107 research outputs found
Breast metastasis of primary colon cancer with micrometastasis in the axillary sentinel node: A metastasis that metastasized?
A case of single breast metastasis from colon adenocarcinoma, with omolateral axillary micrometastasis, is reported with a brief review of the pertinent literature. The originality of the oncological concept of metastasis from metastasis, through lymphatics penetration, is discussed in the setting of a rare condition of breast metastasis from a colorectal carcinoma
The zCOSMOS 10k-Bright Spectroscopic Sample
We present spectroscopic redshifts of a large sample of galaxies with I_(AB) < 22.5 in the COSMOS field, measured from spectra of 10,644 objects that have been obtained in the first two years of observations in the zCOSMOS-bright redshift survey. These include a statistically complete subset of 10,109 objects. The average accuracy of individual redshifts is 110 km s^(–1), independent of redshift. The reliability of individual redshifts is described by a Confidence Class that has been empirically calibrated through repeat spectroscopic observations of over 600 galaxies. There is very good agreement between spectroscopic and photometric redshifts for the most secure Confidence Classes. For the less secure Confidence Classes, there is a good correspondence between the fraction of objects with a consistent photometric redshift and the spectroscopic repeatability, suggesting that the photometric redshifts can be used to indicate which of the less secure spectroscopic redshifts are likely right and which are probably wrong, and to give an indication of the nature of objects for which we failed to determine a redshift. Using this approach, we can construct a spectroscopic sample that is 99% reliable and which is 88% complete in the sample as a whole, and 95% complete in the redshift range 0.5 < z < 0.8. The luminosity and mass completeness levels of the zCOSMOS-bright sample of galaxies is also discussed
EGFR Inhibition Abrogates Leiomyosarcoma Cell Chemoresistance through Inactivation of Survival Pathways and Impairment of CSC Potential
Background: Tumor cells with stem-like phenotype and properties, known as cancer stem cells (CSC), have been identified in most solid tumors and are presumed to be responsible for driving tumor initiation, chemoresistance, relapse, or metastasis. A subpopulation of cells with increased stem-like potential has also been identified within sarcomas. These cells are endowed with increased tumorigenic potential, chemoresistance, expression of embryonic markers, and side population(SP) phenotype. Leiomyosarcomas (LMS) are soft tissue sarcomas presumably arising from undifferentiated cells of mesenchymal origin, the Mesenchymal Stem Cells (MSC). Frequent recurrence of LMS and chemoresistance of relapsed patients may likely result from the failure to target CSC. Therefore, therapeutic cues coming from the cancer stem cell (CSC) field may drastically improve patient outcome. Methodology/Principal Findings: We expanded LMS stem-like cells from patient samples in vitro and examined the possibility to counteract LMS malignancy through a stem-like cell effective approach. LMS stem-like cells were in vitro expanded both as "tumor spheres" and as "monolayers" in Mesenchymal Stem Cell (MSC) conditions. LMS stem-like cells displayed MSC phenotype, higher SP fraction, and increased drug-extrusion, extended proliferation potential, self-renewal, and multiple differentiation ability. They were chemoresistant, highly tumorigenic, and faithfully reproduced the patient tumor in mice. Such cells displayed activation of EGFR/AKT/MAPK pathways, suggesting a possibility in overcoming their chemoresistance through EGFR blockade. IRESSA plus Vincristine treatment determined pathway inactivation, impairment of SP phenotype, high cytotoxicity in vitro and strong antitumor activity in stem-like cell-generated patient-like xenografts, targeting both stem-like and differentiated cells. Conclusions/Significance: EGFR blockade combined with vincristine determines stem-like cell effective antitumor activity in vitro and in vivo against LMS, thus providing a potential therapy for LMS patients. \uc2\ua9 2012 Sette et al
Antibody Responses to NY-ESO-1 in Primary Breast Cancer Identify a Subtype Target for Immunotherapy
The highly immunogenic human tumor antigen NY-ESO-1 (ESO) is a target of choice for anti-cancer immune therapy. In this study, we assessed spontaneous antibody (Ab) responses to ESO in a large cohort of patients with primary breast cancer (BC) and addressed the correlation between the presence of anti-ESO Ab, the expression of ESO in the tumors and their characteristics. We found detectable Ab responses to ESO in 1% of the patients. Tumors from patients with circulating Ab to ESO exhibited common characteristics, being mainly hormone receptor (HR)− invasive ductal carcinomas of high grade, including both HER2− and HER2+ tumors. In line with these results, we detected ESO expression in 20% of primary HR− BC, including both ESO Ab+ and Ab− patients, but not in HR+ BC. Interestingly, whereas expression levels in ESO+ BC were not significantly different between ESO Ab+ and Ab− patients, the former had, in average, significantly higher numbers of tumor-infiltrated lymph nodes, indicating that lymph node invasion may be required for the development of spontaneous anti-tumor immune responses. Thus, the presence of ESO Ab identifies a tumor subtype of HR− (HER2− or HER2+) primary BC with frequent ESO expression and, together with the assessment of antigen expression in the tumor, may be instrumental for the selection of patients for whom ESO-based immunotherapy may complement standard therapy
Mass and environment as drivers of galaxy evolution in SDSS and zCOSMOS and the origin of the Schechter function
We explore the inter-relationships between mass, star-formation rate and
environment in the SDSS, zCOSMOS and other surveys. The differential effects of
mass and environment are completely separable to z ~ 1, indicating that two
distinct processes are operating, "mass-quenching" and "environment-quenching".
Environment-quenching, at fixed over-density, evidently does not change with
epoch to z ~ 1, suggesting that it occurs as large-scale structure develops in
the Universe. The observed constancy of the mass-function shape for
star-forming galaxies, demands that the mass-quenching of galaxies around and
above M*, must be proportional to their star-formation rates at all z < 2. We
postulate that this simple mass-quenching law also holds over a much broader
range of stellar mass and epoch. These two simple quenching processes, plus
some additional quenching due to merging, then naturally produce (a) a
quasi-static Schechter mass function for star-forming galaxies with a value of
M* that is set by the proportionality between the star-formation and
mass-quenching rates, (b) a double Schechter function for passive galaxies with
two components: the dominant one is produced by mass-quenching and has exactly
the same M* as the star-forming galaxies but an alpha shallower by +1, while
the other is produced by environment effects and has the same M* and alpha as
the star-forming galaxies, and is larger in high density environments.
Subsequent merging of quenched galaxies modifies these predictions somewhat in
the denser environments, slightly increasing M* and making alpha more negative.
All of these detailed quantitative relationships between the Schechter
parameters are indeed seen in the SDSS, lending strong support to our simple
empirically-based model. The model naturally produces for passive galaxies the
"anti-hierarchical" run of mean ages and alpha-element abundances with mass.Comment: 66 pages, 19 figures, 1 movie, accepted for publication in ApJ. The
movie is also available at
http://www.exp-astro.phys.ethz.ch/zCOSMOS/MF_simulation_d1_d4.mo
Impact of liver cirrhosis, severity of cirrhosis and portal hypertension on the difficulty of laparoscopic and robotic minor liver resections for primary liver malignancies in the anterolateral segments
Significato prognostico dell'urokinase-type plasminogen activator (uPA) e del suo inibitore (PAI-I) nel cancro del colon - retto
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