序号 专利名 申请号 申请日 公开(公告)号 公开(公告)日 发明人
181 METHODS TO PREDICT AND PREVENT RESISTANCE TO TAXOID COMPOUNDS US14865115 2015-09-25 US20160011211A1 2016-01-14 Bruce R. Zetter; Sabarni K. Chatterjee
Embodiments of the invention are directed to methods for predicting the resistance of cancer to members of the taxoid family by measuring the levels of prohibitin. Methods for treating cancer and taxoid family member resistant cancers using inhibitors of prohibitin, as well as therapeutic complexes that target prohibitin are also provided.
182 TREATMENT-INDUCED DAMAGE TO THE TUMOR MICRO-ENVIRONMENT PROMOTES CANCER THERAPY RESISTANCE THROUGH EXTRACELLULAR PROTEINS US14418789 2013-08-02 US20150309037A1 2015-10-29 Peter S. Nelson; Yu Sun
The present disclosure provides methods for determining the effectiveness of a cancer therapy, as well as methods for increasing the effectiveness of that therapy and determining a prognosis for a patient receiving that therapy.
183 Methods to predict and prevent resistance to taxoid compounds US13404398 2012-02-24 US09151758B2 2015-10-06 Bruce R. Zetter; Sabarni K. Chatterjee
Embodiments of the invention are directed to methods for predicting the resistance of cancer to members of the taxoid family by measuring the levels of prohibitin. Methods for treating cancer and taxoid family member resistant cancers using inhibitors of prohibitin, as well as therapeutic complexes that target prohibitin are also provided.
184 FUNCTIONAL ASSAY FOR CANCER RECURRENCE AND MALIGNANT POTENTIAL US14424948 2013-08-14 US20150212072A1 2015-07-30 Sandra S. Mcallister; Zafira Castano
Embodiments herein provides an in vitro co-culture system comprising a population of cancer responder cells and a population of non-tumor cells wherein the cancer responder cells can convert to a malignant state and exhibit hallmark malignant phenotype when the cells are placed in a tumor supportive environment. The system is useful for prognosis evaluation of cancer recurrence, malignancy development, cancer drug screening and surveillance for resistance to cancer drug therapy.
185 METHODS AND SYSTEMS FOR PREDICTING DRUG-RESPONSE US14380064 2013-02-21 US20150024409A1 2015-01-22 Nahid Razi
Disclosed herein are methods and systems for determining whether a cell is resistant to one or more drugs. Also, disclosed herein are methods and systems for monitoring the treatment of a cancer patient to determine whether the cancerous cells being treated are resistant to the treatment. Further, disclosed herein are methods and systems for predicting the responsiveness of a cell to a drug. Also, disclosed herein are methods and systems to determine the rate of the efficacy of a chemotherapeutic drug on a cancerous, neoplastic or damaged cells
186 Using Adaptive Immunity to Detect Drug Resistance US14365479 2012-12-17 US20140349320A1 2014-11-27 Gregory P. Bisson; Drew Weissman; Harvey Rubin
The present invention relates to a method of using adaptive immunity to detect drug resistance in infectious diseases. The invention provides novel antigens associated with drug resistant MTB infection.
187 Methods for the identification, assessment, and treatment of patients with cancer therapy US13600260 2012-08-31 US08889354B2 2014-11-18 Barbara M. Bryant; Andrew I. Damokosh; George J. Mulligan
The present invention is directed to the identification of predictive markers that can be used to determine whether patients with cancer are clinically responsive or non-responsive to a therapeutic regimen prior to treatment. In particular, the present invention is directed to the use of certain individual and/or combinations of predictive markers, wherein the expression of the predictive markers correlates with responsiveness or non-responsiveness to a therapeutic regimen. Thus, by examining the expression levels of individual predictive markers and/or predictive markers comprising a marker set, it is possible to determine whether a therapeutic agent, or combination of agents, will be most likely to reduce the growth rate of tumors in a clinical setting.
188 QUANTITATIVE ASSAYS FOR RAS P21 IN BODY FLUIDS US14051589 2013-10-11 US20140093890A1 2014-04-03 Walter P. Carney; Peter J. Hamer; Karen Pierce; Sheryl Brown-Shimer
The present invention is directed to the detection and quantification of total ras p21 in body fluids, particularly serial changes of total ras p21 levels in a subject's body fluids. Further, the invention is directed to detecting and quantitating total ras p21 in conjunction with one or more other proteins, such as, oncoproteins, angiogenic factors, tumor markers, inhibitors, growth factor receptors, metastasis proteins, and tumor suppressors. The disclosed methods are diagnostic/prognostic for preneoplastic/neoplastic diseases, and useful to select therapies for patients with preneoplastic/neoplastic diseases. The disclosed methods are further useful to monitor the status of a patient's preneoplastic/neoplastic disease, and/or to monitor how a patient is responding to an anticancer therapy.
189 ANTIBODIES THAT SPECIFICALLY BIND STAPHYLOCOCCUS AUREUS ALPHA TOXIN AND METHODS OF USE US13983804 2012-02-07 US20140072577A1 2014-03-13 Bret Sellman; Christine Tkaczyk; Lei Hua; Partha Chowdhury; Reena Varkey; Melissa Damschroder; Li Peng; Vaheh Oganesyan; Jamese Johnson Hilliard
Herein provided are compositions, methods of manufacture and methods of use pertaining to anti-alpha toxin antibodies and fragments.
190 High Throughput Screening for Antimicrobial Dosing Regimens US13899876 2013-05-22 US20140011762A1 2014-01-09 Vincent H. Tam; Michael Nikolaou
Provided herein are methods and computer-implemented systems for using computer simulations to predict likelihood of a cell population associated with a pathophysiological condition acquiring resistance to a therapeutic agent, to screen for therapeutic agents effective to suppress acquisition of resistance within a cell population and to treat the pathophysiological conditions associated therewith. The computer simulation comprises at least an input/out system and a mathematical model, including operably linked equations, parameter values and constant values, of growth response over a period of time of a cell population in contact with an therapeutic agent. Also provide is a method for determining a best-fit mathematical model of adaptation of a microbial population to a therapeutic agent over time and using the model to simulate microbial population behavior to a therapeutic agent.
191 POLYMORPHISMS IN THE HUMAN GENE FOR THE MULTIDRUG RESISTANCE-ASSOCIATED PROTEIN 1 (MRP-1) AND THEIR USE IN DIAGNOSTIC AND THERAPEUTIC APPLICATIONS US13711281 2012-12-11 US20130309665A1 2013-11-21 Ulrich Brinkmann; Sven Hoffmeyer; Esther Mornhinweg
The present invention relates to a polymorphic MRP-1 polynucleotide, genes or vectors comprising the polynucleotides and a host cell genetically engineered with the polynucleotide or gene. Also provided are methods for producing molecular variant polypeptides, cells capable of expressing a molecular variant polypeptide and a polypeptide encoded by the polynucleotide or the gene or obtainable by the method or cells produced herein. Also provided is an antibody to the polypeptide, a transgenic animal, and a solid support comprising one or a plurality of the provided polynucleotides, genes, vectors, polypeptides, antibodies or host cells. Furthermore, methods of identifying a polymorphism, identifying and obtaining a pro-drug or drug or an inhibitor are also provided. In addition, the invention relates to methods for producing a pharmaceutical composition, diagnosing a disease and detection of the polynucleotide. Furthermore, provided herein are uses of the polynucleotides, genes, vectors, polypeptides or antibodies herein.
192 CD20 negatively converted B-cell malignant lymphoma cell line and utilization thereof US12311281 2007-09-21 US08496927B2 2013-07-30 Tomoki Naoe; Akihiro Tomita; Junji Hiraga
It is intended to provide a tool, a procedure and so on which are useful in developing a therapeutic strategy efficacious in inhibiting or overcoming the resistance against a CD20-directed molecular-targeted drug. Thus, a CD20-negatively converted B-cell malignant lymphocyte cell line is provided. Also, a model animal indicating the pathological conditions of CD20-negatively converted B-cell malignant lymphocyte is provided. Further, a method of screening a substance, which is efficacious against CD20-positive B-cell malignant lymphocyte or CD20-negatively converted B cell malignant lymphocyte, is provided. Furthermore, a drug against CD20-positive B-cell malignant lymphocyte or CD20-negatively converted B-cell malignant lymphocyte, which is characterized by being used together with a CD20-directed molecular-targeted drug, is provided. In one embodiment, a DNA methylase inhibitor or a histone deacetylase inhibitor is employed as the active ingredient.
193 METHODS AND COMPOSITIONS FOR CELL PERMEABLE STAT3 INHIBITOR US13806639 2011-06-22 US20130177979A1 2013-07-11 James Turkson
Disclosed herein are compositions for inhibition of Stat, particularly Stat3. Disclosed herein are compositions comprising cell permeable Stat3 inhibitors. Compositions may comprise peptides, polypeptides, antibodies, nucleic acids, vectors, and host cells for making, using, assaying, and evaluating Stat3 inhibitors. Disclosed herein are methods for making and using the disclosed compositions.
194 MASS SPECTROMETRIC MEASUREMENT OF B-LACTAMASE RESISTANCES US13582372 2011-06-10 US20130095511A1 2013-04-18 Markus Kostrzewa; Karsten Michelmann; Katrin Sparbier
The invention relates to the determination of resistances of microorganisms which produce β-lactamases, in particular “extended spectrum β-lactamases” (ESBL). The invention provides a method whereby the microbial resistance can be measured very simply and quickly by means of the catalytic effect of the microbially produced β-lactamases on β-lactam antibiotics, which consists in a hydrolytic cleavage of the β-lactam ring. The method determines the resistance of the bacteria a few hours after a suitable substrate, either a β-lactam antibiotic or a customized β-lactam derivative, has been added to a suspension of the microbes, by direct mass spectrometric measurement of the substrate breakdown caused by the β-lactamases.
195 Predictive and therapeutic markers in ovarian cancer US11814798 2006-01-19 US08404829B2 2013-03-26 Joe W. Gray; Yinghui Guan; Wen-Lin Kuo; Jane Fridlyand; Gordon B. Mills
Cancer markers may be developed to detect diseases characterized by increased expression of apoptosis-suppressing genes, such as aggressive cancers. Genes in the human chromosomal regions, 8q24, 11q13, 20q11-q13, were found to be amplified indicating in vivo drug resistance in diseases such as ovarian cancer. Diagnosis and assessment of amplification levels certain genes shown to be amplified, including PVT1, can be useful in prediction of poor outcome of patient's response and drug resistance in ovarian cancer patients with low survival rates. Certain genes were found to be high priority therapeutic targets by the identification of recurrent aberrations involving genome sequence, copy number and/or gene expression are associated with reduced survival duration in certain diseases and cancers, specifically ovarian cancer. Therapeutics to inhibit amplification and inhibitors of one of these genes, PVT1, target drug resistance in ovarian cancer patients with low survival rates is described.
196 Method of reversing carboplatin resistance by inhibition of HGFIN US13085612 2011-04-13 US08383806B2 2013-02-26 Pranela Rameshwar
The present invention discloses the cloning of a new cDNA, HGFIN, from stimulated bone marrow stromal cells that was retrieved with a probe specific for the neurokinin-1 (NK-1) receptor. The novel gene, HGFIN, encodes a protein receptor that is involved in the regulation of hematopoietic proliferation and differentiation. HGFIN is implicated in the treatment of hyperproliferative disorders, particularly bone and breast cancer, because it acts to suppress the proliferating cells.
197 DIAGNOSTIC MARKER FOR EFFECT OF ANTICANCER AGENT US13635911 2011-03-18 US20130029357A1 2013-01-31 Nobuyuki Ise; Daisuke Nambara; Kazuya Omi
The present invention enables to realize a convenient determination of a therapeutic effect of an anticancer agent on a cancer. Specifically, the present invention provides a diagnostic marker for an effect of an anticancer agent on a cancer, comprising a substance having an affinity for a fragment of an extracellular domain of c-MET; a diagnostic reagent for an effect of an anticancer agent on a cancer, comprising a substance having an affinity for a fragment of an extracellular domain of c-MET and the fragment of the extracellular domain of c-MET; and a method of testing an effect of an anticancer agent on a cancer, comprising (a) measuring a concentration of a fragment of an extracellular domain of c-MET in a biological sample from a subject, and (b) comparing the measured concentration of the fragment of the extracellular domain of c-MET with an indicator which presents a relationship between a concentration of the fragment of the extracellular domain of c-MET and the effect of the anticancer agent on the cancer.
198 METHODS TO PREDICT AND PREVENT RESISTANCE TO TAXOID COMPOUNDS US13404398 2012-02-24 US20130028885A1 2013-01-31 Bruce R. Zetter; Sabarni K. Chatterjee
Embodiments of the invention are directed to methods for predicting the resistance of cancer to members of the taxoid family by measuring the levels of prohibitin. Methods for treating cancer and taxoid family member resistant cancers using inhibitors of prohibitin, as well as therapeutic complexes that target prohibitin are also provided.
199 Methods for the identification, assessment, and treatment of patients with cancer therapy US11449195 2006-06-08 US08278038B2 2012-10-02 Barbara M. Bryant; Andrew I. Damokosh; George Mulligan
The present invention is directed to the identification of predictive markers that can be used to determine whether patients with cancer are clinically responsive or non-responsive to a therapeutic regimen prior to treatment. In particular, the present invention is directed to the use of certain individual and/or combinations of predictive markers, wherein the expression of the predictive markers correlates with responsiveness or non-responsiveness to a therapeutic regimen. Thus, by examining the expression levels of individual predictive markers and/or predictive markers comprising a marker set, it is possible to determine whether a therapeutic agent, or combination of agents, will be most likely to reduce the growth rate of tumors in a clinical setting.
200 Agents and Methods Related to Reducing Resistance to Apoptosis-Inducing Death Receptor Agonists US13356739 2012-01-24 US20120122724A1 2012-05-17 Tong Zhou; Robert P. Kimberly
Provided herein is a method of reversing or preventing a target cell's resistance to a death receptor agonist. Also provided are methods of screening for biomarkers resistance of and monitoring resistance to death receptor agonists. Also provided are methods of selectively inducing apoptosis in a target cell, treating a subject with cancer, autoimmune or inflammatory diseases, comprising administering compositions provided herein. Further provided are compositions comprising agents that modulate CARD containing proteins.
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