In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

[Q]: Coarctation of the aorta (CofA) has been associated with an increased risk of intracranial aneurysm (IA). This magnetic resonance angiography (MRA) study investigates the prevalence of IAs in 80 children treated in early life for CofA. MRA was performed at mean age of 15.7 7.1 years, and surgical or endovascular treatment for CofA occurred at a mean age of 2.6 4.4 years. No IA was found. In contrast with earlier findings in adult patients with late treatment for CofA, this first systematic study of very early treated patients for CofA failed to confirm the association between CofA and IAs. Our results call the abnormal developmental relation between CofA and IAs into question and suggest that modifiable risk factors like hypertension may be responsible for IA development in patients with CofA with adult diagnosis and treatment. In conclusion, our data suggest that early treatment of CofA can reduce the formation of IAs in children so as to make MRA screening less valuable in this young population.
[A]: Frequency of Intracranial Aneurysms Determined by Magnetic Resonance Angiography in Children (Mean Age 16) Having Operative or Endovascular Treatment of Coarctation of the Aorta (Mean Age 3).

[Q]: DNA replication stress promotes genome instability in cancer. However, the contribution of the replication stress response to the development of malignancies remains unresolved. The DNA replication stress response protein SMARCAL1 stabilizes DNA replication forks and prevents replication fork collapse, a cause of DNA breaks and apoptosis. While the fork regression/remodeling functions of SMARCAL1 have been investigated, its in vivo functions in replication stress and cancer are unclear. Using a gamma radiation (IR)-induced replication stress T-cell lymphoma mouse model, we observed a significant inhibition of lymphomagenesis in mice lacking one or both alleles of Smarcal1. Notably, a quarter of the Smarcal1-deficient mice did not develop tumors. Moreover, hematopoietic stem/progenitor cells (HSPCs) and developing thymocytes in Smarcal1-deficient mice showed increased DNA damage and apoptosis during the proliferation burst following IR and an impaired ability to repopulate the thymus after IR. Additionally, mice lacking Smarcal1 showed significant HSPC defects when challenged to respond to other replication stress stimuli. Thus, our data reveal the critical function of the DNA replication stress response and, specifically, Smarcal1 in hematopoietic cell survival and tumor development. Our results also provide important insight into the immunodeficiency observed in individuals with mutations in SMARCAL1 by suggesting that it is an HSPC defect.
[A]: Defective replication stress response inhibits lymphomagenesis and impairs lymphocyte reconstitution

[Q]: Hoxa9, Meis1 and Pbx1 encode homeodomaincontaining proteins implicated in leukemic transformation in both mice and humans. Hoxa9, Meis1 and Pbx1 proteins have been shown to physically interact with each other, as Hoxa9 cooperatively binds consensus DNA sequences with Meis1 and with Pbx1, while Meis1 and Pbx1 form heterodimers in both the presence and absence of DNA. In this study, we sought to determine if Hoxa9 could transform hemopoietic cells in collaboration with either Pbx1 or Meis1. Primary bone marrow cells, retrovirally engineered to overexpress Hoxa9 and Meis1a simultaneously, induced growth factor-dependent oligoclonal acute myeloid leukemia in <3 months when transplanted into syngenic mice. In contrast, overexpression of Hoxa9, Meis1a or Pbx1b alone, or the combination of Hoxa9 and Pbx1b failed to transform these cells acutely within 6 months post-transplantation. Similar results were obtained when FDC-P1 cells, engineered to overexpress these genes, were transplanted to syngenic recipients. Thus, these studies demonstrate a selective collaboration between a member of the Hox family and one of its DNA-binding partners in transformation of hemopoietic cells.
[A]:
Hoxa9 transforms primary bone marrow cells through specific collaboration with Meis1a but not Pbx1b.