Abstract: The present disclosure relates generally to compounds that bind to and act as degraders of an IKAROS Family Zinc Finger (IKZF) protein, such as IKZF2 (Helios) and/or IKZF4 (Eos). The disclosure further relates to the use of the compounds for the preparation of a medicament for the treatment of diseases and/or conditions through binding and degradation of an IKZF protein, such as IKZF2 and/or IKZF4, including cancer.

Abstract: Apparatuses, systems, and techniques to annotate images using neural models. In at least one embodiment, neural networks generate mask information from labels of one or more objects within one or more images identified by one or more other neural networks.

Abstract: The present disclosure relates generally to certain 6-azabenzimidazole compounds, pharmaceutical compositions comprising said compounds, and methods of making and using said compounds and pharmaceutical compositions. The compounds and compositions disclosed herein may be used for the treatment or prevention of diseases, disorders, or infections modifiable by hematopoietic progenitor kinase 1 (HPK1) inhibitors, such as HBV, HIV, cancer, and/or a hyper-proliferative disease.

Abstract: A method of treating cancer in a subject includes contacting an enriched population of T-cells obtained from cancer or tumor draining lymph nodes ex-vivo with: an anti-CD3 antibody, an anti-CD28 antibody, and/or functional fragments thereof, and optionally a VEGF inhibitor and/or an IL-2 receptor agonist, at amounts effective to activate and expand the T-cells and administering the activated and expanded T-cells to the subject.

Abstract: A method of treating a subject having cancer is described that includes administering a therapeutically effective amount of a ?-(1,3)-(1,4) glucan to the subject. Methods of immunostimulating in a subject by administering an effective amount of a ?-(1,3)-(1,4) glucan to the subject are also described.

Abstract: A method of treating a subject having cancer is described that includes administering a therapeutically effective amount of a ?-(1,3)-(1,4) glucan to the subject. Methods of immunostimulating in a subject by administering an effective amount of a ?-(1,3)-(1,4) glucan to the subject are also described.

Abstract: A method of treating a subject having cancer is described that includes administering a therapeutically effective amount of a ?-(1,3)-(1,4) glucan to the subject. Methods of immunostimulating in a subject by administering an effective amount of a ?-(1,3)-(1,4) glucan to the subject are also described.

Abstract: A method of treating cancer in a subject includes contacting an enriched population of T-cells obtained from cancer or tumor draining lymph nodes ex-vivo with: an anti-CD3 antibody, an anti-CD28 antibody, and/or functional fragments thereof, and optionally a VEGF inhibitor and/or an IL-2 receptor agonist, at amounts effective to activate and expand the T-cells and administering the activated and expanded T-cells to the subject.

Abstract: A method for the expansion of tumor-specific T-cells includes obtaining an enriched population of T-cells from a subject with cancer; and contacting the enriched population of T-cells ex-vivo with: (i) an anti-CD3 antibody, an anti-CD28 antibody, and/or functional fragments thereof, and (ii) a VEGF inhibitor, to activate and expand the T-cells.

Abstract: A method for the expansion of tumor-specific T-cells includes obtaining an enriched population of T-cells from a subject with cancer; and contacting the enriched population of T-cells ex-vivo with: (i) an anti-CD3 antibody, an anti-CD28 antibody, and/or functional fragments thereof, and (ii) a VEGF inhibitor, to activate and expand the T-cells.

Abstract: The present invention relates to nucleic acid molecules such as ribozymes, DNAzymes, short interfering RNA (siRNA), short interfering nucleic acid (siNA), and antisense which modulate the synthesis, expression and/or stability of an mRNA encoding one or more receptors of vascular endothelial growth factor, such as flt-1 (VEGFR1) and/or KDR (VEGFR2). Nucleic acid molecules and methods for the inhibition of angiogenesis and treatment of cancer and other conditions associated with VEGF-R are provided, optionally in conjunction with other therapeutic agents such as interferons.

Abstract: The present invention relates to nucleic acid molecules such as ribozymes, DNAzymes, short interfering RNA (siRNA), short interfering nuleic acid (siNA), and antisense which modulate the synthesis, expression and/or stability of an mRNA encoding one or more receptors of vascular endothelial growth factor, such as flt-1 (VEGFR1) and/or KDR (VEGFR2). Nucleic acid molecules and methods for the inhibition of angiogenesis and treatment of cancer and other conditions associated with VEGF-R are provided, optionally in conjunction with other therapeutic agents such as interferons.

Abstract: Disclosed is a method for improving the treatment of a cancer patient which is undergoing (adjuvant) chemotherapy. Prior to or concomitant with the patient receiving adjuvant chemotherapy, the patient is administered mitogenically stimulated lymph node lymphocytes or the supernatant therefrom. The lymph node lymphocytes are patient excised lymph node lymphocytes enriched in tumor reactive cells, such as CD4+ tumor reactive cells. Radiolabeled locators (e.g., antibodies) can be used along with a portable radiation detector to intraoperatively determine which lymph nodes bear lymph node lymphocytes enriched in tumor reactive cells. The patient excised lymph node lymphocytes enriched in tumor reactive cells then are subjected to mitogenic stimulation for their expansion and administration to the patient.

Abstract: The present invention is directed to a method for reliably determining lymph nodes enriched in tumor reactive cells, e.g., CD4+tumor-specific lymphocytes. This method includes the steps of administering to a patient an effective amount of a radiolabeled locator which specifically binds a marker produced by or associated with neoplastic tissue. Time is permitted to elapse following the administration for the radiolabeled locator to preferentially concentrate in any neoplastic tissue and for unbound radiolabeled locator to be cleared, so as to increase the ratio of photon emissions from neoplastic tissue to background photon emissions in the patient. After the time has elapsed, the patient is accessed with a radiation detection probe for determining lymph node sites exhibiting accretion of the radiolabeled locator by detecting with the probe elevated levels of radiation at the lymph node sites.