In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Q: Context: We utilized whole-genome mapping of promoters that are activated by DNA hypomethylation in hepatocellular carcinoma (HCC) clinical samples to shortlist novel targets for anticancer therapeutics. We provide a proof of principle of this approach by testing six genes short-listed in our screen for their essential role in cancer growth and invasiveness.', 'We used siRNA- or shRNA-mediated depletion to determine whether inhibition of these genes would reduce human tumor xenograft growth in mice as well as cell viability, anchorage-independent growth, invasive capacities, and state of activity of nodal signaling pathways in liver, breast, and bladder cancer cell lines.', 'Depletion of EXOSC4, RNMT, SENP6, WBSCR22, RASAL2, and NENF effectively and specifically inhibits cancer cell growth and cell invasive capacities in different types of cancer, but, remarkably, there is no effect on normal cell growth, suggesting a ubiquitous causal role for these genes in driving cancer growth and metastasis. Depletion of RASAL2 and NENF in vitro reduces their growth as explants in vivo in mice. RASAL2 and NENF depletion interferes with AKT, WNT, and MAPK signaling pathways as well as regulation of epigenetic proteins that were previously demonstrated to drive cancer growth and metastasis.\Question: Does genome-wide study of hypomethylated and induced genes in patients with liver cancer unravel novel anticancer targets?

A: Our results prove that genes that are hypomethylated and induced in tumors are candidate targets for anticancer therapeutics in multiple cancer cell types. Because these genes are particularly activated in cancer, they constitute a group of targets for specific pharmacologic inhibitors of cancer and cancer metastasis. Clin Cancer Res; 20(12); 3118-32. ©2014 AACR.
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Q: Context: Glucocorticoids (GCs) are highly effective in the treatment of asthma. However, some individuals have GC-insensitive asthma.', 'To evaluate the functional response to steroids of bronchoalveolar lavage (BAL) cells from sites of airway inflammation from patients with GC-insensitive versus GC-sensitive asthma. As well, to attempt to define the functional role of glucocorticoid receptor (GCR)beta (a splicing variant, and dominant negative inhibitor of, the classic GCRalpha) in controlling GCRalpha nuclear translocation and transactivation at a molecular level.', 'Fiberoptic bronchoscopy with collection of BAL fluid was performed on seven patients with GC-sensitive asthma and eight patients with GC-insensitive asthma. GCRalpha cellular shuttling in response to 10(-6) M dexamethasone treatment and GCRbeta expression were analyzed in BAL cells by immunofluorescence staining. The effects of overexpression and silencing of GCRbeta mRNA on GCRalpha function were assessed.', 'Significantly reduced nuclear translocation of GCRalpha in response to steroids was found in BAL cells from patients with GC-insensitive asthma. BAL macrophages from patients with GC-insensitive asthma had significantly increased levels of cytoplasmic and nuclear GCRbeta. It was demonstrated that GCRalpha nuclear translocation and its transactivation properties were proportionately reduced by level of viral transduction of the GCRbeta gene into the DO-11.10 cell line. RNA silencing of GCRbeta mRNA in human BAL macrophages from patients with GC-insensitive asthma resulted in enhanced dexamethasone-induced GCRalpha transactivation.\Question: Does increased glucocorticoid receptor beta alter steroid response in glucocorticoid-insensitive asthma?

A: GC insensitivity is associated with loss of GCRalpha nuclear translocation in BAL cells and elevated GCRbeta, which may inhibit GCRalpha transactivation in response to steroids.
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Q: Context: Low serum levels of vitamin D have been associated with depression in non-stroke subjects. Our aim was to examine the possible association between serum vitamin D levels and the development of post-stroke depression (PSD).', 'In total, 189 patients with acute ischaemic stroke were consecutively recruited. Serum levels of 25-hydroxyvitamin D [25(OH)D] were measured by competitive protein-binding assay within 24 h after admission. The 17-item Hamilton Depression Scale was used for screening for the existence of depressive symptoms at 1 month after stroke. Patients with a Hamilton Depression Scale score of ≥7 were given the Structured Clinical Interview of the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, for diagnosis of PSD. Meanwhile, 100 healthy control subjects were also recruited and underwent measurement of 25(OH)D.', 'Fifty-five patients (29.1%) were diagnosed as having PSD at 1 month. Serum vitamin D levels within 24 h after admission were significantly lower in both non-PSD patients and PSD patients than in normal controls. PSD patients had significantly lower vitamin D than non-PSD patients. Serum vitamin D levels (≤37.1 and ≥64.1 nmol/l) were independently associated with the development of PSD (odds ratio 8.824, 95% confidence interval 2.011-38.720, P = 0.004, and odds ratio 0.127, 95% confidence interval 0.022-0.718, P = 0.020, respectively).\Question: Are low serum levels of vitamin D associated with post-stroke depression?

A:
Serum vitamin D levels within 24 h after admission are found to be associated with PSD and may predict its development at 1 month post-stroke.
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