Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

Many different cellular pathways have evolved to protect the genome from the deleterious effects of DNA damage that result from exposure to chemical and physical agents. Among these is a process called transcription-coupled repair (TCR) that catalyzes the removal of DNA lesions from the transcribed strand of expressed genes, often resulting in a preferential bias of damage clearance from this strand relative to its non-transcribed counterpart. Lesions subject to this type of repair include cyclobutane pyrimidine dimers that are normally repaired by nucleotide excision repair (NER) and thymine glycols (TGs) that are removed primarily by base excision repair (BER). While the mechanism underlying TCR is not completely clear, it is known that its facilitation requires proteins used by other repair pathways like NER. It is also believed that the signal for TCR is the stalled RNA polymerase that results when DNA damage prevents its translocation during transcription elongation. While there is a clear role for some NER proteins in TCR, the involvement of BER proteins is less clear. To explore this further, we studied the removal of 7-methylguanine (7MeG) and 3-methyladenine (3MeA) from the dihydrofolate reductase (dhfr) gene of murine cell lines that vary in their repair phenotypes. 7MeG and 3MeA constitute the two principal N-methylpurines formed in DNA following exposure to methylating agents. In mammalian cells, alkyladenine DNA alkyladenine glycosylase (Aag) is the major enzyme required for the repair of these lesions via BER, and their removal from the total genome is quite rapid. There is no observable TCR of these lesions in specific genes in DNA repair proficient cells; however, it is possible that the rapid repair of these adducts by BER masks any TCR. The repair of 3MeA and 7MeG was examined in cells lacking Aag, NER, or both Aag and NER to determine if rapid overall repair masks TCR. The results show that both 3MeA and 7MeG are removed without strand bias from the dhfr gene of BER deficient (Aag deficient) and NER deficient murine cell lines. Furthermore, repair of 3MeA in this region is highly dependent on Aag, but repair of 7MeG is equally efficient in the repair proficient, BER deficient, and NER deficient cell lines. Strikingly, in the absence of both BER and NER, neither 7MeG nor 3MeA is repaired. These results demonstrate that NER, but not TCR, contributes to the repair of 7MeG, and to a lesser extent 3MeA.
Which gene strand is targeted by transcription-coupled repair (TCR)?

NGC 65 (ESO 473-10A/PGC 1229) is a galaxy in the constellation Cetus.
What is the constellation that is made with NGC 65?

Philadelphia (Ph) chromosome positive acute lymphoblastic leukemia (ALL) is a common cytogenetic abnormality associated with poor outcome in adults. This preliminary study, in the absence of substantial evidence, reported the prevalence of the BCR-ABL gene fusion in ALL patients by RT-PCR in Pakistan. Moreover, the prognostic significance of BCR-ABL fusion along with other characteristics was also ascertained. One hundred forty six newly diagnosed ALL patients treated at our center between 2005 and 2008 comprised the study group. The patients were treated with a Children and Leukemia Group B induction regimen. Among these patients, BCR-ABL fusion oncogene was present in 43 of 78 patients (55%). A statistically significant difference in BCR-ABL-positivity within three age groups (<20 years, 20-50 years, >50 years) was observed (P= 0.001). The median age was significantly higher in the BCR-ABL+ group (30 vs 19 years; P= 0.001). BCR-ABL+ patients were also characterized by higher median WBC counts (96,000/L vs 23,000//L, P= 0.002). Complete remission was achieved in 74% BCR-ABL- patients and 35% BCR-ABL+ patients (P= 0.001). Only 10% of BCR-ABL- patients achieved continued complete remission (CR). None of the BCR-ABL+ patients maintained a CR further to induction therapy. With the available therapeutic protocol, the presence of a BCR-ABL fusion predicted a lower survival (P= 0.001). A high prevalence of BCR-ABL gene fusion was observed that appeared as a poor prognostic factor. Identification of this genetic entity at diagnosis is crucial for understanding the nature of adult ALL and for deciding optimal treatment.
Which gene fusion is the result of the "philadelphia translocation" or the "philadelphia chromosome" mutation?