Breast metastasis and lung large-cell neuroendocrine carcinoma: first clinical observation

The lung Large-cell neuroendocrine carcinoma (LCNEC) is a very rare aggressive neuroendocrine tumor with a high propensy to metastasize and very poor prognosis. We report an atypical presentation of lung large-cell neuroendocrine carcinoma was diagnosed from a metastatic nodule on the breast. Our patient is a 59 years-old woman that presented in March 2014 non productive cough. A CT scan showed multiple brain, lung, adrenal gland and liver secondary lesions; moreover, it revealed a breast right nodule near the chest measuring 1.8 cm. The breast nodule and a lung lesions were biopsied and their histology and molecular diagnosis were LCNEC of the lung. To our knowledge, this is the first documented case of breast metastasis from LCNEC of the lung. Furthermore, breast metastasis from extramammary malignancy is uncommon and its diagnosis is difficult but important for proper management and prediction of prognosis. Therefore, a careful clinical history with a thorough clinical examination is needed to make the correct diagnosis. Moreover, metastasis to the breast should be considered in any patient with a known primary malignant tumor history who presents with a breast lump. Anyhow, pathological examination should be performed to differentiate the primary breast cancer from metastatic tumor. Therefore, an accurate diagnosis of breast metastases may not only avoid unnecessary breast resection, more importantly it is crucial to determine an appropriate and systemic treatment

Capecitabine and Temozolomide (CAPTEM) in advanced neuroendocrine neoplasms (NENs): a systematic review and pooled analysis

Background Retrospective studies and single center experiences suggest a role of capecitabine combined with temozolomide (CAPTEM) in neuroendocrine tumors (NENs). Methods We performed a systematic review to assess the efficacy and safety of CAPTEM in patients affected with NENs, with the aim to better clarify the role of this regimen in the therapeutic algorithm of NENs. Results A total of 42 articles and 1818 patients were included in our review. The overall disease control rate was 77% (range 43.5%-100%). The median progression free survival ranged from 4 to 38.5 months, while the median overall survival ranged from 8 to 103 months. Safety analysis showed an occurrence of G3-G4 toxicities in 16.4% of the entire population. The most common toxicities were hematological (27.2%), gastrointestinal (8.3%,) and cutaneous (3.2%). Conclusion This systematic review demonstrated that CAPTEM was an effective and relatively safe treatment for patients with advanced well-moderate differentiated NENs of gastroenteropancreatic, lung and unknown origin

Star Formation Suppression by Tidal Removal of Cold Molecular Gas from an Intermediate-redshift Massive Post-starburst Galaxy

Observations and simulations have demonstrated that star formation in galaxies must be actively suppressed to prevent the formation of overly massive galaxies. Galactic outflows driven by stellar feedback or supermassive black hole accretion are often invoked to regulate the amount of cold molecular gas available for future star formation but may not be the only relevant quenching processes in all galaxies. We present the discovery of vast molecular tidal features extending up to 64 kpc outside of a massive z = 0.646 post-starburst galaxy that recently concluded its primary star-forming episode. The tidal tails contain (1.2 ± 0.1) × 1010 M⊙ of molecular gas, 47% ± 5% of the total cold gas reservoir of the system. Both the scale and magnitude of the molecular tidal features are unprecedented compared to all known nearby or high-redshift merging systems. We infer that the cold gas was stripped from the host galaxies during the merger, which is most likely responsible for triggering the initial burst phase and the subsequent suppression of star formation. While only a single example, this result shows that galaxy mergers can regulate the cold gas contents in distant galaxies by directly removing a large fraction of the molecular gas fuel, and plausibly suppress star formation directly, a qualitatively different physical mechanism than feedback-driven outflows

KPNB1 (karyopherin (importin) beta 1)

Review on KPNB1 (karyopherin (importin) beta 1), with data on DNA, on the protein encoded, and where the gene is implicated

The Compact Structures of Massive z ∼ 0.7 Post-starburst Galaxies in the SQuIGGL⃗E Sample

We present structural measurements of 145 spectroscopically selected intermediate-redshift (z ∼ 0.7), massive (M⋆ ∼ 1011 M⊙) post-starburst galaxies from the $\mathrm{SQuIGG}\vec{L}{\rm{E}}$ sample measured using wide-depth Hyper Suprime-Cam i-band imaging. This deep imaging allows us to probe the sizes and structures of these galaxies, which we compare to a control sample of star-forming and quiescent galaxies drawn from the LEGA-C Survey. We find that post-starburst galaxies systematically lie ∼0.1 dex below the quiescent mass–size (half-light radius) relation, with a scatter of ∼0.2 dex. This finding is bolstered by nonparametric measures, such as the Gini coefficient and the concentration, which also reveal these galaxies to have more compact light profiles than both quiescent and star-forming populations at similar mass and redshift. The sizes of post-starburst galaxies show either negative or no correlation with the time since quenching, such that more recently quenched galaxies are larger or similarly sized. This empirical finding disfavors the formation of post-starburst galaxies via a purely central burst of star formation that simultaneously shrinks the galaxy and shuts off star formation. We show that the central densities of post-starburst and quiescent galaxies at this epoch are very similar, in contrast with their effective radii. The structural properties of z ∼ 0.7 post-starburst galaxies match those of quiescent galaxies that formed in the early universe, suggesting that rapid quenching in the present epoch is driven by a similar mechanism to the one at high redshift

Early targets of miR-34a in neuroblastoma

Several genes encoding for proteins involved in proliferation, invasion, and apoptosis are known to be direct miR-34a targets. Here, we used proteomics to screen for targets of miR-34a in neuroblastoma (NBL), a childhood cancer that originates from precursor cells of the sympathetic nervous system. We examined the effect of miR-34a overexpression using a tetracycline inducible system in two NBL cell lines (SHEP and SH-SY5Y) at early time points of expression (6, 12, and 24 h). Proteome analysis using post-metabolic labeling led to the identification of 2,082 proteins, and among these 186 were regulated (112 proteins down-regulated and 74 up-regulated). Prediction of miR-34a targets via bioinformatics showed that 32 transcripts held miR-34a seed sequences in their 3′-UTR. By combining the proteomics data with Kaplan Meier geneexpression studies, we identified seven new gene products (ALG13, TIMM13, TGM2, ABCF2, CTCF, Ki67, and LYAR) that were correlated with worse clinical outcomes. These were further validated in vitro by 3′-UTR seed sequence regulation. In addition, Michigan Molecular Interactions searches indicated that together these proteins affect signaling pathways that regulate cell cycle and proliferation, focal adhesions, and other cellular properties that overall enhance tumor progression (including signaling pathways such as TGF-β, WNT, MAPK, and FAK). In conclusion, proteome analysis has here identified early targets of miR-34a with relevance to NBL tumorigenesis. Along with the results of previous studies, our data strongly suggest miR-34a as a useful tool for improving the chance of therapeutic success with NBL