Abstract: A method of distinguishing between lung squamous cell carcinoma and head and neck squamous cell carcinoma using a 22-gene biomarker signature is presented.

Abstract: A method of distinguishing between urothelial carcinoma and squamous cell carcinoma of head and neck and lung primaries is presented. A 19-gene signature was developed which differentiates between metastatic urothelial carcinoma and squamous cell carcinoma in a metastatic site when the primary site is either known or unknown.

Abstract: A method of distinguishing between urothelial carcinoma and squamous cell carcinoma of head and neck and lung primaries is presented. A 19-gene signature was developed which differentiates between metastatic urothelial carcinoma and squamous cell carcinoma in a metastatic site when the primary site is either known or unknown.

Abstract: A method of determining disease diagnosis, progression and response to therapy through the use of xenograft animal models for determining cancer biomarkers is presented. In use, a tumor from a patient is transplanted into an animal model such as a mouse. Expression levels of biomarkers for a disease are assessed in the serum of the animal model. A personalized gene expression profile or biomarker gene signature may be obtained from the expression levels of the biomarkers which can be used to determine disease recurrence, progression and response to therapy.

Abstract: The present invention concerns materials and methods useful for distinguishing between liposarcoma and non-liposarcoma. The invention further includes methods for treating a patient having a lesion from which a sample has been analyzed. The invention also includes arrays useful for distinguishing between liposarcoma and non-liposarcoma.

Abstract: A method of distinguishing between lung squamous cell carcinoma and head and neck squamous cell carcinoma using a 22-gene biomarker signature is presented.

Abstract: A method of determining disease diagnosis, progression and response to therapy through the use of xenograft animal models for determining cancer biomarkers is presented. In use, a tumor from a patient is transplanted into an animal model such as a mouse. Expression levels of biomarkers for a disease are assessed in the serum of the animal model. A personalized gene expression profile or biomarker gene signature may be obtained from the expression levels of the biomarkers which can be used to determine disease recurrence, progression and response to therapy.

Abstract: Systems and methods for culturing and monitoring, ex vivo, pharmacologic and metabolic response in a biological sample, including receiving at a fluidic apparatus the biological sample retrieved from the patient, retaining the biological sample within a channel of the fluidic apparatus, providing for the culture of the biological sample within the channel of the fluidic apparatus, flowing a fluid past the biological sample, retrieving and analyzing the fluid to determine a pharmacologic and/or metabolic response of the sample.

Abstract: The subject invention pertains to a non-human animal model of human cancer, methods of producing a non-human animal model of human cancer, methods of using a non-human animal model to propagate human cancer cells, methods of using a non-human animal model to study cancer, methods of using a non-human animal model to screen potential treatments for a subject's cancer, methods of using a non-human animal model for treating cancer in a subject (providing personalized therapy), methods of using a non-human animal model for identifying a biomarker of cancer treatment; and methods of using a non-human animal model for selecting cancer patients for a clinical trial.

Abstract: Assays are provided that can effectively assess tumor response to one or more therapeutic agents. Preferred assays of the invention include assessment of posttranslation modification and expression of target proteins.

Abstract: Assays are provided that can effectively assess tumor response to one or more therapeutic agents. Preferred assays of the invention include assessment of posttranslation modification and expression of target proteins.

Abstract: The present invention is based on the finding that activation of PPAR? plays a key role in inducing growth arrest and differentiation of certain actively proliferating cells. We show that administration of PPAR? agonists, such as thiazolidinedione ligands (TZDs), is effective both in vitro and in vivo at inhibiting the proliferation of such cells.

Abstract: The invention shows that 12-oxo-phytodienoic acid, coronatine, 6-azido-1-oxo-indanoyl isoleucine and related compounds arrest growth and induce cell death of exponentially proliferating cancer cells and malignant B-cell lymphoma cell lines in a dose dependant manner. It appears that the compounds of the present invention are not toxic to cancer cells but rather irreversibly effect cell growth, differentiation and the interaction between the cancer cell and the extracellular matrix.

Abstract: The present invention is based on the finding that activation of PPAR&ggr; plays a key role in inducing growth arrest and differentiation of certain actively proliferating cells. We show that administration of PPAR&ggr; agonists, such as thiazolidinedione ligands (TZDs), is effective both in vitro and in vivo at inhibiting the proiferation of such cells.

Abstract: The present invention is based on the finding that activation of PPAR&ggr; plays a key role in inducing growth arrest and differentiation of certain actively proliferating cells. We show that administration of PPAR&ggr; agonists, such as thiazolidinedione ligands (TZDs), is effective both in vitro and in vivo at inhibiting the proiferation of such cells.

Abstract: The present invention is based on the finding that activation of PPAR&ggr; plays a key role in inducing growth arrest and differentiation of certain actively proliferating cells. We show that administration of PPAR&ggr; agonists, such as thiazolidinedione ligands (TZDs), is effective both in vitro and in vivo at inhibiting the proiferation of such cells.

Abstract: A method for inhibiting proliferation of a PPAR &ggr;-responsive hyperproliferative cell which comprises the step of contacting the cell with (I) an inhibitory amount of a PPAR&ggr; agonist and (II) a MAP kinase inhibitor is disclosed. A method for treating or prophylactically preventing in an animal subject a disorder characterized by unwanted proliferation of PPAR&ggr;-responsive hyperproliferative cells which comprises administering to the subject (I) an inhibitory amount of a PPAR&ggr; agonist and (II) a MAP kinase inhibitor is also disclosed. Pharmaceutical compositions comprising a therapeutically effective amount of a PPAR&ggr; agonist and a MAP kinase inhibitor are disclosed for use in the methods.