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.

Example Input: Context: To determine whether macrophages in human reproductive tissues contain luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptor mRNA and receptor protein that can bind 125I-hCG.', 'Macrophages isolated from term pregnancy human decidua were used for LH/hCG receptor detection by in situ hybridization for receptor mRNA and immunocytochemistry for a macrophage marker, CD68, performed alone and in combination, reverse transcription-nested polymerase chain reaction, Western and ligand blotting. The LH/hCG receptor presence in macrophages in late luteal phase human endometria and corpora lutea was determined by sequential performance of in situ hybridization and immunocytochemistry.', 'The macrophages present in term pregnancy human decidua and late luteal phase human endometria and corpora lutea contain LH/hCG receptors.\Question: Do macrophages in human reproductive tissues contain luteinizing hormone/chorionic gonadotropin receptors?
Example Output: This is the first demonstration of macrophages present in human reproductive tissues containing LH/hCG receptors. The receptor presence suggests that LH and hCG may regulate macrophage functions in gonadal as well as in non-gonadal target tissues.

Example Input: Context: To determine the role of factor V Leiden and prothrombin gene mutation in the pathogenesis of unexplained second and third trimester nonrecurrent fetal loss.', 'One hundred and fourteen women with unexplained nonrecurrent late fetal loss made up the study group, and 106 normal pregnant women with a history of delivery of at least one healthy fetus and no history of late fetal loss made up the control group. The study group was further divided into two subgroups: second (n = 36) and third (n = 78) trimester fetal loss. All women were tested for factor V Leiden and G20210A prothrombin gene mutations.', 'Twenty-one (18.4%) of the women in the study group and seven (6.6%) of the women in the control group were heterozygous carriers of factor V Leiden mutation (OR = 3.19). Eleven (9.6%) of the women in the study group and three (2.8%) of the women in the control group were heterozygous carriers of prothrombin gene mutation (OR = 3.66). In assessing with regard to trimesters, 18 (23%) factor V Leiden and 10 (12.8%) prothrombin gene mutations were present in the group of third trimester fetal loss (OR = 4.24 and OR = 5.04, respectively). Three (8.3%) factor V Leiden and one (2.7%) prothrombin gene mutation were detected in women with second trimester fetal loss (OR = 1.28 and OR = 0.40, respectively).\Question: Is third trimester nonrecurrent fetal loss associated with factor V Leiden and prothrombin gene mutations?
Example Output: Factor V Leiden and prothrombin gene mutations were associated with third trimester nonrecurrent fetal loss. These mutations should be screened in women with third trimester but not second trimester unexplained nonrecurrent late fetal loss.

Example Input: Context: Neuroblastomas harboring activating point mutations in anaplastic lymphoma kinase (ALK) are differentially sensitive to the ALK inhibitor crizotinib, with certain mutations conferring intrinsic crizotinib resistance. To overcome this clinical obstacle, our goal was to identify inhibitors with improved potency that can target intractable ALK variants such as F1174L. We find that PF-06463922 has high potency across ALK variants and inhibits ALK more effectively than crizotinib in vitro. Most importantly, PF-06463922 induces complete tumor regression in both crizotinib-resistant and crizotinib-sensitive xenograft mouse models of neuroblastoma, as well as in patient-derived xenografts harboring the crizotinib-resistant F1174L or F1245C mutations. These studies demonstrate that PF-06463922 has the potential to overcome crizotinib resistance and exerts unprecedented activity as a single targeted agent against F1174L and F1245C ALK-mutated xenograft tumors, while also inducing responses in an R1275Q xenograft model. Taken together, these results provide the rationale to move PF-06463922 into clinical trials for treatment of patients with ALK-mutated neuroblastoma.\Question: Does the ALK/ROS1 Inhibitor PF-06463922 overcome Primary Resistance to Crizotinib in ALK-Driven Neuroblastoma?
Example Output:
The next-generation ALK/ROS1 inhibitor PF-06463922 exerts unparalleled activity in ALK-driven neuroblastoma models with primary crizotinib resistance. Our biochemical and in vivo data provide the preclinical rationale for fast-tracking the development of this agent in children with relapsed/refractory ALK-mutant neuroblastoma.