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.

Context: Women diagnosed with pregnancy-associated breast cancer postpartum have a worse prognosis, stage for stage, than other women with breast cancer. The time of breast involution is tumor promotional. The extracellular matrix protein tenascin-C is upregulated during involution in animal models and promotes breast cancer progression. It interacts with transforming growth factor (TGF), which also is involved in breast involution and breast cancer progression. Little is known about the expression of tenascin-C during human breast involution, nor its relationship to TGF. The purpose of this study was to investigate the expression of tenascin-C throughout lactation, as well as its relationship to TGF1 and TGF2.', 'Three milk samples from 25 lactating women (transitional, whole, and wean) were collected, separated into components (cells, fat, and skim), and the skim fraction analyzed for total protein, tenascin-C, TGF1, and TGF2. Tenascin-C, TGF1, and TGF2 were detectable in all milk samples.', 'Highest tenascin-C levels on average were found in whole milk, whereas highest mean TGF1 and TGF2 levels were in wean milk. Wean samples on average had higher levels of both TGF1 (26%) and TGF2 (>500%) than matched transitional milk samples. Tenascin-C levels in wean milk were associated with nursing length (p = 0.048). Combining all three milk collection time points, tenascin-C exhibited a weak inverse correlation with TGF1 and TGF2 (p < 0.1). The inverse correlation at the wean time point was stronger for TGF2 than -1 (-0.37 versus -0.25). Tenascin-C, a protein known to promote breast cancer progression, is expressed throughout lactation.\Question: Does expression of the Extracellular Matrix Protein Tenascin-C vary During Lactation?
The inverse correlation with TGF2 in wean milk suggests a possible interaction during breast involution, which should be further investigated.

Context: To elucidate the importance of hepatitis C Virus (HCV) genotype in HIV disease progression.', 'This study was conducted among 126 HIV/HCV co-infected drug users with a known interval of HIV seroconversion whose HCV genotype was known early in HIV infection. Both clinical progression (to AIDS) and immunological progression (to a CD4+ T-cell count of 200 x 10(6) cells/l) by HCV genotype were studied using Cox proportional hazards analysis.', 'The median duration of follow-up was 7.3 years [interquartile range (IQR), 4.6-10.1 years]. The majority of the HCV infections concerned genotype 1 and genotype 3; The distribution was: HCV type 1: 48%, HCV type 3: 34%, HCV type 4: 13%, multiple HCV types: 5%. Concurrent multiple infections consisted of HCV genotypes 1b+3a, 1b+4 and 3a+4. HCV genotype 1 and multiple HCV genotype infections were associated with faster immunological progression [hazard ratio (HR), 2.02; 95% confidence interval (CI), 1.04-3.92 and HR, 2.74; 95% CI, 0.95-7.90, respectively]. Multiple HCV genotype infection was also associated with faster clinical progression (HR, 3.36; 95% CI, 0.82-13.79). These hazard ratios increased further and were all significant when analyses were limited to data in the pre-HAART era (HR, 3.92; 95% CI, 1.51-10.20; HR, 4.38; 95% CI, 1.04-18.40 and HR, 6.54; 95% CI, 1.39-30.76, respectively).\Question: Is infection with concurrent multiple hepatitis C virus genotypes associated with faster HIV disease progression?
HIV disease progression differs by HCV genotype and is especially faster in individuals whose HCV infection involves more than one HCV genotype. The effect of HCV genotype on HIV progression was greater in the pre-highly active antiretroviral therapy (HAART) era, suggesting that the effectiveness of HAART may diminish the effect of HCV genotype on HIV disease progression.

Context: To determine whether deguelin can regulate the expression of nuclear factor kappa B (NF-kappaB) binding protein (IkappaBalpha) in U937 human leukemia cells and Raji human B lymphoma cells.', 'The localization of IkappaBalpha protein was investigated by using an immunofluorescence method. The expression of IkappaBalpha and NF-kappaB /p65 proteins in Raji and U937 cells were investigated by using Western blotting. Apoptosis was detected through annexin V/PI double-labeled cytometry.', 'IkappaBalpha localized in the cytoplasm in untreated and deguelin-treated cells. After treatment with tumor necrosis factor alpha (TNF-alpha) or deguelin plus TNF-alpha for 15 min, there was a substantial reduction in the amount of IkappaBalpha protein. The expression of IkappaBalpha was downregulated by deguelin in Raji and U937 cells. Deguelin induced apoptosis in U937 cells.\Question: Does deguelin inhibit expression of IkappaBalpha protein in Raji and U937 cells?
Deguelin inhibited the expression of IkappaBalpha protein in U937 and Raji cells. The anti-proliferative activity of deguelin is related to the signal pathway of NF-kappaB.