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: Due to lack of a targeted therapy for the triple-negative breast cancer (TNBC) patients, it is important to explore this aggressive breast cancer type in more detail and to establish novel therapeutic approaches. TNBC is defined negative for the protein expression of oestrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2). One prominent feature of this cancer type is the frequent overexpression of major components of the urokinase-type plasminogen activator system (uPAS) including uPA, its receptor uPAR and the inhibitor PAI-1, which may be valuable as therapeutic targets.', 'Direct interactions of uPAR with interactors were demonstrated by immunoprecipitations and proximity ligation assays. For stable knockdowns of target proteins, lentiviral vectors were used and the effects were analysed by immunoblottings and using in vitro cell viability, migration and invasion assays. Immunohistochemical and statistical analyses of biomarkers and clinical parameters were conducted in a TNBC cohort (n=174).', 'Direct tumour-promoting interactions of uPAR with uPA and the insulin-like growth factor receptor 1 (IGF1R) were shown in TNBC cells and these interactions were significantly reduced (p=0.001) when uPAR was downregulated. The combined knockdown of uPAR and uPA or IGF1R additively and significantly reduced cell viability, migration and invasion of the model cell lines. In TNBC tissue, the complexes formed by uPAR with uPA or with IGF1R significantly correlated with the histological grade (p=0.0019) as well as with cathepsin B and D (p0.0001) that are implicated in cell invasion and metastasis.\Question: Does uPAR enhance malignant potential of triple-negative breast cancer by directly interacting with uPA and IGF1R?
[A]: Our outcomes show that not only overexpressed biomarkers promote tumourigenesis, but rather their interactions further potentiate tumour progression. This study emphasises the potential of combined approaches targeting uPAR and its interactors with regard to an improved therapy of TNBC.

[Q]: Context: Neoadjuvant chemotherapy (NACT) improves the prognosis of patients with esophageal cancer who respond, but it is not effective in nonresponders. Therefore, it is crucial to establish a reliable method of predicting response before initiation of chemotherapy. Hypercoagulability, which is thought to be because of upregulation of tissue factor (TF) in cancer cells, was reported to be associated with chemoresistance. The aim of this study was to investigate the association between TF expression and response to NACT in esophageal cancer.', 'In 67 patients with advanced esophageal cancer, TF expression in pretreatment biopsy samples was evaluated immunohistochemically and correlated with clinicopathologic factors and response to chemotherapy.', 'TF was expressed by 43.3% of the tumors, but there were no correlations observed with any clinicopathologic parameters examined. Clinical and histologic responses to chemotherapy were significantly worse in TF-positive patients compared with TF-negative patients. Multivariate analysis revealed that TF expression was significantly associated with a poor clinical response (P=0.0431). TF expression was also independently associated with poor progression-free survival (P=0.0353).\Question: Does tissue factor predict response to chemotherapy in esophageal cancer?
[A]: TF expression levels in pretreatment biopsy samples are useful for predicting response to NACT in advanced esophageal cancer. Further studies of mechanisms underlying the relationship between TF expression and chemosensitivity are needed.

[Q]: Context: Sufentanil is an intravenous opioid often used as a component of anesthesia during neurosurgical procedures. However, the effects of sufentanil on intracranial pressure in patients with diminished intracranial compliance are not well established, and remain controversial.', 'Ten patients with head trauma, in each of whom the trachea was intubated, were studied for the effects of sufentanil on intracranial pressure (ICP) and on cerebral perfusion pressure (CPP). In all patients, ICP monitoring was instituted before the study. Sedation was obtained using a propofol infusion, and paralysis was achieved with vecuronium. After obtaining control of ICP (between 15 and 25 mmHg) hemodynamic values and blood gas tensions (PaCO2 between 30 and 35 mmHg), the level of sedation was deepened with an intravenous injection of sufentanil (1 microgram/kg over 6 min), followed by an infusion of 0.005 microgram.kg-1min-1. Mean arterial pressure (MAP), ICP (fiberoptic intracranial pressure monitor), and end-tidal CO2 were continuously measured and recorded at 1-min intervals throughout the 30-min study period.', 'Sufentanil injection was associated with a statistically significant increase in ICP of 9 +/- 7 mmHg (+ 53%), which peaked at 5 min. Then ICP gradually decreased and returned to baseline after 15 min. This was accompanied by a significant decrease in MAP (24% decrease) and, thus, CPP (38% decrease). After 5 min, MAP and CPP gradually increased, but remained significantly decreased throughout the study.\Question: Does sufentanil increase intracranial pressure in patients with head trauma?
[A]:
The results of the current study indicate that caution should be exercised in the administration of sufentanil bolus to patients with abnormal intracranial elastance, particularly if ICP is significantly increased.