N-(3-Methyl­phen­yl)-N′-(4-nitro­benzo­yl)thio­urea

Two mol­ecules of the title compound, C15H13N3O3S, are linked by an inter­molecular N—H⋯S hydrogen bond. There is also an intra­molecular N—H⋯O hydrogen bond, forming a six-membered ring. The steric restriction of the m-methyl and p-nitro groups, as well as the intra­molecular hydrogen bond, are the main factors influencing the mol­ecular conformation

On the scalar nonet in the extended Nambu Jona-Lasinio model

We discuss the lightest scalar resonances, $f_0(600)$, $\kappa(800)$, $a_0(980)$ and $f_0(980)$ in the extended Nambu Jona-Lasinio model. We find that the model parameters can be tuned, but unnaturally, to accommodate for those scalars except the $f_0(980)$. We also discuss problems encountered in the K Matrix unitarization approximation by using $N_c$ counting technique.Comment: 23 pages 3 eps figures, To appear in Nucl. Phys.

Elevated neoantigen levels in tumors with somatic mutations in the HLA-A, HLA-B, HLA-C and B2M genes.

BackgroundThe major histocompatibility complex class I (MHC-I) molecule is a protein complex that displays intracellular peptides to T cells, allowing the immune system to recognize and destroy infected or cancerous cells. MHC-I is composed of a highly polymorphic HLA-encoded alpha chain that binds the peptide and a Beta-2-microglobulin (B2M) protein that acts as a stabilizing scaffold. HLA mutations have been implicated as a mechanism of immune evasion during tumorigenesis, and B2M is considered a tumor suppressor gene. However, the implications of somatic HLA and B2M mutations have not been fully explored in the context of antigen presentation via the MHC-I molecule during tumor development. To understand the effect that B2M and HLA MHC-I molecule mutations have on mutagenesis, we analyzed the accumulation of mutations in patients from The Cancer Genome Atlas according to their MHC-I molecule mutation status.ResultsSomatic B2M and HLA mutations in microsatellite stable tumors were associated with higher overall mutation burden and a larger fraction of HLA-binding neoantigens when compared to B2M and HLA wild type tumors. B2M and HLA mutations were highly enriched in patients with microsatellite instability. B2M mutations tended to occur relatively early during patients' respective tumor development, whereas HLA mutations were either early or late events. In addition, B2M and HLA mutated patients had higher levels of immune infiltration by natural killer and CD8+ T cells and higher levels of cytotoxicity.ConclusionsOur findings add to a growing body of evidence that somatic B2M and HLA mutations are a mechanism of immune evasion by demonstrating that such mutations are associated with a higher load of neoantigens that should be presented via MHC-I

Breast metastasis from rectal carcinoma: A case report and review of the literature

BackgroundMetastasis from extramammary primary tumor to breast is extremely rare. Case SummaryA 59-year-old woman with 1-year history of rectal cancer presented with asymptomatic breast mass. At 16 months after the diagnosis of rectal mucinous adenocarcinoma, a breast mass was confirmed by ultrasonography and identified by pathology and immunohistochemistry as a metastasis from the rectal cancer. Treatments included chemotherapy (6 cycles: 300 mg irinotecan on day 1, 4.5 mg raltitrexed on day 2, 450 mg bevacizumab on day 3), radiotherapy, and surgical resection. Two years of follow-up examinations (6-months intervals) showed no evidence of recurrence or novel distant metastasis. ConclusionBreast metastasis from rectal carcinoma is a rare secondary malignancy. Final diagnosis can be established by histopathology and immunohistochemistry