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Abstract
Purpose Radionuclide therapy (RNT) is a rapidly growing area of clinical nuclear medicine, wherein radionuclides are employed to deliver cytotoxic dose of radiation to the diseased cells/tissues. During RNT, radionuclides are either directly administered or delivered through biomolecules targeting the diseased site. RNT has been clinically used for diverse range of diseases including cancer, which is the focus of the review.
Conclusions The major emphasis in RNT has so far been given towards developing peptides/antibodies and other molecules to conjugate a variety of therapeutic radioisotopes for improved targeting/delivery of radiation dose to the tumor cells. Despite that, many of the RNT approaches have not achieved their desired therapeutic success probably due to poor knowledge about complex and dynamic (i) fate of radiolabeled molecules; (ii) radiation dose delivered; (iii) cellular heterogeneity in tumor mass; and (iv) cellular radiobiological response. Based on understanding gathered during recent years, it may be stated that besides the absorbed dose, the net radiobiological response of tumor/normal cells also determines the clinical response of radiotherapeutic modalities including RNT. The radiosensitivity of tumor/normal cells is governed by radiobiological phenomenon such as radiation-induced bystander effect, genomic instability, adaptive response and low dose hyper-radiosensitivity. These concepts have been well investigated in the context of external beam radiotherapy, but their clinical implications during RNT have received meagre attention. In this direction, a few studies performed using in vitro and in vivo models envisage the possibilities of exploiting the radiobiological knowledge for improved therapeutic outcome of RNT.
| Abbreviations | ||
| ALL | = | Acute Lymphoid Leukaemia |
| AML | = | Acute Myeloid Leukaemia |
| CEA | = | Carcinoembryonic Antigen |
| CD | = | Cluster of Differentiation |
| CLL | = | Chronic Lymphocytic Leukaemia |
| CNS | = | Central Nervous System |
| CPP | = | Cell Penetrating Peptide, DC, Dendritic Cell |
| DOTA | = | 1,4,7,10-Tetraazacyclododecane-1,4,7,10-Tetraacetic Acid |
| DTPA | = | Diethylene Triamine Pentaacetic Acid |
| EDTMP | = | Ethylenediamine Tetra(methylene Phosphonic Acid); EGFR, Epidermal Growth Factor Receptor |
| EU | = | European Union |
| FDA | = | Food and Drug Administration |
| Her2 | = | Human Epidermal Growth Factor Receptor 2 |
| HEDP | = | 1-Hydroxy Ethylidene-1,1-Diphosphonic Acid |
| GI | = | Gastro Intestinal |
| HLA | = | Human Leukocyte Antigen |
| HRS | = | Hyper-radiosensitivity |
| LET | = | Linear Energy Transfer |
| MCL | = | Mantle Cell Lymphoma |
| MIBG | = | Metaiodobenzylguanidine |
| MN | = | Micronuclie |
| 4-NCS-Bz-TCMC | = | S-2-(4-isothiocyanatobenzyl) -1,4,7,10-tetraaza-1,4,7,10-tetra(2-carbamoylmethyl) cyclododecane |
| NHL | = | Non-Hodgkin’s Lymphoma |
| PSMA | = | Prostate Specific Membrane Antigen |
| RGD | = | Arginylglycylaspartic Acid |
| RIAR | = | Radiation-Induced Adaptive Response |
| RIBE | = | Radiation-Induced Bystander Effect |
| RIGI | = | Radiation-Induced Genomic Instability |
| RNT | = | Radionuclide Therapy |
| TAT | = | Targeted Alpha Therapy |
| TATE | = | Tyr3-octreotate |
| TIMP | = | Tissue Inhibitor of Metalloproteinase |
| TOC | = | Tyr3-octreotide |
| VEGF | = | Vascular Endothelial Growth Factor. |
Acknowledgements
Sejal Desai would like to acknowledge DAE Graduate Fellowship provided from Department of Atomic Energy, Government of India.
Disclosure statement
The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.