Investigation of X-ray timing and spectral properties of ESO 243-49 HLX-1 with long-term Swift Monitoring

The long-term Swift monitoring of ESO???243???49 HLX???1 provides an opportunity to investigate the detailed timing and spectral behaviour of this hyperluminous X-ray source. Swift has detected seven outbursts since 2009 mid-August. Using different dynamical timing algorithms, we confirm an increasing trend for the time intervals between outbursts, which is manifest in the delays between the latest outbursts. The X-ray spectra of HLX???1 in quiescence can be described with a single power-law model while the thermal component dominates the X-ray emission during outburst. There is only marginal evidence for photon index (or spectral hardness) changes between quiescent states with about 1?? deviation. With the updated temporal and spectral features, we re-examine different scenarios to explain the origin of the quasi-periodic modulation of HLX???1. A significantly increasing trend without obvious stochastic fluctuations on the time-scale of the detected quasi-period may not fully support an orbital period origin as might be due to mass transfer episodes from a donor star at periastron of an extremely eccentric orbit. The outburst profile seems to be consistent with the effect of tidal-induced-precession of an accretion disc or an oscillating wind scenario in the inner disc. Based on these models, we speculate that the true orbital period is much shorter than the detected quasi-periodicity

Colorectal Adenocarcinomas Harboring ALK Fusion Genes

This study determined the frequency, clinicopathologic, and genetic features of colorectal carcinomas driven by oncogenic fusions of the anaplastic lymphoma kinase gene (ALK). Out of 8150 screened tumors, 12 (0.15%) were immunohistochemically ALK-positive with D5F3 antibody. These cancers harbored CAD-ALK (n=1), DIAPH2-ALK (n=2), EML4-ALK (n=2), LOC101929227-ALK (n=1), SLMAP-ALK (n=1), SPTBN1-ALK (n=4) and STRN-ALK (n=1) fusions as detected by an RNA-based NGS assay. ALK fusion carcinomas were diagnosed mostly in older patients with a 9:3 female predominance (median age, 72 years). All tumors, except a rectal one, occurred in the right colon. Most tumors were stage T3 (n=7) or T4 (n=3). Local lymph node and distant metastases were seen at presentation in 9 and 2 patients. These tumors showed moderate (n=6) or poor (n=3) glandular differentiation, solid medullary growth pattern (n=2), and pure mucinous morphology (n=1). DNA mismatch repair deficient phenotype was identified in 10 cases. Tumor-infiltrating lymphocytes were prominent in 9 carcinomas. In 4 carcinomas, tumor cells showed strong, focal (n=3) or diffuse PD-L1 immunoreactivity. CDX2 expression and loss of CK20 and MUC2 expression were frequent. CK7 was expressed in 5 tumors. Four patients died of disease within 3 years and 7 were alive with follow-up ranging from 1–8 years. No mutations in BRAF, RAS and genes encoding components of PI3K-AKT/MTOR pathway were identified. However, one tumor had a loss-of-function PTEN mutation. Aberration of p53 signaling, TP53 mutations and/or nuclear accumulation of p53 protein was seen in 9 cases. ALK fusion colorectal carcinomas are a distinct and rare subtype of colorectal cancers displaying some features of mismatch repair-deficient tumors