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Colorectal cancer (CRC) is a malignant tumor with persistently high incidence and mortality worldwide, and its associated disease burden keeps rising year by year. Statistics predict that the global burden of colorectal cancer will increase by 60% by 2030. As a highly heterogeneous and complex malignancy, patients with distinct molecular phenotypes of CRC exhibit markedly different clinical responses to identical therapeutic regimens. During malignant progression, tumor cells continuously acquire novel phenotypic features, which further aggravate tumor heterogeneity and bring great challenges to clinical treatment. Traditional anti-tumor drug screening mainly relies on tumor cell line models. Nevertheless, long-term serial in vitro culture of cell lines tends to induce genomic variations such as genetic drift, leading to gradual loss of inherent molecular signatures of primary tumors. Consequently, these models fail to faithfully recapitulate the biological characteristics of in vivo tumors. Patient-derived tumor organoids serve as superior preclinical research models, which can largely preserve the molecular profiles and heterogeneity of primary tumors and effectively overcome the limitations of conventional models. Under light microscopy, CRC organoids appear as well-demarcated, translucent cell clusters and are morphologically categorized into compact, loose, vesicular and mixed subtypes. Cells within organoids display typical cytological features of malignancy, including hyperchromatic nuclei, abnormal mitotic figures and disturbed nucleocytoplasmic ratios. Immunohistochemical examination reveals specific positive expression of CDX2 and CK20, accompanied by loss of cell polarity and disordered cellular arrangement. Genetic sequencing confirms that the mutation spectrum of key oncogenes and tumor suppressor genes including KRAS, NRAS, HRAS, BRAF, APC, TP53 and SMAD4 in CRC organoids is highly consistent with that in matched primary tumor tissues. Numerous studies have demonstrated that tumor organoids can accurately predict the sensitivity of CRC patients to chemotherapy and targeted therapy, and thereby guide clinical management. The core applications of colorectal cancer organoids in basic tumor research and clinical translation are summarized as follows: Disease model construction: Precisely simulating tumor heterogeneity and the tumor microenvironment of colorectal cancer, providing a reliable in vitro model to elucidate the molecular mechanisms underlying tumor initiation, malignant progression and distant metastasis. Drug screening and individualized therapy: Systematically evaluating the anti-tumor efficacy and cytotoxicity of various anti-cancer agents, supplying experimental evidence for formulating individualized and precise therapeutic regimens for colorectal cancer patients. Gene function research: Combining gene-editing technology to perform knock-out and knock-in modifications of specific genes in colorectal cancer organoids, so as to clarify the biological functions and regulatory mechanisms of target genes during CRC malignant progression. Early diagnosis and prevention research: Recapitulating the initiation and progression of early colorectal lesions, offering an innovative research platform for developing early tumor diagnostic techniques and disease prevention strategies. Metabolic mechanism research: Exploring unique metabolic reprogramming pathways in colorectal tumor cells based on organoid models, and identifying novel metabolic targets and therapeutic strategies for tumor targeted intervention.

Breast cancer is the most prevalent malignant tumor in women and the second leading cause of cancer-associated mortality among female patients. Characterized by prominent subtype heterogeneity, breast cancer arises from stepwise accumulation of gene mutations in mammary epithelial cells, exhibiting complex genomic profiles and divergent biological phenotypes. At present, standard clinical therapeutic regimens are formulated mainly according to patients’ pathological features and the expression status of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2). Such strategies fail to fully match the tumor characteristics of individual patients, imposing considerable restrictions on individualized precision therapy. Accordingly, systematic elucidation of normal mammary gland development, tumor initiation mechanisms and malignant progression is of great significance for developing novel personalized therapeutic approaches. Compared with conventional breast cancer cell line models, breast cancer organoids support long-term stable in vitro culture and can faithfully recapitulate the histopathological features, hormone receptor expression patterns, HER2 status, copy number variations and gene mutation landscapes of patients’ primary tumors, maximally preserving the tumor heterogeneity of breast cancer. These organoid models can be applied to in vitro evaluation of drug efficacy; meanwhile, the establishment of in vivo xenograft models enables verification of the therapeutic effects of novel anti-tumor agents. Combined with the mammary imaging window technique, real-time dynamic monitoring of xenograft growth and invasive behaviors of tumor cells can be achieved. Most importantly, breast cancer organoids steadily retain the genetic background and histological characteristics of matched primary tumors, allowing accurate testing of individualized drug sensitivity. They serve as an excellent preclinical platform to facilitate mechanistic research on breast cancer and advance the clinical translation of precision oncology.

Hepatocellular carcinoma (HCC) possesses distinctive tumorigenic mechanisms, a characteristic tumor microenvironment, robust angiogenic capacity and prominent chemoresistance. These biological traits endow HCC with high tumor heterogeneity, which greatly complicates basic mechanistic research and clinical intervention. At present, there is a shortage of micro-morphological and molecular biomarkers for early clinical screening. Early detection of HCC mainly relies on imaging examinations, which are limited by delayed diagnosis and insufficient sensitivity. Compared with conventional animal experimental models, organoids can steadily retain human-specific biological and histological features and accurately recapitulate the genomic, epigenomic and microenvironmental landscapes of primary tumors, serving as an ideal in vitro research system for screening early diagnostic markers and prognostic factors for tumors. By reconstructing the extracellular matrix microenvironment required for liver development and regeneration, supplemented with key cytokines including hepatocyte growth factor (HGF), epidermal growth factor (EGF), fibroblast growth factor (FGF) and R‑Spondin 1, relevant studies have effectively overcome the technical bottleneck of poor long-term expansion of adult stem cell-derived organoids and successfully established a culture system for normal liver organoids capable of stable long-term passaging. At present, HCC organoids have been widely adopted to dissect the mechanisms underlying malignant tumor progression and provide novel technical support for research on individualized liver cancer therapy. Furthermore, this model can faithfully recapitulate the early evolutionary stages of tumorigenesis, facilitating the discovery of novel molecular markers for early diagnosis as well as the screening and validation of key regulatory genes governing HCC progression, invasion and malignant transformation.

The 5-year survival rate of patients with locally advanced and metastatic pancreatic cancer is less than 3.0%. Characterized by insidious early onset and high malignancy, most patients miss the optimal treatment window upon diagnosis, leading to persistently high overall mortality. Accordingly, there is an urgent clinical demand to establish efficient early diagnostic systems and develop novel targeted therapeutic strategies. More than 95% of pancreatic malignancies are of exocrine origin, mainly derived from pancreatic acinar cells and ductal epithelial cells. To date, the cellular origin of pancreatic ductal adenocarcinoma (PDAC) has not been fully elucidated. Abnormal expression and dysfunction of key genes including KRAS, p16INK4A/CDKN2A, TP53 and SMAD4/DPC4 represent core molecular events driving the malignant progression of PDAC. As an innovative in vitro research platform, tumor organoids provide powerful experimental support for in-depth dissection of pathogenic mechanisms of pancreatic cancer and the development of innovative therapeutic regimens. Human pancreatic cancer organoids are established via three-dimensional in vitro culture using clinical tumor tissues or malignant effusion specimens obtained from patients. This model can faithfully recapitulate the cytological features, histopathological morphology and molecular profiles of primary tumors, maximally preserving the authentic biological traits of tumors and effectively overcoming the limitations of conventional research models. Pancreatic cancer organoids possess diverse application values in basic tumor research and clinical translation, as summarized below: Precisely simulating tumor heterogeneity and the complex microenvironment of pancreatic cancer, providing a stable and reliable in vitro model for systematically investigating the molecular mechanisms underlying tumor initiation, malignant progression and distant metastasis. Patient-derived organoids can steadily maintain the inherent biological phenotypes and genetic characteristics of primary tumors during long-term in vitro culture. High-throughput drug screening and individualized therapeutic evaluation: Drug sensitivity and cytotoxicity assays based on organoid models yield results highly consistent with actual clinical treatment responses, enabling accurate prediction of patient prognosis and offering experimental evidence for formulating individualized clinical regimens. Combined with CRISPR/Cas9 gene-editing technology, specific gene knock-out and knock-in modifications can be performed on pancreatic organoids, providing technical support for exploring the biological functions of key genes and screening novel anti-tumor therapeutic targets. Establishing co-culture systems of tumor organoids with immune cells, fibroblasts and other stromal cells enables faithful reconstruction of the complex in vivo tumor microenvironment. Such systems help clarify the interaction mechanisms between tumor cells and stromal cells, uncover core mechanisms of tumor immune evasion, and facilitate the research, development and clinical translation of innovative tumor immunotherapeutic strategies.

Lung cancer is the malignancy with the highest mortality worldwide and possesses prominent histological heterogeneity. It mainly consists of three major subtypes: lung adenocarcinoma, lung squamous cell carcinoma and small cell lung cancer, along with rare pathological types such as adenosquamous carcinoma and large cell neuroendocrine carcinoma. Conventional tumor cell line models feature easy operation, rapid culture and suitability for high-throughput screening, which serve as classic in vitro tools for investigating the mechanisms underlying tumor targeted therapy. Nevertheless, genomic studies have verified that lung cancer exhibits remarkable inter-tumoral and intra-tumoral heterogeneity; phenotypic and genetic characteristics vary drastically among patients and even within distinct regions of a single tumor. Tumor cell lines alone cannot recapitulate the three-dimensional architecture and heterogeneity of primary tumors, failing to faithfully mimic the complex biological behaviors of lung cancer, which results in prominent model limitations. Patient-derived xenograft (PDX) models can well preserve the tissue architecture, genetic profiles and pathological phenotypes of human tumors, and can be stably passaged for up to 14 times, overcoming the shortcomings of cell line models. However, PDX models have inherent drawbacks: the establishment success rate is merely 30%–40%, the modeling period lasts 2–10 months, accompanied by high experimental costs and low screening throughput. These factors greatly restrict their wide application in high-throughput drug screening and large-sample mechanistic research [21]. In contrast, lung cancer organoids have a short modeling period and can be stably passaged long-term. They are capable of highly recapitulating the morphological structure, pathological features and molecular genetic phenotypes of primary lung tumors, acting as a more ideal novel in vitro tumor model. Human lung cancer organoids derived from patients’ tumor cells have been widely adopted in various cancer research fields, with core applications summarized as follows: Disease model construction: Precisely recapitulate tumor heterogeneity and microenvironmental features of lung cancer, providing a reliable in vitro system to dissect molecular mechanisms governing lung cancer initiation, malignant progression, invasion and metastasis. Drug screening and personalized therapy: Enable in vitro evaluation of the efficacy, sensitivity and toxicity of various anti-tumor drugs, offering experimental evidence and guidance for personalized precision treatment of lung cancer patients. Gene function research: Combine gene-editing technology to achieve specific knockout and knock-in of target genes, so as to accurately explore the regulatory roles of key genes in the malignant progression of lung cancer. Tumor microenvironment research: Co-culture with stromal cells including immune cells and fibroblasts to biomimetically reconstruct the tumor microenvironment, and further elucidate the interaction mechanisms between tumor cells and their microenvironment. Basic biological research: Utilize the organoid biomimetic system to investigate the development and physiological functions of normal alveolar epithelial cells, and advance the systematic understanding of lung cancer pathogenesis. Research on invasion and metastasis mechanisms: Effectively simulate the dynamic invasion and metastasis processes of lung cancer cells, providing an innovative research platform to uncover core molecular regulatory mechanisms driving malignant tumor evolution.

More than 650,000 new cases of head and neck cancer are diagnosed worldwide each year, and approximately half of these patients ultimately succumb to the disease. Head and neck squamous cell carcinoma (HNSCC) accounts for over 90% of all head and neck malignancies, arising from the squamous epithelial tissues of the oral cavity, pharynx, and larynx. The incidence of HNSCC exhibits prominent geographical disparities, with tobacco exposure, alcohol consumption, and human papillomavirus (HPV) infection serving as its major risk factors. Tumor organoids are capable of recapitulating the three-dimensional spatial architecture of primary tumors, stably retaining patient-specific genomic mutations and gene expression profiles, and preserving the core biological features of tumors during long-term in vitro passaging. Compared with patient-derived xenograft (PDX) models, HNSCC organoids achieve a markedly higher success rate of establishment. Furthermore, their morphological and histological characteristics are highly consistent with those of parental tumors, enabling faithful recapitulation of patients’ drug response profiles. Therefore, HNSCC organoids possess broad application prospects in the research of individualized precision cancer therapy.

Gastric cancer ranks as the fifth most prevalent malignancy worldwide and represents the second leading cause of cancer-related mortality. It encompasses multiple histological subtypes, among which gastric adenocarcinoma accounts for over 90% of all cases. The overall prognosis of gastric cancer remains poor. Owing to the absence of characteristic clinical manifestations in the early stage, most patients are diagnosed with incurable advanced disease, thus missing the optimal window for diagnosis and treatment. Organoid technology establishes an innovative technical system for preclinical drug screening in individualized precision therapy. Compared with xenograft models, organoids feature a shorter establishment cycle, straightforward operation, and great convenience for genetic editing modification. Organoid biobanks constructed from large-scale patient samples serve as living human biological repositories, which can support high-throughput drug screening, the formulation of clinical individualized therapeutic strategies, and the research and development of novel anti-tumor agents. In addition to primary tumor tissues, metastatic lesions can also be utilized to generate gastrointestinal tumor organoids; the drug response profiles of such organoids are highly consistent with the clinical therapeutic efficacy observed in corresponding patients.

Prostate cancer (PCa) ranks as the most prevalent malignancy in men worldwide and represents the second leading cause of cancer-related death among the male population. Epidemiological statistics from the United States predict that approximately 20 million new cancer cases and 10 million cancer-related deaths occur globally every year. The number of new global cancer cases is projected to rise to 30 million by 2040, indicating that cancer incidence will keep increasing in the future. Widespread tumor heterogeneity exists among patients, which creates an urgent clinical demand for developing more effective therapeutic strategies. As an emerging in vitro/ex vivo model system, organoids serve as highly promising research vehicles for basic and translational studies of prostate cancer. Organoids are capable of recapitulating the core genomic, histopathological and phenotypic features of parental tumors. With the support of genetic manipulation technology, researchers can accurately elucidate the molecular regulatory mechanisms underlying tumor initiation and drug resistance. This model system features relatively manageable costs; it can simulate tumor heterogeneity in vitro and reconstruct the interactions between tumor cells and the tumor microenvironment.

Ovarian cancer is the most aggressive gynecological tumor and poses a severe threat to the life and health of women worldwide. In recent years, a variety of novel targeted therapies have been successively developed and introduced into clinical practice. Although the mortality rate of ovarian cancer has been partially controlled, the 5-year survival rate of patients remains at approximately 50%. Multiple factors contribute to the persistently high mortality of ovarian cancer: the disease presents occult clinical manifestations at the early stage, and there is a lack of early screening biomarkers with both high sensitivity and specificity verified by large-sample clinical trials; additionally, tumor recurrence is frequent and chemotherapy resistance is prevalent. Conventional in vitro models such as cell lines fail to recapitulate the prominent heterogeneity of ovarian cancer and tend to undergo substantial genomic drift during long-term passaging. Patient-derived xenograft (PDX) models remedy some of these deficiencies, yet they still suffer from drawbacks including low establishment success rates, long experimental cycles, and the inability to simulate in vivo immune responses. Furthermore, safety regulations and ethical constraints on clinical trials hinder the research and development of candidate new drugs, and numerous findings from basic research cannot be translated into clinical practice. Faced with the above research bottlenecks, the emergence of organoid technology provides a stable and reliable in vitro platform for investigating the basic mechanisms and translational medicine of ovarian cancer. Ovarian cancer is a highly heterogeneous tumor with diverse pathological subtypes, and distinct subtypes exhibit markedly different clinical phenotypes and molecular features. Even within the same pathological subtype, significant heterogeneity exists among different patients and across different regions of a single tumor, which serves as a key cause of treatment failure and drug resistance in ovarian cancer. The organoid system can effectively recapitulate inter-tumoral and intra-tumoral heterogeneity. Organoid models established from patients’ tumor tissues enable rapid in vitro drug screening and facilitate research on individualized therapeutic strategies. The formation of various ovarian cancer subtypes results from the synergistic effects of multiple genetic alterations. The combination of gene-editing technology and organoid platforms helps uncover the regulatory roles of genetic abnormalities in the initiation and malignant progression of ovarian cancer.

Glioblastoma (GBM) is a highly malignant central nervous system tumor with dismal prognosis, and radical curative approaches are still lacking in clinical practice. The prominent intratumoral heterogeneity of GBM constitutes the core factor leading to difficult treatment and unsatisfactory therapeutic outcomes. Malignant GBM cells can differentiate into four canonical cell states: neural progenitor cell-like (NPC-like), oligodendrocytic progenitor cell-like (OPC-like), astrocytic-like (AC-like) and mesenchymal-like (MES-like). NPC-like and OPC-like cells primarily take part in tumor invasion into brain tissues and mediate electrical communication with the neuronal microenvironment. In contrast, AC-like and MES-like cells form interconnected tumor microtube networks, through which they establish signal crosstalk with normal cells within the tumor microenvironment (TME) to drive malignant tumor progression. To thoroughly investigate the biological functions underlying malignant cell heterogeneity in GBM, experimental models with high fidelity, reproducibility and operability are urgently required. Such models should accurately recapitulate human tumor cell states, reconstruct interactions within the tumor microenvironment, and support standardized experimental manipulation. Patient-derived xenograft models are widely adopted for GBM mechanistic research at present. Nevertheless, they require long preparation periods and complicated operations; additionally, species differences prevent them from faithfully recapitulating the authentic biological characteristics of human tumors. Although conventional monolayer cell culture enables rapid mechanistic research on human tumors, it lacks an intact neural microenvironment and fails to reproduce sophisticated in vivo cell-cell interaction patterns [14]. In recent years, human organoid technology has been progressively optimized and applied to glioblastoma research, overcoming numerous limitations of traditional models. GBM organoids can closely mimic the pathological phenotypes and biological features of human tumors, which facilitates the exploration of oncogenic mechanisms, the illustration of regulatory rules in the tumor microenvironment, as well as targeted drug screening and pharmacodynamic evaluation. Organoid models established using patients’ autologous tumor tissues can fully reflect individual tumor heterogeneity. They provide experimental evidence for designing individualized clinical regimens, precisely predict patients’ therapeutic responses, help optimize clinical intervention strategies, and ultimately improve the overall treatment efficacy of glioblastoma. Generation of patient-derived glioblastoma organoids (PD-GBOs) and models for investigating GBM invasiveness. Two mainstream construction protocols are available: Protocol 1: Fresh surgically resected tumor specimens are dissociated or thoroughly minced, embedded in Matrigel, and cultured in Neurobasal complete medium (NBM) supplemented with exogenous growth factors (epidermal growth factor EGF / basic fibroblast growth factor bFGF). Protocol 2: Tumor tissues are only finely minced without single-cell dissociation, seeded onto ultra-low attachment plates, and cultured in plain Neurobasal medium free of exogenous growth factors, relying on endogenous extracellular matrix from the tissue to sustain growth.

Renal cell carcinoma (RCC) is one of the most common malignancies of the urinary system. Its global incidence has been rising year by year in recent decades, imposing a heavy burden on public health systems. Clinically, early-stage RCC can achieve favorable prognosis through surgical resection. Nevertheless, there remains a lack of effective and comprehensive therapeutic regimens for advanced and metastatic lesions, leading to enormous challenges in clinical treatment. Conventional in vitro cell culture models fail to faithfully recapitulate the complex pathological phenotypes and disease characteristics of RCC, making them inadequate for in-depth mechanistic research. Although animal models can simulate the in vivo tumor microenvironment to a certain extent, they are restricted by interspecies differences, ethical limitations, high experimental costs and lengthy research cycles. These drawbacks hinder their seamless translation toward clinical research and greatly reduce their translational value. With the innovation of biological experimental techniques, organoid technology has achieved groundbreaking progress, opening up a brand-new avenue for precision oncology research of renal cell carcinoma. RCC organoids derived from patient tumor tissues are generated via in vitro culture systems. They can highly recapitulate the cellular biological properties, histopathological architecture and molecular expression profiles of primary tumors, and effectively improve the accuracy and reliability of preclinical drug screening. Meanwhile, the combination of organoid technology with cutting-edge approaches including single-cell sequencing, multi-omics profiling and microfluidic chips can further optimize the in vitro simulation system of the tumor microenvironment and substantially strengthen the translational efficiency and application prospects of this model. Schematic workflow of renal cancer organoid-based precision medicine pipeline. This diagram illustrates the translational application roadmap of renal cell carcinoma (RCC) organoids in precision oncology.

Cholangiocarcinoma (CCA) ranks as the second most prevalent primary malignant tumor of the liver with an extremely poor overall prognosis, and the five-year survival rate of patients remains merely 5%–15%. The incidence and mortality of CCA have kept rising globally in recent decades. Epidemiological projections indicate that its case load may increase tenfold within the next 20 to 30 years. At present, effective targeted therapies for CCA are severely limited. Accordingly, exploring innovative targeted strategies and improving the efficacy of chemotherapy and immunotherapy are critical to ameliorating clinical outcomes and breaking therapeutic bottlenecks for CCA patients. Human intrahepatic cholangiocarcinoma organoids are generated via in vitro culture of cells isolated from patients’ clinical tumor specimens, which can faithfully mimic the cellular biological properties, histopathological morphology and molecular signatures of primary tumors. As a high-performance preclinical research model, CCA organoids are capable of recapitulating tumor heterogeneity and tumor microenvironment features, establishing a stable in vitro system to systematically investigate the initiation, malignant progression and metastatic mechanisms of intrahepatic cholangiocarcinoma. Patient-derived organoids can sustainably preserve the core biological phenotypes of primary tumors over long-term culture, and are applicable to high-throughput drug screening and evaluation of individualized therapeutic efficacy. The drug response profiles of this model are highly consistent with patients’ clinical treatment outcomes, enabling accurate prediction of therapeutic effects and providing credible experimental evidence for designing individualized therapeutic regimens. Combined with CRISPR/Cas9 gene-editing technology, CCA organoids support specific knockout or overexpression of target genes, which facilitates the analysis of biological functions of key genes and the discovery of novel potential therapeutic targets for cholangiocarcinoma. Furthermore, CCA organoids can be co-cultured with various stromal cells including immune cells and cancer-associated fibroblasts to reconstruct the physiological tumor microenvironment in vitro. Such co-culture systems can effectively simulate the dynamic interactions between tumor-stroma and tumor-immune cells, offering vital support for elucidating tumor immune escape mechanisms and developing innovative immunotherapeutic strategies. Meanwhile, organoid models can be adopted to explore characteristic pathological mechanisms of CCA, analyze the crosstalk between tumors and the extracellular matrix, and clarify the specific metabolic disorders and aberrant signaling pathways during tumor progression. Hence, organoids serve as an innovative research platform for mechanistic studies and translational applications of cholangiocarcinoma.

Melanoma is a highly aggressive malignancy with an extremely low clinical cure rate, imposing a severe burden on the global public health system. Its worldwide incidence has increased year by year in recent years. In-depth analysis of the complex molecular features, pathogenic mechanisms and cell-cell interaction networks underlying melanoma initiation and progression has become a key and challenging research priority. Conventional animal models cannot accurately recapitulate the authentic biological properties of human melanoma. Interspecies differences in immune responses and the emergence of non-specific tumor phenotypes greatly reduce the precision and reproducibility of preclinical experiments. Meanwhile, such models are accompanied by uncontrollable tumor evolution, unstable metastatic phenotypes and poor consistency of experimental outcomes. Furthermore, relevant experiments are strictly restricted by animal ethics and welfare regulations, leading to evident application limitations. In contrast, organoid models feature manageable costs and are capable of faithfully reconstructing the tissue architecture and pathological characteristics of human tumors, which have established them as a core technical platform for tumor mechanistic research. The organoid-based research system enables precise analysis of the biological behaviors, drug response patterns and disease progression mechanisms of melanoma, effectively overcoming numerous drawbacks of traditional animal experiments. The application of organoid models in preclinical studies not only promotes a more systematic understanding of melanoma pathogenesis, but also provides solid support for the discovery of novel therapeutic targets and the development of clinical intervention strategies, thereby greatly improving the clinical translational efficiency and practical value of basic tumor research.

Bladder cancer ranks as the ninth most prevalent malignancy worldwide and takes the lead in the incidence of urinary system malignant tumors. This disease tends to affect the elderly population, with the peak onset age at 60, and men face a markedly higher risk of developing the disease than women. Characterized by high recurrence and progression rates, bladder cancer leads to distant tumor metastasis in nearly half of patients, which constitutes the primary cause of death among individuals with advanced bladder cancer. Tumor heterogeneity acts as the core contributor to inconsistent clinical therapeutic outcomes, and patients exhibit dramatically variable responses to standardized treatment regimens. Conventional tumor cell lines are derived from patients’ primary tumor tissues and can reflect the features of tumor gene mutations at the cellular level. Widely used bladder cancer cell lines such as T24, 5637 and J82 are easy to obtain and convenient to culture, yet they suffer from limited diversity of cell subtypes. During long-term serial passaging, cell lines are prone to phenotypic shift, making them incapable of accurately recapitulating the authentic pathological features of primary tumors and fully restoring the inherent heterogeneity of tumors. Patient-derived xenograft (PDX) models are established by implanting human tumor tissues into immunodeficient mice. These models can preserve the heterogeneity and complex biological traits of primary tumors to a certain extent, serving as favorable preclinical models for bladder cancer research. Nevertheless, PDX models have evident drawbacks: complicated operational procedures, excessive experimental costs, incompatibility with high-throughput drug screening, and the inability to simulate the regulatory effects of the human immune system on tumor growth and drug responses. Besides, the construction of PDX models for drug screening generally takes several months, resulting in extremely low experimental efficiency. Patient-derived bladder cancer organoids (BCa PDOs) represent an innovative and groundbreaking technical system in oncology research. They can faithfully recapitulate the tissue architecture and biological functions of human bladder cancer, offering an ideal research vehicle for individualized exploration of tumor heterogeneity, drug sensitivity and the mechanisms underlying drug resistance. Making up for the deficiencies of conventional experimental models, this system bridges the translational gap between basic research and clinical practice and provides novel support for the advancement of individualized precision medicine for bladder cancer.