Abstract: The invention relates to the field of tumor disease stratification, in particular melanoma disease stratification. In particular it relates to the methods for tumor analysis, such as for determining tumor cell heterogeneity during treatment. These methods are helpful in selecting or optimizing tumor therapy, or in predicting responses to tumor therapy. The invention further relates to methods for screening for cytotoxic or cytostatic compounds targeting one or more of the heterogeneous tumor cell populations occurring such as during therapy, such as during the minimal residual disease phase.

Abstract: The invention relates to the field of tumor treatment, in particular to melanoma tumor treatment. In particular it relates to the use of CD36 antagonists for use in tumor treatment, in particular for use in reducing tumor cell heterogeneity during minimal residual disease (MRD), and thus for use in treating MRD. Even more in particular, the invention relates to the use of CD36 antagonists in combination with clinically established treatments such as treatment with a combination of BRAF and MEK inhibitors, and optionally other anticancer agents.

Abstract: The invention relates to the field of tumor treatment, in particular to melanoma tumor treatment. In particular it relates to the use of retinoid X receptor antagonists for use in tumor treatment, in particular for use in reducing tumor cell heterogeneity during minimal residual disease (MRD), and thus for use in treating MRD. Even more in particular, the invention relates to the use of retinoid X receptor antagonists in combination with clinically established treatments such as treatment with a combination of BRAF and MEK inhibitors, and optionally other anticancer agents.

Abstract: The present application relates to the field of cancer, particularly that of cancers with high MDM4 protein levels (such as melanoma, breast, colon or lung cancers, glioblastoma, retinoblastoma, etc.). It is shown herein that direct and selective inhibition of MDM4, e.g., by antisense RNA, leads to growth inhibition of cancer cells and sensitization to chemo or targeted therapies. Also provided are simple ways of determining which patients are most amenable for such treatment by comparing specific transcript levels.

Abstract: The present application relates to the field of cancer, particularly that of cancers with high MDM4 protein levels (such as melanoma, breast, colon or lung cancers, glioblastoma, retinoblastoma, etc.). It is shown herein that direct and selective inhibition of MDM4, e.g., by antisense RNA, leads to growth inhibition of cancer cells and sensitization to chemo or targeted therapies. Also provided are simple ways of determining which patients are most amenable for such treatment by comparing specific transcript levels.

Abstract: This disclosure relates to the field of cancer, particularly the field of melanoma. It was found that a particular long non-coding RNA (lncRNA) is specifically up-regulated in melanoma (but not other tumor) cells as compared to melanocytes. Inhibition of this lncRNA in melanoma cells leads to induction of apoptosis and is a novel therapeutic strategy in the treatment of melanoma.

Abstract: The present application relates to the field of cancer, particularly that of cancers with high MDM4 protein levels (such as melanoma, breast, colon or lung cancers, glioblastoma, retinoblastoma, etc.). It is shown herein that direct and selective inhibition of MDM4, e.g., by antisense RNA, leads to growth inhibition of cancer cells and sensitization to chemo or targeted therapies. Also provided are simple ways of determining which patients are most amenable for such treatment by comparing specific transcript levels.

Abstract: The application relates to the field of cancer, particularly to the field of solid tumors. It was found that a particular long non-coding RNA (lncRNA), NEAT1, an essential architectural component of nuclear paraspeckles, is required for the survival of cancer, but not that of normal, non-transformed, cells. Inhibition of NEAT1 reduces cell viability of cancer cells and induces apoptosis. These data identify NEAT1 as a novel therapeutic target for treatment of solid tumors.

Abstract: The application relates to the field of cancer, particularly to the field of solid tumors. It was found that a particular long non-coding RNA (lncRNA), NEAT1, an essential architectural component of nuclear paraspeckles, is required for the survival of cancer, but not that of normal, non-transformed, cells. Inhibition of NEAT1 reduces cell viability of cancer cells and induces apoptosis. These data identify NEAT1 as a novel therapeutic target for treatment of solid tumors.

Abstract: This disclosure relates to the field of cancer, particularly the field of melanoma. It was found that a particular long non-coding RNA (lncRNA) is specifically up-regulated in melanoma (but not other tumor) cells as compared to melanocytes. Inhibition of this lncRNA in melanoma cells leads to induction of apoptosis and is a novel therapeutic strategy in the treatment of melanoma.

Abstract: The present disclosure relates to the field of oncology, more particularly to the field of melanoma. Provided are methods of treating melanoma, particularly advanced cutaneous melanoma, with a combination of pharmaceutical agents comprising MDM4-specific antagonists (such as an inhibitor of the MDM4-p53 interaction or a molecule that decreases MDM4 protein stability) or MDM4-MDM2 dual inhibitors (i.e., molecules that disrupt the interactions between p53 and MDM2 and p53 and MDM4) and one or more chemotherapeutic agents such as for example alkylating agents (i.e., Dacarbazine (DITC) or melphalan), alkylating-like agents (i.e., cisplatin or carboplatin) or mitotic inhibitors (taxanes docetaxel or paclitaxel) and PI3K-AKT, B-RAF and MEK inhibitors. Further provided are pharmaceutical formulations of MDM4-specific antagonists (be it an inhibitor of the MDM4-p53 interaction or a molecule that decreases MDM4 protein stability) or MDM4-MDM2 dual inhibitors (i.e.

Abstract: It has now been found that the p53 pathway is inactivated in ocular cancers such as retinoblastoma. As such, the present invention is a method for inducing ocular cancer cell death using a p53 activator. In particular embodiments, the p53 activator blocks the interaction between DM2 or DMX and p53. As the p53 activator induces ocular cancer cell death, a method for preventing or treating ocular cancer is also provided.

Abstract: It has now been found that the p53 pathway is inactivated in ocular cancers such as retinoblastoma. As such, the present invention is a method for inducing ocular cancer cell death using a p53 activator. In particular embodiments, the p53 activator blocks the interaction between DM2 or DMX and p53. As the p53 activator induces ocular cancer cell death, a method for preventing or treating ocular cancer is also provided.

Abstract: The present disclosure relates to the field of oncology, more particularly to the field of melanoma. Provided are methods of treating melanoma, particularly advanced cutaneous melanoma, with a combination of pharmaceutical agents comprising MDM4-specific antagonists (such as an inhibitor of the MDM4-p53 interaction or a molecule that decreases MDM4 protein stability) or MDM4-MDM2 dual inhibitors (i.e., molecules that disrupt the interactions between p53 and MDM2 and p53 and MDM4) and one or more chemotherapeutic agents such as for example alkylating agents (i.e., Dacarbazine (DITC) or melphalan), alkylating-like agents (i.e., cisplatin or carboplatin) or mitotic inhibitors (taxanes docetaxel or paclitaxel) and PI3K-AKT, B-RAF and MEK inhibitors. Further provided are pharmaceutical formulations of MDM4-specific antagonists (be it an inhibitor of the MDM4-p53 interaction or a molecule that decreases MDM4 protein stability) or MDM4-MDM2 dual inhibitors (i.e.

Abstract: Compositions and methods for treating ocular cancer are provided. The composition is a subconjunctival formulation of nutlin-3 and its analogs. The composition provides for methods of treating ocular cancer, including retinoblastoma. The formulation has high penetration into ocular tissue with low toxicity.

Abstract: Compositions and methods for treating ocular cancer are provided. The composition is a subconjunctival formulation of nutlin-3 and its analogs. The composition provides for methods of treating ocular cancer, including retinoblastoma. The formulation has high penetration into ocular tissue with low toxicity.

Abstract: It has now been found that the p53 pathway is inactivated in ocular cancers such as retinoblastoma. As such, the present invention is a method for inducing ocular cancer cell death using a p53 activator. In particular embodiments, the p53 activator blocks the interaction between DM2 or DMX and p53. As the p53 activator induces ocular cancer cell death, a method for preventing or treating ocular cancer is also provided.

Abstract: This disclosure relates to the field of cancer, particularly the field of melanoma. It was found that a particular long non-coding RNA (lncRNA) is specifically up-regulated in melanoma (but not other tumor) cells as compared to melanocytes. Inhibition of this lncRNA in melanoma cells leads to induction of apoptosis and is a novel therapeutic strategy in the treatment of melanoma.

Abstract: The application relates to the field of cancer, particularly to the field of solid tumors. It was found that a particular long non-coding RNA (lncRNA), NEAT1, an essential architectural component of nuclear paraspeckles, is required for the survival of cancer, but not that of normal, non-transformed, cells. Inhibition of NEAT1 reduces cell viability of cancer cells and induces apoptosis. These data identify NEAT1 as a novel therapeutic target for treatment of solid tumors.