?