Abstract: Provided herein are placental perfusate, placental perfusate cells, and placenta-derived intermediate natural killer cells, and combinations thereof. Also provided herein are compositions comprising the same, and methods of using placental perfusate, placental perfusate cells, and placenta-derived intermediate natural killer cells, and combinations thereof, to suppress the growth or proliferation of tumor cells, cancer cells, and the like, and to treat individuals having tumor cells.

Abstract: Provided herein are methods of producing erythrocytes from hematopoietic cells, particularly hematopoietic cells from placental perfusate in combination with hematopoietic cells from umbilical cord blood, wherein the method results in accelerated expansion and differentiation of the hematopoietic cells to more efficiently produce administrable erythrocytes. Further provided herein is a bioreactor in which hematopoietic cell expansion and differentiation takes place.

Abstract: Methods of treating individuals having sarcoidosis or a sarcoidosis-related disease or disorder using placental cells are described. Also describe are kits comprising placental stem cells or a composition thereof that can be used in methods of treating sarcoidosis or a sarcoidosis-related disease or disorder.

Abstract: Provided herein are methods of producing enhanced placental stem cells by modulatory RNA molecules. Also provided herein are methods of using enhanced placental stem cells, for example, to treat individuals having a disease, disorder or condition caused by, or relating to, an unwanted or harmful immune response. Further provided herein are compositions comprising said enhanced placental stem cells.

Abstract: Provided herein are placental perfusate, placental perfusate cells, and placenta-derived intermediate natural killer cells, and combinations thereof. Also provided herein are compositions comprising the same, and methods of using placental perfusate, placental perfusate cells, and placenta-derived intermediate natural killer cells, and combinations thereof, to suppress the growth or proliferation of tumor cells, cancer cells, and the like, and to treat individuals having tumor cells.

Abstract: Provided herein are methods of producing natural killer cells using a two-step expansion and differentiation method. Also provided herein are methods of suppressing tumor cell proliferation, of treating individuals having cancer or a viral infection, comprising administering the NK cells produced by the method to an individual having the cancer or viral infection.

Abstract: Provided herein are compositions and methods of treating individuals having sarcoidosis or a sarcoidosis-related disease or disorder, using placental cells, e.g., the placental stem cells and placental multipotent cells (PDACs) described herein. Also provided herein are kits comprising said cells or a composition thereof.

Abstract: Provided herein are methods of suppressing tumor cell proliferation, of treating individuals having cancer or a viral infection, comprising contacting the tumor cells, or administering to the individual, placental perfusate, placental perfusate cells, or natural killer cells, e.g., placenta-derived intermediate natural killer cells, with an immunomodulatory compound or thalidomide.

Abstract: Provided herein are methods of suppression of proliferation and growth of cells of bone-related cancers, e.g., multiple myeloma or chondrosarcoma cells, using placental cells, e.g., the placental stem cells described herein, and populations of such placental cells. Also provided herein are methods of treating individuals having cells of a bone-related cancer.

Abstract: Provided herein are methods of producing erythrocytes from hematopoietic cells, particularly hematopoietic cells from placental perfusate in combination with hematopoietic cells from umbilical cord blood, wherein the method results in accelerated expansion and differentiation of the hematopoietic cells to more efficiently produce administrable erythrocytes. Further provided herein is a bioreactor in which hematopoietic cell expansion and differentiation takes place.

Abstract: Provided herein are placental perfusate, placental perfusate cells, and placenta-derived intermediate natural killer cells, and combinations thereof. Also provided herein are compositions comprising the same, and methods of using placental perfusate, placental perfusate cells, and placenta-derived intermediate natural killer cells, and combinations thereof, to suppress the growth or proliferation of tumor cells, cancer cells, and the like, and to treat individuals having tumor cells.

Abstract: Provided herein are the production of vasculogenic or angiogenic cells from placental perfusate. Also provided are methods of treating an individual having a cardiac or vascular insufficiency, disease, disorder or condition comprising administering to said individual placental perfusate, placental perfusate cells, or combinations of placental perfusate or perfusate cells with placental or non-placental hematopoietic stem cells or adherent placental stem cells.

Abstract: The present invention relates to methods for identifying interacting regions of transcription factors, and methods for identifying agents which modulate the interactions, useful for affecting gene regulation, for example, cellular transformation. A site within residues 130–154 and within residues 343–358 in Stat3 were found to interact with the transcription factor c-Jun. On c-Jun, a site within residues 105 and 334, and more particularly, between 105 and 263, interact with Stat3. These sites of interactions permit methods for identifying agents which modulate the interaction between these transcription factors to modulate gene transcription.

Abstract: The present invention relates to methods for identifying interacting regions of transcription factors, and methods for identifying agents which modulate the interactions, useful for affecting gene regulation, for example, cellular transformation. A site within residues 130-154 and within residues 343-358 in Stat3 were found to interact with the transcription factor c-Jun. On c-Jun, a site within residues 105 and 334, and more particularly, between 105 and 263, interact with Stat3. These sites of interactions permit methods for identifying agents which modulate the interaction between these transcription factors to modulate gene transcription.

Abstract: The present invention relates to methods for identifying interacting regions of transcription factors, and methods for identifying agents which modulate the interactions, useful for affecting gene regulation, for example, cellular transformation. A site within residues 130-154 and within residues 343-358 in Stat3 were found to interact with the transcription factor c-Jun. On c-Jun, a site within residues 105 and 334, and more particularly, between 105 and 263, interact with Stat3. These sites of interactions permit methods for identifying agents which modulate the interaction between these transcription factors to modulate gene transcription.

Abstract: The present invention relates to methods for identifying interacting regions of transcription factors, and methods for identifying agents which modulate the interactions, useful for affecting gene regulation, for example, cellular transformation. A site within residues 130-154 and within residues 343-358 in Stat3 were found to interact with the transcription factor c-Jun. On c-Jun, a site within residues 105 and 334, and more particularly, between 105 and 263, interact with Stat3. These sites of interactions permit methods for identifying agents which modulate the interaction between these transcription factors to modulate gene transcription.

Abstract: The present invention relates to methods for identifying interacting regions of transcription factors, and methods for identifying agents which modulate the interactions, useful for affecting gene regulation, for example, cellular transformation. A site within residues 130-154 and within residues 343-358 in Stat3 were found to interact with the transcription factor c-Jun. On c-Jun, a site within residues 105 and 334, and more particularly, between 105 and 263, interact with Stat3. These sites of interactions permit methods for identifying agents which modulate the interaction between these transcription factors to modulate gene transcription.