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This article will explore the design and implementation of quantum networks in space integrated with quantum networks on Earth. We propose a three-layer approach, involving GEO and LEO satellites integrated with terrestrial ground stations. We first analyze the channel conditions between the three layers, and then highlight the key role of LEO satellites in the integrated space-terrestrial system – namely the source of entanglement distribution between specified terrestrial stations via direct downlink quantum-optical channels. The GEO satellites in the considered system are used primarily as “coordination” stations, managing and directing the LEO satellites regarding the positioning and timing of entanglement distribution. Complexity, in the form of entanglement distillation and quantum-state correction, is concentrated at the terrestrial stations, and teleportation is used as the primary quantum channel in the LEO uplinks and the inter-terrestrial channels. Although our designs are futuristic in that they assume limited quantum memory at the transceivers, we also discuss some near-term uses of our network in which no quantum memory is available.

Quantum routing, the entanglement of an input quantum signal over multiple output paths, will be an important aspect of future quantum networks. Implementation of such routing in nearterm quantum networks via the noisy quantum devices currently under development is a distinct possibility. Quantum error correction, suitable for the arbitrary noisy quantum channels experienced in the routing process, will be required. In this work, we design a combined circuit for quantum routing and quantum error correction, and carry out an implementation of such a circuit on a noisy real-world quantum device. Under the assumption of statistical knowledge on the channel, we experimentally verify the quantum nature of the error-corrected quantum routing by determining the path-entanglement through quantum state tomography, measuring also its probability of success. The quantum error correction deployed is identified as successful in terms of improving the routing. Our experiments validate, for the first time, that error-corrected quantum routing in near-term quantum networks is feasible, provided enough statistical information on the noise intrinsic to the routing device is a priori known.

Limited sampling for imperiled taxa inhibits effective management by obscuring windows into ecological and evolutionary processes and ultimately thwarting thoughtful conservation efforts. We report eight new locations for the endangered New Mexico Meadow Jumping Mouse (Zapus luteus luteus) detected across three states that expand their known distribution. When combined with existing curated museum records, we develop an ensemble species distribution model to evaluate persistence of populations over the next 50 years. Predicted distributions indicate complex future changes, including regional expansion and the likelihood that half of the designated critical habitat areas will be unsuitable by 2070. Three of the newly discovered populations occur where predicted climate conditions suggest extirpation is likely. Importantly, indices of historical sampling efforts show that recognized and potential distributions are mismatched, highlighting vast areas that have been insufficiently surveyed. Ongoing habitat degradation and climate disruption are projected to synergistically erode genetic diversity across four of the five divergent phylogroups. Considering these combined results, a holistic sampling strategy is needed to more completely document the distribution of jumping mice and facilitate genomic analyses aimed at establishing a roadmap for improving our understanding of geographic variation and adaptive potential. Current management efforts are not only costly, but they are lacking key biological insights, essentially wagering actions with an incomplete deck of cards.

High-purity single-photon sources (SPS) that can operate at room temperature are highly desirable for a myriad of applications, including quantum photonics and quantum key distribution. In this work, we realize an ultra-bright solid-state SPS based on an atomic defect in hexagonal boron nitride (hBN) integrated with a solid immersion lens (SIL). The SIL increases the source efficiency by a factor of six, and the integrated system is capable of producing over ten million single photons per second at room temperature. Our results are promising for practical applications of SPS in quantum communication protocols.

ABSTRACTNimesulide is a nonsteroidal anti-inflammatory drug and a COX-2 inhibitor with antitumor and antiproliferative activities that induces apoptosis in oral, esophagus, breast, and pancreatic cancer cells. Despite being removed from the market due to hepatotoxicity, nimesulide is still an important research tool being used to develop new anticancer drugs. Multiple studies have been done to modify the nimesulide skeleton to develop more potent anticancer agents and related compounds are promising scaffolds for future development. As such, establishing a mechanism of action for nimesulide remains an important part of realizing its potential. Here, we show that nimesulide enhances TRAIL-induced apoptosis in resistant pancreatic cancer cells by promoting clustering of DR5 in the plasma membrane. In this way, nimesulide acts like a related compound, DuP-697, which sensitizes TRAIL-resistant colon cancer cells in a similar manner. Our approach applies a time-resolved FRET-based biosensor that monitors DR5 clustering and conformational states in the plasma membrane. We show that this tool can be used for future high-throughput screens to identify novel, nontoxic small molecule scaffolds to overcome TRAIL resistance in cancer cells.

Background: Protein biogenesis is a complex process involving nucleoliand ribosomes. Alterations in any step could lead to alterations in ribosome functionality and protein synthesis. Hnrnpk is an RNA-binding protein (RBP) involve in these processes, finding that an overexpression (OE) produces nucleus and nucleolar stress (NS), decreases transcription, and drives an imbalance in ribosome biogenesis, causing a reduced translation.

Deletion of the long arm of chromosome 9, del(9q), is a recurrent genetic abnormality involving the haploinsufficient loss of the RNA binding protein hnRNPK and is often associated with poor treatment responses in AML. In addition to reduced hnRNP K expression, other critical proteins, not localized to this locus, are also aberrantly expressed in del9q AML. One protein of critical interest is CEBPα, a well-established myeloid differentiation transcription factor. Recently, CEBPα was discovered to have a novel role in ribosomal RNA (rRNA) synthesis. However, as opposed to CEBPα, hnRNP K's role in RNA stability, rRNA processing, and ribosomal functions is already firmly rooted. Collectively, these results suggest that del(9q) AML dysregulations in hnRNP K and CEBPα expression may have a multi-faceted influence on ribosomal biogenesis and protein translation.

URLLC is one category of service to be provided by next-generation wireless networks. Motivated by increasing security concerns in such networks, this article focuses on physical layer security in the context of URLLC. The physical layer security technique mainly uses transmission designs based on the intrinsic randomness of the wireless medium to achieve secrecy. As such, physical layer security is of a lower complexity and incurs less latency than traditional cryptography. In this article, we first introduce appropriate performance metrics for evaluating physical layer security in URLLC and investigate the trade-off between latency, reliability, and security. We then identify the key challenging problems for achieving physical layer security in URLLC, and discuss the role that channel state information can have in providing potential solutions to these problems. Finally, we present our recommendations on future research directions in this emerging area.

Natural history collections have stimulated insights into systematics and evolution, but the extensive biodiversity sampling held in museums is increasingly employed to address other critical societal concerns, especially those related to changing environmental conditions on our planet. Due to large-scale digitization efforts in the last decade, specimen information can now be collated across natural history museums. Here, we leverage the availability of digital records of specimens in the United States that span the past ~135 years to explore the vitality of this resource. Using mammals as an example, we document a significant decline in recent specimen acquisition at a time of extreme environmental degradation and loss of mammalian populations. To stimulate rigorous assessments of the impacts of changing conditions and future-proof this basic infrastructure for mammalogy, we recommend a renewed effort to build temporally deep, geographically extensive, and site-intensive collections of holistic specimens. Targeted fieldwork should be designed to leverage historic sampling to enable retrospective environmental analyses and derive more complete perspectives of change.

ABSTRACTPTEN phosphorylation at its C-terminal (C-tail) serine/threonine cluster negatively regulates its tumor suppressor function. However, the consequence of such inhibition and its downstream effects in driving lung cancer remain unexplored. Herein, we ascertain the molecular mechanisms by which phosphorylation compromises PTEN function, contributing to lung cancer. Replacement of the serine/threonine residues with alanine generated PTEN-4A, a phosphorylation-deficient PTEN mutant, which suppressed lung cancer cell proliferation and migration. PTEN-4A preferentially localized to the nucleus where it suppressed E2F1-mediated transcription of cell cycle genes. PTEN-4A physically interacted with the transcription factor E2F1 and associated with chromatin at gene promoters with E2F1 DNA-binding sites, a likely mechanism for its transcriptional suppression function. Deletion analysis revealed that the C2 domain of PTEN was indispensable for suppression of E2F1-mediated transcription. Further, we uncovered cancer-associated C2 domain mutant proteins that had lost their ability to suppress E2F1-mediated transcription, supporting the concept that these mutations are oncogenic in patients. Consistent with these findings, we observed increased PTEN phosphorylation and reduced nuclear PTEN levels in lung cancer patient samples establishing phosphorylation as a bona fide inactivation mechanism for PTEN in lung cancer. Thus, use of small molecule inhibitors that hinder PTEN phosphorylation is a plausible approach to activate PTEN function in the treatment of lung cancer.AbbreviationsAKTV-Akt Murine Thymoma Viral OncogeneCACancer adjacentCDK1Cyclin dependent kinase 1CENPC-CCentromere Protein CChIPChromatin Immunoprecipitationco-IPCo-immunoprecipitationCOSMICCatalog of Somatic Mutations In CancerCREBcAMP Responsive Element Binding ProteinC-tailCarboxy terminal tailE2F1E2F Transcription Factor 1ECISElectric Cell-substrate Impedance SensingEGFREpidermal Growth Factor ReceptorGSIGamma Secretase InhibitorHDAC1Histone Deacetylase 1HP1Heterochromatin protein 1KAP1/TRIM28KRAB-Associated Protein 1/Tripartite Motif Containing 28MAF1Repressor of RNA polymerase III transcription MAF1 homologMCM2Minichromosome Maintenance Complex Component 2miRNAmicro RNAMTF1Metal-Regulatory Transcription Factor 1PARPPoly(ADP-Ribose) PolymerasePD-1Programmed Cell Death 1PD-L1Programmed Cell Death 1 Ligand 1PI3KPhosphatidylinositol-4,5-Bisphosphate 3-KinasePLKPolo-like KinasepPTENPhosphorylated PTENPTENPhosphatase and Tensin Homolog deleted on chromosome tenPTMPost Translational ModificationRad51RAD51 RecombinaseRad52RAD52 RecombinaseRPA1Replication protein ASILACStable Isotope Labeling with Amino Acids in Cell CultureSRFSerum Response FactorTKITyrosine Kinase inhbitorsTMATissue MicroarrayTOP2ADNA Topoisomerase 2A

DCLK1 expression is critically required for maintaining growth of human colon cancer cells (hCCCs). Human colorectal tumors (CRCs) and hCCCs express a novel short isoform of DCLK1 (DCLK1-S; isoform 2) from β-promoter of hDCLK1 gene, while normal colons express long isoform (DCLK1-L; isoform 1) from 5′(α)-promoter, suggesting that DCLK1-S, and not DCLK1-L, marks cancer stem cells (CSCs). Even though DCLK1-S differs from DCLK1-L by only six amino acids, we succeeded in generating a monospecific DCLK1-S-Antibody (PS41014), which does not cross-react with DCLK1-L, and specifically detects CSCs. Subcellular localization of S/L-isoforms was examined by immune-electron-microscopy (IEM). Surprisingly, besides plasma membrane and cytosolic fractions, S/L also localized to nuclear/mitochondrial fractions, with pronounced localization of S-isoform in the nuclei and mitochondria. Sporadic CRCs develop from adenomas. Screening colonoscopy is used for detection/resection of growths, and morphological/pathological criteria are used for risk assessment and recommendations for follow-up colonoscopy. But, these features are not precise and majority of the patients will never develop cancer. We hypothesized that antibody-based assay(s), which identify CSCs, will significantly improve prognostic value of morphological/pathological criteria. We conducted a pilot retrospective study with PS41014-Ab, by staining archived adenoma specimens from patients who developed (high-risk), or did not develop (low-risk) adenocarcinomas within 10–15 years. PS41014-Ab stained adenomas from initial and follow-up colonoscopies of high-risk patients, at significantly higher levels (three to fivefold) than adenomas from low-risk patients, suggesting that PS41014-Ab could be used as an additional tool for assessing CRC risk. CRC patients, with high DCLK1-S-expressing tumors (by qRT-PCR), were reported to have worse overall survival than low expressers. We now report that DCLK1-S-specific Ab may help to identify high-risk patients at the time of index/screening colonoscopy.

DCLK1 expression is critically required for maintaining growth of human colon cancer cells (hCCCs). Human colorectal tumors (CRCs) and hCCCs express a novel short isoform of DCLK1 (DCLK1-S; isoform 2) from β-promoter of hDCLK1gene, while normal colons express long isoform (DCLK1-L; isoform 1) from 5′(α)-promoter, suggesting that DCLK1-S, and not DCLK1-L, marks cancer stem cells (CSCs). Even though DCLK1-S differs from DCLK1-L by only six amino acids, we succeeded in generating a monospecific DCLK1-S-Antibody (PS41014), which does not cross-react with DCLK1-L, and specifically detects CSCs. Subcellular localization of S/L-isoforms was examined by immune-electron-microscopy (IEM). Surprisingly, besides plasma membrane and cytosolic fractions, S/L also localized to nuclear/mitochondrial fractions, with pronounced localization of S-isoform in the nuclei and mitochondria. Sporadic CRCs develop from adenomas. Screening colonoscopy is used for detection/resection of growths, and morphological/pathological criteria are used for risk assessment and recommendations for follow-up colonoscopy. But, these features are not precise and majority of the patients will never develop cancer. We hypothesized that antibody-based assay(s), which identify CSCs, will significantly improve prognostic value of morphological/pathological criteria. We conducted a pilot retrospective study with PS41014-Ab, by staining archived adenoma specimens from patients who developed (high-risk), or did not develop (low-risk) adenocarcinomas within 10–15 years. PS41014-Ab stained adenomas from initial and follow-up colonoscopies of high-risk patients, at significantly higher levels (three to fivefold) than adenomas from low-risk patients, suggesting that PS41014-Ab could be used as an additional tool for assessing CRC risk. CRC patients, with high DCLK1-S-expressing tumors (by qRT-PCR), were reported to have worse overall survival than low expressers. We now report that DCLK1-S-specific Ab may help to identify high-risk patients at the time of index/screening colonoscopy.

In this letter, the use of quantum information as a security enabler for the future driverless vehicle is explored. Specifically, the role combined classical and quantum information can have on the most important characteristic of the driverless vehicle paradigm—the vehicle location is investigated. By using information-theoretic verification frameworks, coupled with emerging quantum-based location-verification procedures, how vehicle positions can be authenticated with a probability of error simply not attainable in classical-only networks is shown. How other quantum applications can be seamlessly encapsulated within the same vehicular communication infrastructure required for location verification is also discussed. The two technology enablers required for the driverless quantum vehicle are an increase in current quantum memory timescales (likely) and wide-scale deployment of classical vehicular communication infrastructure (underway). It is argued that the enhanced safety features delivered by the “quantum car” mean its eventual deployment is inevitable.

Death receptor 5 (DR5) is an apoptosis-inducing membrane receptor that mediates cell death in several life-threatening conditions. There is a crucial need for the discovery of DR5 antagonists for the therapeutic intervention of conditions in which the overactivation of DR5 underlies the pathophysiology. DR5 activation mediates cell death in non-alcoholic fatty liver disease (NAFLD) and neurodegenerative processes including amyloid-beta (Aβ) accumulation, spinal cord injury (SCI), and brain ischemia. In the current work, we used fluorescence resonance energy transfer (FRET) to monitor the conformational dynamics of DR5 that mediate death signaling. We used a time-resolved FRET screening platform to screen the Selleck library of 2863 U.S. Food and Drug Administration (FDA)-approved compounds. The high-throughput screen (HTS) identified 13 compounds that modulated the FRET between DR5 monomers beyond 5 median absolute deviations (MADs) from the DMSO controls. Of these 13 compounds, indirubin was identified to specifically inhibit tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced caspase-8 activity without modulating DR5 surface expression or TRAIL binding. Indirubin inhibited Fas-associated death domain (FADD) oligomerization and increased cellular FLICE-inhibitory protein (c-FLIP) expression; both are molecular mechanisms involved in inhibiting the DR5 signaling cascade. This study has elucidated previously unknown properties of indirubin that make it a promising candidate for therapeutic investigation of diseases in which overactivation of DR5 underlies pathology.

Understanding how diversity is partitioned across the landscape provides perspectives on the environmental processes that have influenced the evolutionary history of organisms. We analyzed spatial demography, historical biogeography, and niche divergence of the western jumping mouse (Zapus princeps) using molecular sequence data from mitochondrial and nuclear DNA recovered from 7 of the 11 subspecies in western North America. Phylogeographic structure within Z. princepswas partitioned across 5 clades (Boreal, Northern Sierra, Southern Rockies, Southern Sierra, and Uinta). Two lineages detected in the Sierra Nevada of California (Northern Sierra and Southern Sierra) were more closely allied to Z. trinotatusthan to other lineages of Z. princepsand species distribution models mirror these phylogenetic signatures by detecting wide overlap in niches for Sierran jumping mice and Z. trinotatusas compared to other Z. princeps. Four southern lineages are deeply divergent and limited to disjunct mesic and montane habitats within the xeric southwestern United States, whereas the 5th lineage is widespread, extending from Wyoming to Alaska and reflecting expansion northward following deglaciation, a common pattern in boreal mammals.

AbstractAn experimental facility for in situ measurements of high-temperature spectral emissivity of materials in environments of interest to the gas-cooled very high temperature reactor (VHTR) has been developed. The facility is capable of measuring emissivities of seven materials in a single experiment, thereby enhancing the accuracy in measurements due to even minor systemic variations in temperatures and environments. The system consists of a cylindrical silicon carbide (SiC) block with seven sample cavities and a deep blackbody cavity, a detailed optical system, and a Fourier transform infrared spectrometer. The reliability of the facility has been confirmed by comparing measured spectral emissivities of SiC, boron nitride, and alumina (Al2O3) at 600°C against those reported in literature. The spectral emissivities of two candidate alloys for VHTR, INCONEL® alloy 617 (INCONEL is a registered trademark of the Special Metals Corporation group of companies) and SA508 steel, in air environment at 700°C were measured.

The purpose of this study was to examine how pretransfer experiences and preparation, along with posttransfer experiences, influence the adjustment of community college transfer students (as measured by academic achievement and satisfaction with various aspects of the university experience) to life on a four-year university campus. A survey of 372 community college transfer students attending a large, public four-year university provides empirical evidence that those students who are best informed and who have most actively prepared for transfer are most likely to achieve higher grades and be more satisfied in the university environment. The findings from this study also suggested that patterns of academic and social involvement shift as students move from two-year college settings to a four-year university. The article concludes with a discussion of strategies that can be instituted at both two and four-year institutions to assist community college transfer students in making a successful transition to a four-year college or university.

The study investigated Asian American students’ perceptions of racial climate in comparison with those of White counterparts at a large public university. It also examined students’ reporting behaviors upon encountering incidents of racial harassment as well as their awareness of reporting procedures, the Student Code of Conduct, and civil rights. The results indicated that Asian American students were more likely to report negative perceptions and were found to be less aware of their rights and procedures. The study included several implications for student affairs practitioners in order to better understand and serve this population of students.

The purpose of this study was to examine how pretransfer experiences and preparation, along with posttransfer experiences, influence the adjustment of community college transfer students (as measured by academic achievement and satisfaction with various aspects of the university experience) to life on a four-year university campus. A survey of 372 community college transfer students attending a large, public four-year university provides empirical evidence that those students who are best informed and who have most actively prepared for transfer are most likely to achieve higher grades and be more satisfied in the university environment. The findings from this study also suggested that patterns of academic and social involvement shift as students move from two-year college settings to a four-year university. The article concludes with a discussion of strategies that can be instituted at both two and four-year institutions to assist community college transfer students in making a successful transition to a four-year college or university.

The study investigated Asian American students’ perceptions of racial climate in comparison with those of White counterparts at a large public university. It also examined students’ reporting behaviors upon encountering incidents of racial harassment as well as their awareness of reporting procedures, the Student Code of Conduct, and civil rights. The results indicated that Asian American students were more likely to report negative perceptions and were found to be less aware of their rights and procedures. The study included several implications for student affairs practitioners in order to better understand and serve this population of students.

This essay examines the meaning of scholarship in student affairs from teaching and research perspectives. It suggests that the scholarship of teaching needs more emphasis within the field of student affairs. Several concerns related to what is taught, how it is taught, and to whom it is taught are addressed. The essay also suggests that the scholarship of research should not be limited to empiricism and the generation and testing of theories. It argues that various notions of research should be considered as scholarship as long as rigorous, traditional, methodological standards are practiced.

This essay examines the meaning of scholarship in student affairs from teaching and research perspectives. It suggests that the scholarship of teaching needs more emphasis within the field of student affairs. Several concerns related to what is taught, how it is taught, and to whom it is taught are addressed. The essay also suggests that the scholarship of research should not be limited to empiricism and the generation and testing of theories. It argues that various notions of research should be considered as scholarship as long as rigorous, traditional, methodological standards are practiced.

We report the results of NMR studies and computer simulations of potent antagonists reflective of the αIIbβ3 receptor-bound conformations. The peptides c[Mpa–¹⁵N-Arg¹–¹⁵N-Gly²–¹⁵N-Asp³–¹⁵N-Phe⁴–¹⁵N-Arg⁵–Cys]-NH2 (Phe–Arg analog) (Mpa: 3-mercaptopropionic acid) and c[Mpa–¹⁵N-Arg¹–¹⁵N-Gly²–¹⁵N-Asp³–¹⁵N-Asp⁴–¹⁵N-Val⁵–Cys]-NH2 (Asp–Val analog) were subjected to ¹⁵N-edited NMR experiments to study the conformations of these peptides in the absence and in the presence of αIIbβ3 receptor. The NMR studies of the Phe–Arg analog, a selective αIIbβ3 antagonist, resulted in distinctly different experimental data in the presence and absence of the receptor. The computer simulations for this peptide resulted in one large family of structures consistent with the experimental data. This conformation suggests a type I β-turn spanning residues Arg¹ and Gly² when bound to the receptor and we were able to establish a model for the three dimensional arrangement of the pharmacophores. The studies on the Asp–Val analog, an αvβ3 antagonist that binds to the αIIbβ3 with moderate affinity, resulted in conformations that are not as well defined as those for the Phe–Arg analog but are consistent with the model established for this analog. These results are important for the design of novel αIIbβ3 antagonists. © 2003 Wiley Periodicals, Inc. Biopolymers (Pept Sci) 66: 326–338, 2002

Subunit 7 or the Qcr7 protein of the cytochrome bc1 complex in yeast is a nuclear-encoded 14-kDa protein and is essential for formation of a functional bc1 complex and respiration. It was shown previously that the N-terminal region of the Qcr7 protein might play little role in import but may be essential for correct assembly of the bc1 complex. To examine the role of the N-terminus in assembly of the bc1 complex, various N-terminus deletion and point mutants of the QCR7 gene were expressed in yeast strains where the endogenous QCR7 gene has been inactivated. Deletion of the first 8–15 residues after methionine at the N-terminus of the Qcr7 protein was studied and it was shown that except for the Qcr7p-Δ7 mutant, the strains overexpressing deletion mutants (Qcr7p-Δ8 to Qcr7p-Δ14) displayed decreased steady-state levels of iron–sulfur protein (ISP) and 14-kDa (Qcr7) and 11-kDa (Qcr8) subunits, as well as a respiratory defect. It was shown that introducing mutations at the N-terminus of the QCR7 gene in the Δ7 context had more drastic effects on respiration and assembly than in the full-length context, suggesting that the first seven residues at the N-terminus have a role in increasing the stability of the holocomplex. This led to a respiratory-deficient phenotype and drastic decrease in the steady-state levels of Qcr7 (14-kDa) and Qcr8 (11-kDa) proteins. The mutants Qcr7p-Δ7 (R10I), Qcr7p-Δ7 (G12V), Qcr7p-Δ7 (D13G), Qcr7p-Δ7 (D13V), and Qcr7p-Δ7 (D13Y) showed decreases in the steady-state levels of ISP and 14- and 11-kDa subunits, as well as defects in respiration. These results are interpreted in the light of the X-ray crystal structure of the yeast bc1 complex.

The Internet and its varied applications have redefined the student affairs landscape. The most commonly used resources include e-mail, Internet discussion groups (listservs), and the World Wide Web. While these technological tools have become widespread throughout the profession, no empirical studies have been conducted to gauge their pervasiveness.

The Internet and its varied applications have redefined the student affairs landscape. The most commonly used resources include e-mail, Internet discussion groups (listservs), and the World Wide Web. While these technological tools have become widespread throughout the profession, no empirical studies have been conducted to gauge their pervasiveness.

The Ras superfamily of GTPases act as important regulatory switches to co-ordinate extracellular stimuli with activation of intracellular signaling pathways and appropriate biological responses. The Ras branch of this superfamily includes H-, K- and N-Ras, which are commonly mutated in particular human cancers, but notably not in those of the breast. Instead, in breast cancer the signaling pathways involving these GTPases may be upregulated due to increased coupling to growth factor receptors or other tyrosine kinases commonly overexpressed in this disease, or increased expression of regulators, the Ras protein itself, or downstream effectors. Functional studies utilizing both in vitro and in vivo models demonstrate that Ras signaling can regulate a variety of endpoints relevant to breast cancer progression, including anchorage dependent and independent growth, tumorigenesis, steroid sensitivity and invasion. Finally, analysis of the processing and signaling mechanisms of the Ras superfamily has identified potential targets for therapeutic intervention.