Abstract: Granulin-epithelin precursor (GEP), a pluripotent growth factor, is a hepatic oncofetal protein defining a cancer stem cell (CSC) population in liver cancer. The present invention provides the use of GEP inhibitors (including anti-GEP antibody) for inhibiting immune evasion by liver cancer cells and for eliminating liver cancer stem cells.

Abstract: Compositions and methods for diagnosing, treating and/or preventing cancers characterized by CDH17 overexpression based on the detection of CDH17 or the use of CDH17 as a target for therapeutic intervention or prophylactic intervention are provided. Methods for diagnosing and/or monitoring liver cancers using the expressing of CDH17 involve detecting and/or quantitating the CDH17 protein or encoding nucleic acids (DNA or RNA) in a biological sample such as urine from the subject. Methods for treating liver cancers using CDH17 as a target and of sensitizing cells with aberrant expression of CDH17 have also been developed. The methods include suppression or knockdown of the expression of CDH17 by administering an effective amount of a CDH17 inhibitor.

Abstract: Granulin-epithelin precursor (GEP), a pluripotent growth factor, is a hepatic oncofetal protein defining a cancer stem cell (CSC) population in liver cancer. The present invention provides the use of GEP inhibitors (including anti-GEP antibody) for inhibiting immune evasion by liver cancer cells and for eliminating liver cancer stem cells.

Abstract: This invention relates to the diagnosis and treatment of cancerous diseases, particularly to the mediation of cytotoxicity of primary and metastatic human tumor cells; and most particularly to the use of an isolated monoclonal antibody or cancerous disease modifying antibodies (CDMAB) thereof, optionally in combination with one or more chemotherapeutic agents, as a means for initiating the cytotoxic response in such human tumors, e.g. any primary or metastatic tumor sites which arise from hepatocytes. The invention further relates to binding assays which utilize the CDMAB of the instant invention.

Abstract: This invention relates to the diagnosis and treatment of cancerous diseases, particularly to the mediation of cytotoxicity of primary and metastatic human tumor cells; and most particularly to the use of an isolated monoclonal antibody or cancerous disease modifying antibodies (CDMAB) thereof, optionally in combination with one or more chemotherapeutic agents, as a means for initiating the cytotoxic response in such human tumors, e.g. any primary or metastatic tumor sites which arise from hepatocytes. The invention further relates to binding assays which utilize the CDMAB of the instant invention.

Abstract: This invention relates to the diagnosis and treatment of cancerous diseases, particularly to the mediation of cytotoxicity of primary and metastatic human tumor cells; and most particularly to the use of an isolated monoclonal antibody or cancerous disease modifying antibodies (CDMAB) thereof, optionally in combination with one or more chemotherapeutic agents, as a means for initiating the cytotoxic response in such human tumors, e.g. any primary or metastatic tumor sites which arise from hepatocytes. The invention further relates to binding assays which utilize the CDMAB of the instant invention.

Abstract: This invention provides a composition comprising the following polynucleotide probes: IL7R (AA485865) (SEQ ID NO:7), NDRGI (AA486403) (SEQ ID NO:8), EST1 (H50345) (SEQ ID NO:9), TRPC1 (AA017132) (SEQ ID NO:10), GFRA1 (AA512935) (SEQ ID NO:11), EST2 (AA454543) (SEQ ID NO:12), CLDN10 (R54559) (SEQ ID NO:13), DNALI1 (R93087) (SEQ ID NO:14), RBP5 (AA453198) (SEQ ID NO:15), EST3 (AA621761) (SEQ ID NO:16), EST4 (N63706) (SEQ ID NO:17), PCOLCE (AA670200) (SEQ ID NO:18), TDO2 (T72398) (SEQ ID NO:19), EST5 (T47454) (SEQ ID NO:20), HIST1H2BD (N33927) (SEQ ID NO:21), PXMP2 (N70714) (SEQ ID NO:22), ACAS2 (AA455146) (SEQ ID NO:23), ANAPC7 (T68445) (SEQ ID NO:24), EST6 (AA576580) (SEQ ID NO:25), RBP5 (N92148) (SEQ ID NO:26), ANXAI (H63077) (SEQ ID NO:27), CKB (AA894557) (SEQ ID NO:28), ITGBL1 (N52533) (SEQ ID NO:29), KPNA2 (AA676460) (SEQ ID NO:30), EST7 (W90740) (SEQ ID NO:31) and MEG3 (W85841) (SEQ ID NO:32).

Abstract: Described herein are methods for manipulating GEP and/or drug transporters (e.g., ABCB5 and/or ABCF1) on a cell, as well as related products. Also described herein are methods for treating cancer cells using GEP and/or drug transporter and/or their binding molecules and suppression thereof. Methods of cancer treatment targeting the GEP and/or drug transporters, alone or in combination with chemotherapy are also described herein. Also provided herein are sets of markers whose expression patterns can be used to differentiate clinical conditions, such as high or low levels of GEP and drug transporters. Based on the levels of GEP and drug transporters, the likelihood of cancer recurrences, drug sensitivity, and prognosis can be determined. Methods of classifying and treating patients based on the prognosis are also provided herein.

Abstract: This invention relates to the diagnosis and treatment of cancerous diseases, particularly to the mediation of cytotoxicity of primary and metastatic human tumor cells; and most particularly to the use of an isolated monoclonal antibody or cancerous disease modifying antibodies (CDMAB) thereof, optionally in combination with one or more chemotherapeutic agents, as a means for initiating the cytotoxic response in human tumors, e.g. any primary or metastatic tumor sites which arise from hepatocytes and to binding assays which utilize the CDMAB of the instant invention.

Abstract: Bacterial lipopolysaccharide (LPS) in systemic circulation triggers deleterious super-inflammatory response, which is key pathogenesis of many disorders like gram-negative sepsis and necrotizing enterocolitis. No effective therapeutic interventions are currently available for protection of patients against mortality. Disclosed are methods and therapeutic agents that ablate the biological toxicity of LPS in circulation (Integrin Peptide), and abrogate leukocyte infiltration into lung and liver and suppress adhesion molecule expression (Integrin Peptide and Anti-CD18 ?A scFv). These therapeutic agents can be used alone, or in combination for treatment of endotoxin-mediated pro-inflammatory responses, particularly in cases of acute sepsis and necrotizing enterocolitis.

Abstract: Compositions and methods for diagnosing, treating and/or preventing cancers characterized by CDH17 overexpression based on the detection of CDH17 or the use of CDH17 as a target for therapeutic intervention or prophylactic intervention are provided. Methods for diagnosing and/or monitoring liver cancers using the expressing of CDH17 involve detecting and/or quantitating the CDH17 protein or encoding nucleic acids (DNA or RNA) in a biological sample such as urine from the subject. Methods for treating liver cancers using CDH17 as a target and of sensitizing cells with aberrant expression of CDH17 have also been developed. The methods include suppression or knockdown of the expression of CDH17 by administering an effective amount of a CDH17 inhibitor.

Abstract: Bacterial lipopolysaccharide (LPS) in systemic circulation triggers deleterious super-inflammatory response, which is key pathogenesis of many disorders like gram-negative sepsis and necrotizing enterocolitis. No effective therapeutic interventions are currently available for protection of patients against mortality. Disclosed are methods and therapeutic agents that ablate the biological toxicity of LPS in circulation (Integrin Peptide), and abrogate leukocyte infiltration into lung and liver and suppress adhesion molecule expression (Integrin Peptide and Anti-CD18 ?A scFv). These therapeutic agents can be used alone, or in combination for treatment of endotoxin-mediated pro-inflammatory responses, particularly in cases of acute sepsis and necrotizing enterocolitis.

Abstract: This invention provides a composition comprising the following polynucleotide probes: IL7R (AA485865) (SEQ ID NO:7), NDRGI (AA486403) (SEQ ID NO:8), EST1 (H50345) (SEQ ID NO:9), TRPC1 (AA017132) (SEQ ID NO:10), GFRA1 (AA512935) (SEQ ID NO:11), EST2 (AA454543) (SEQ ID NO:12), CLDN10 (R54559) (SEQ ID NO:13), DNALI1 (R93087) (SEQ ID NO:14), RBP5 (AA453198) (SEQ ID NO:15), EST3 (AA621761) (SEQ ID NO:16), EST4 (N63706) (SEQ ID NO:17), PCOLCE (AA670200) (SEQ ID NO:18), TDO2 (T72398) (SEQ ID NO:19), EST5 (T47454) (SEQ ID NO:20), HIST1H2BD (N33927) (SEQ ID NO:21), PXMP2 (N70714) (SEQ ID NO:22), ACAS2 (AA455146) (SEQ ID NO:23), ANAPC7 (T68445) (SEQ ID NO:24), EST6 (AA576580) (SEQ ID NO:25), RBP5 (N92148) (SEQ ID NO:26), ANXAI (H63077) (SEQ ID NO:27), CKB (AA894557) (SEQ ID NO:28), ITGBL1 (N52533) (SEQ ID NO:29), KPNA2 (AA676460) (SEQ ID NO:30), EST7 (W90740) (SEQ ID NO:31) and MEG3 (W85841) (SEQ ID NO:32).

Abstract: This invention relates to the diagnosis and treatment of cancerous diseases, particularly to the mediation of cytotoxicity of primary and metastatic human tumor cells; and most particularly to the use of an isolated monoclonal antibody or cancerous disease modifying antibodies (CDMAB) thereof, optionally in combination with one or more chemotherapeutic agents, as a means for initiating the cytotoxic response in such human tumors, e.g. any primary or metastatic tumor sites which arise from hepatocytes. The invention further relates to binding assays which utilize the CDMAB of the instant invention.

Abstract: This invention provides methods for detecting serum GEP level. This invention further provides methods for determining whether a subject is afflicted with Hepatocellular carcinoma (HCC) by measuring serum GEP level. In another embodiment, this invention provides methods for the suppression of HCC growth and progression both in vitro and in vivo by treating a patient with anti-GEP monoclonal antibody A23.

Abstract: The present invention provides adeno-associated viral (AAV) vectors encoding an angiostatin protein (“AAV-angiostatin vector”) and/or a costimulatory molecule B7.1 (“AAV-B7.1 vector”). The AAV-angiostatin vector can be administered to a subject, alone or in combination, sequentially or simultaneously, with a AAV-B7.1 vector for treatment, management or prevention of metastatic tumors. Pharmaceutical compositions and vaccines comprising the AAV-angiostatin vector and/or the AAV-B7.1 vector and methods of manufacturing are also described. Administration of AAV-angiostatin and AAV-B7.1 vectors by intraportal and muscular injections are also provided.