Determination of coordinates of control points in the Wieruszów District area

W pracy przedstawiono metodykę pomiaru i opracowania osnowy szczegółowej GPS III na obszarze powiatu wieruszowskiego. Pomiary 988 punktów wykonano metodą statyczną w ciągu dziesięciu dni z wykorzystaniem 12 odbiorników GPS Ashtech Z-XII, Z-Surveyor, Z-Xtreme. W pracy przedstawiono także analizy wyrównania i transformacji z układu ETRF-89 do państwowych układów współrzędnych: "1965" i "2000". Z uwagi na liczne zasłony drzew nad wyznaczanymi punktami, obserwacje GPS powtórzono na około trzydziestu punktach, aby uzyskać wymaganą dokładność i niezależną kontrolę pomiarów. Dodatkowo przy takiej liczbie odbiorników bardzo skuteczne okazały się analizy zamknięć przyrostów w trójkątach jak również warunki geometryczne nieoznaczoności pomiarów fazowych stosowane przy rozwiązaniach multistacyjnych.The paper presents the methodology of GPS measurements and data elaboration for control points in the Wieruszów District area. GPS measurements of 988 points were executed with the use of static method during ten days of measurements and twelve GPS receivers of Ashtech company i.e. Z-XII, Z-Surveyor, Z-Xtreme. The results and analyses of adjustment and transformation from ETRF-89 to the national coordinate systems: ,,1965" and ,,2000" were also presented. Due to bad observational conditions of GPS measurements there were about thirty points on which GPS measurements were repeated in order to achieve reliable and accurate results. Additionally, loop closures of baselines and geometric conditions of ambiguity network solutions were successfully useful before final adjustment

Stem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition.

Inhibitors of the mechanistic target of rapamycin (mTOR) are currently used to treat advanced metastatic breast cancer. However, whether an aggressive phenotype is sustained through adaptation or resistance to mTOR inhibition remains unknown. Here, complementary studies in human tumors, cancer models and cell lines reveal transcriptional reprogramming that supports metastasis in response to mTOR inhibition. This cancer feature is driven by EVI1 and SOX9. EVI1 functionally cooperates with and positively regulates SOX9, and promotes the transcriptional upregulation of key mTOR pathway components (REHB and RAPTOR) and of lung metastasis mediators (FSCN1 and SPARC). The expression of EVI1 and SOX9 is associated with stem cell-like and metastasis signatures, and their depletion impairs the metastatic potential of breast cancer cells. These results establish the mechanistic link between resistance to mTOR inhibition and cancer metastatic potential, thus enhancing our understanding of mTOR targeting failure

Stem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition

Inhibitors of the mechanistic target of rapamycin (mTOR) are currently used to treat advanced metastatic breast cancer. However, whether an aggressive phenotype is sustained through adaptation or resistance to mTOR inhibition remains unknown. Here, complementary studies in human tumors, cancer models and cell lines reveal transcriptional reprogramming that supports metastasis in response to mTOR inhibition. This cancer feature is driven by EVI1 and SOX9. EVI1 functionally cooperates with and positively regulates SOX9, and promotes the transcriptional upregulation of key mTOR pathway components (REHB and RAPTOR) and of lung metastasis mediators (FSCN1 and SPARC). The expression of EVI1 and SOX9 is associated with stem cell-like and metastasis signatures, and their depletion impairs the metastatic potential of breast cancer cells. These results establish the mechanistic link between resistance to mTOR inhibition and cancer metastatic potential, thus enhancing our understanding of mTOR targeting failure