作者
Hamidreza Aboulkheyr Es,Leila Montazeri,Amir Reza Aref,Massoud Vosough,Hossein Baharvand
摘要
Personalized cancer medicine is an approach to tailoring effective therapeutic strategies for each patient according to a tumor's genomic characterization. There is an urgent demand for research in personalized tumor modeling to confirm the functional aspects of genomic drug response predictions in the preclinical setting. While different tumor models, such as tumor cell lines and patient-derived tumor xenografts, have been proposed, the drawbacks of each model have limited their applications as personalized tumor models. A tumor organoid, in which cellular and molecular heterogeneity of tumor cells is preserved, has emerged as a promising platform. Recently, numerous studies highlighted the application of tumor organoids in personalized cancer medicine in terms of gene–drug association treatment, the identification of new therapies, and prediction of patient outcome. Personalized cancer therapy applies specific treatments to each patient. Using personalized tumor models with similar characteristics to the original tumors may result in more accurate predictions of drug responses in patients. Tumor organoid models have several advantages over pre-existing models, including conserving the molecular and cellular composition of the original tumor. These advantages highlight the tremendous potential of tumor organoids in personalized cancer therapy, particularly preclinical drug screening and predicting patient responses to selected treatment regimens. Here, we highlight the advantages, challenges, and translational potential of tumor organoids in personalized cancer therapy and focus on gene–drug associations, drug response prediction, and treatment selection. Finally, we discuss how microfluidic technology can contribute to immunotherapy drug screening in tumor organoids. Personalized cancer therapy applies specific treatments to each patient. Using personalized tumor models with similar characteristics to the original tumors may result in more accurate predictions of drug responses in patients. Tumor organoid models have several advantages over pre-existing models, including conserving the molecular and cellular composition of the original tumor. These advantages highlight the tremendous potential of tumor organoids in personalized cancer therapy, particularly preclinical drug screening and predicting patient responses to selected treatment regimens. Here, we highlight the advantages, challenges, and translational potential of tumor organoids in personalized cancer therapy and focus on gene–drug associations, drug response prediction, and treatment selection. Finally, we discuss how microfluidic technology can contribute to immunotherapy drug screening in tumor organoids. a tyrosine kinase inhibitor for EGFR and ErbB 2 (HER2). adenomatous polyposis coli, a negative regulator of beta catenin and a modulator of its interaction with E-cadherin. Mutations in the APC gene can result in colon cancer. extraction of small pieces of tissue from a specific site (e.g., tumor tissue). a targeted therapy drug that inhibits the pan-class I phosphatidylinositol 3-kinase (PI3K) family of lipid kinases. resistance of tumor cells to the effects of chemotherapeutics. a category of cancer treatment that uses one or more anticancer drugs. treatment in which a patient is given two or more drugs. a type of targeted drug therapy that inhibits EGFR on cancer cells. a chemotherapy regimen composed of folinic acid, 5-fluorouracil, and oxaliplatin. selection of a drug based on the genomic abnormalities of a tumor. small molecules that inhibit histone deacetylase. a cancer treatment that attempts to stimulate the immune system to destroy tumors. a protein that plays a key role in regulation of lineage commitment and maturation of myeloid cells. common methods for a 3D culture of cancer cells. the use of chemotherapy regimens prior to surgery. drugs used as treatment that lack FDA approval. a poly (ADP-ribose) polymerase (PARP) inhibitor. small-molecule agents that inhibit HER1, HER2, and HER4 receptors on cancer cells. the transplantation of patient's tumor cells into immune-deficient mice. also called 'copy number variation' when a section of the genome is repeated. The numbers of these repeats play key roles in cancer diagnosis and prognosis. white blood cells located in the spleen. a cancer treatment that employs small-molecule inhibitors to specifically target cancer cells.