SDF-1 binding nucleic acids and the use thereof in cancer treatment
The present invention is related to a nucleic acid molecule capable of binding to SDF-1, preferably capable of inhibiting SDF-1, whereby the nucleic acid molecule is for use in a method for the treatment and/or prevention of a disease or disorder, for use in a method for the treatment of a subject suffering from a disease or disorder or being at risk of developing a disease or disorder as an adjunct therapy, or for use as a medicament for the treatment and/or prevention of a disease or disorder, whereby the disease or disorder is cancer.
1. A method for the treatment of a subject suffering from cancer, wherein the method comprises a) administering to the subject a pharmaceutically effective amount of a type B L-nucleic acid, or a homolog thereof, that binds SDF-1, wherein said type B L-nucleic acid comprises, in order, a 5′ flanking sequence, SEQ ID NO:52 and a 3′ flanking sequence, wherein said 5′ and 3′ flanking sequences can hybridize to each other.
2. The method according to claim 1 , wherein the method further comprises b) irradiating the subject, conducting surgery on said subject, exposing said subject to a cellular therapy and/or administering a pharmaceutically effective amount of a further pharmaceutically active agent to the subject.
3. The method of claim 1 , wherein the cancer comprises a hematological cancer or a solid tumor.
4. The method of claim 2 , wherein said L-nucleic acid is administered as an adjunct therapy or part of an adjunct therapy, with a primary treatment.
5. The method of claim 3 , wherein said hematological cancer comprises leukemia or myeloma.
6. The method of claim 3 , wherein said solid tumor comprises glioblastoma, colorectal cancer, breast cancer, lymphoma, prostate cancer, pancreatic cancer, renal cancer, ovarian cancer or lung cancer.
7. The method of claim 4 , wherein the adjunct therapy sensitizes the subject to said primary treatment.
8. The method of claim 4 , wherein said primary treatment comprises administrating a further pharmaceutically active agent to said subject, irradiating the subject, conducting surgery on said subject and/or exposing said subject to a cellular therapy.
9. The method of claim 8 , wherein the further pharmaceutically active agent is selected from the group consisting of an antibody, an alkylating agent, an anti-metabolite, a plant alkaloid, a plant terpenoid, and a topoisomerase inhibitor.
10. The method of claim 8 , wherein said further pharmaceutically active agent is selected from the group consisting of leucovorin, methotrexate, tamoxifen, sorafenib, lenalidomide, bortezomib, dexamethasone, flurouracil and prednisone.
11. The method of claim 9 , wherein the antibody is selected from the group consisting of Rituximab, Ofatumumab, Cetuximab, Ibritumomab-Tiuxetan, Tositumomab, Trastuzumab, Bevacizumab, and Alemtuzumab.
12. The method of claim 9 , wherein the alkylating agent is selected from the group consisting of cisplatin, carboplatin, oxaliplatin, mechlorethamine, cyclophosphamide, chlorambucil, doxorubicin, lioposomal doxorubicin, bendamustine, temozolomide and melphalan.
13. The method of claim 9 , wherein the anti-metabolite is selected from the group consisting of purineazathioprine, mercaptopurine, fludarabine, pentostatin, and cladribine.
14. The method of claim 9 , wherein the plant terpenoid comprises a taxane.
15. The method of claim 9 , wherein the topoisomerase inhibitor is selected from the group consisting of camptothecin, irinotecan, and mitoxantrone.
16. The method of claim 1 , wherein the L-nucleic acid comprises a modification.
17. The method of claim 16 , wherein the modification is selected from the group consisting of an HES moiety, a PEG moiety, biodegradable modifications and combinations thereof.
18. The method of claim 16 , wherein said modification enhances residence time in an animal or human host.