Given a passage, 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]: Cervical carcinoma is the second most common malignancy in females and most of the cases are found in developing countries. The objectives of the present study were (a): to demonstrate the antiproliferative and apoptotic effects of Achillea falcata (A.falcata) extract in human cervical cancer cells (HeLa), and (b): to study the effect of the extract on cellular morphology, cell cycle phase distribution and mitochondrial membrane potential.', 'MTT assay was used to evaluate the anticancer effect of the extract on HeLa cells. Phase contrast, fluorescence microscopy and transmission electron microscopy (TEM) were used to investigate the morphological changes in these cancer cells after extract treatment. Flow cytometry was used to evaluate the effects of the extract on cell cycle and mitochondrial membrane potential.', 'The results revealed that A. falcata extract led to a significant antiproliferative effect in HeLa cancer cells. The extract induced cellular shrinkage, chromatin condensation and appearance of apoptotic bodies which are the hallmarks of cellular apoptosis. TEM results showed that extract-treated cells had nuclear membrane which was hemispherical and the nuclear chromatin was concentrated and bundled on the inner border of karyotheca. The endoplasmic reticulum also became enlarged in the inner segment. The extract also induced G2/M phase cell cycle arrest along with loss of mitochondrial membrane potential.
[EX A]: Are antiproliferative and apoptotic effects of the ethanolic herbal extract of Achillea falcata in human cervical cancer cells mediated via cell cycle arrest and mitochondrial membrane potential loss?

[EX Q]: Cardiometabolic disorders are rapidly becoming major public health challenges. Valproic acid (VPA) is a widely prescribed anticonvulsant drug.', 'We hypothesized that treatment with VPA would improve the regulation of glucose and atherogenic dyslipidemia through reduction in circulating corticosterone.', 'Female Wistar rats recieved (p.o.) combined oral contraceptive (COC) containing 1.0\u2009µg ethinylestradiol plus 5.0\u2009µg levonorgestrel and valproic acid (VPA; 20\u2009mg) for 8 weeks.', 'Treatment with COC led to elevated fasting blood glucose, insulin, corticosterone, triglycerides (TG), TG/HDL-cholesterol ratio, insulin resistance (IR) and impaired glucose tolerance. VPA significantly attenuated the alterations induced by COC treatment, but did not affect the corticosterone level. However, VPA treatment led to significant increases in plasma insulin, corticosterone, atherogenic lipids and impaired glucose tolerance in rats not treated with COC.
[EX A]: Is improvement of oral contraceptive-induced glucose dysregulation and dyslipidemia by valproic acid independent of circulating corticosterone?

[EX Q]: Most melanomas harbor oncogenic BRAF(V600) mutations, which constitutively activate the MAPK pathway. Although MAPK pathway inhibitors show clinical benefit in BRAF(V600)-mutant melanoma, it remains incompletely understood why 10% to 20% of patients fail to respond. Here, we show that RAF inhibitor-sensitive and inhibitor-resistant BRAF(V600)-mutant melanomas display distinct transcriptional profiles. Whereas most drug-sensitive cell lines and patient biopsies showed high expression and activity of the melanocytic lineage transcription factor MITF, intrinsically resistant cell lines and biopsies displayed low MITF expression but higher levels of NF-κB signaling and the receptor tyrosine kinase AXL. In vitro, these MITF-low/NF-κB-high melanomas were resistant to inhibition of RAF and MEK, singly or in combination, and ERK. Moreover, in cell lines, NF-κB activation antagonized MITF expression and induced both resistance marker genes and drug resistance. Thus, distinct cell states characterized by MITF or NF-κB activity may influence intrinsic resistance to MAPK pathway inhibitors in BRAF(V600)-mutant melanoma.
[EX A]:
Does a melanoma cell state distinction influence sensitivity to MAPK pathway inhibitors?