THOR 42: A touchstone ∼24 Myr-old eclipsing binary spanning the fully convective boundary

We present the characterization of CRTS J055255.7-004426 (=THOR 42), a young eclipsing binary comprising two pre-main sequence M dwarfs (combined spectral type M3.5). This nearby (103 pc), short-period (0.859 d) system was recently proposed as a member of the ∼24 Myr-old 32 Orionis Moving Group. Using ground- and space-based photometry in combination with medium- and high-resolution spectroscopy, we model the light and radial velocity curves to derive precise system parameters. The resulting component masses and radii are 0.497 ± 0.005 and 0.205 ± 0.002 {M}_{⊙ }, and 0.659 ± 0.003 and 0.424 ± 0.002 {R}_{⊙ }, respectively. With mass and radius uncertainties of ∼1 per cent and ∼0.5 per cent, respectively, THOR 42 is one of the most precisely characterized pre-main sequence eclipsing binaries known. Its systemic velocity, parallax, proper motion, colour-magnitude diagram placement, and enlarged radii are all consistent with membership in the 32 Ori Group. The system provides a unique opportunity to test pre-main sequence evolutionary models at an age and mass range not well constrained by observation. From the radius and mass measurements we derive ages of 22-26 Myr using standard (non-magnetic) models, in excellent agreement with the age of the group. However, none of the models can simultaneously reproduce the observed mass, radius, temperature, and luminosity of the coeval components. In particular, their H-R diagram ages are 2-4 times younger and we infer masses ∼50 per cent smaller than the dynamical values

Improved survival outcomes despite older age at diagnosis: an era‐by‐era analysis of patients with primary central nervous system lymphoma treated at a single referral centre in the United Kingdom

Observational studies with long-term follow-up of patients with primary central nervous system lymphoma (PCNSL) are scarce. Patient data over a period of four decades were retrospectively analysed from databases at Not-tingham University Hospitals Trust, UK. The cohort was delineated by two distinct therapeutic eras; the first from 01/01/1982 to 31/12/2010 (n = 147) and the second 01/01/2011 to 31/07/2020 (n = 125). The median age at diagnosis was significantly older in the second era compared to the first (69 and 65 years respectively, P = 0·003). The 3-, 6-and 12-month overall survival (OS) rates in the second era were significantly higher compared to the first, at 85%, 77%, 62% versus 56%, 49%, 38% respectively (log-rank test P < 0·0001). On multivariate analysis, high-dose methotrexate (HD-MTX)-based induction protocols employed in the second era were associated with improved OS compared to those used in the first [hazard ratio (HR) 0·40, 95% confidence interval (CI) 0·28–0·57]. Within the second era, superior OS rates were seen with the use of intensive HD-MTX protocols (including consolidation with high-dose chemotherapy and autologous stem cell transplantation) compared to non-intensive HD-MTX schedules (HR 0·47, 95% CI 0·22–0·99). Initiating chemotherapy within 14 days of biopsy and use of rituximab were independently associated with improved OS and progression-free survival during the second era. These data suggest that prompt treatment initiation and use of intensive HD-MTX-and rituximab-based protocols have resulted in improved survival outcomes for patients

Common variation near CDKN1A, POLD3 and SHROOM2 influences colorectal cancer risk

We performed a meta-analysis of five genome-wide association studies to identify common variants influencing colorectal cancer (CRC) risk comprising 8,682 cases and 9,649 controls. Replication analysis was performed in case-control sets totaling 21,096 cases and 19,555 controls. We identified three new CRC risk loci at 6p21 (rs1321311, near CDKN1A; P = 1.14 × 10 -10), 11q13.4 (rs3824999, intronic to POLD3; P = 3.65 × 10 -10) and Xp22.2 (rs5934683, near SHROOM2; P = 7.30 × 10 -10) This brings the number of independent loci associated with CRC risk to 20 and provides further insight into the genetic architecture of inherited susceptibility to CRC.</p