Cancer type | Sample source | No. | Niche factor supplements | Success rate | Key findings | Ref |
---|---|---|---|---|---|---|
CRC | Surgery | 20 | Wnt, Noggin, R-Spondin, EGF, Gastrin, A83–01, SB202190, PGE2 | 81% | The features of genetic changes in CRC PDOs largely resembles the mutational analyses of CRC tissues. | [22] |
CRC | NM | 55 | Wnt-3A, Noggin, R-spondin-1, EGF, Gastrin I, A83–01, SB202190 | 100% | CRC PDOs of various pathological types have been established. The histopathological grading and differentiation of CRC PDOs were nearly the same as those of their parental tumors in vitro and in vivo. | [23] |
CRC | Biopsy and surgery | 35 | Wnt-3A, Noggin, R-spondin-1, EGF, Gastrin, A83–01, SB202190 | 60% | PDXs appear closer to the CRC molecular groups than PDOs. PDOs has less complex molecular subpopulations than PDXs due to their loss of matrix and higher expression of xenobiotic and fatty acid processes related genes. | [26] |
CRC | NM | 7 | Wnt, R-Spondin, Noggin, EGF, Gastrin, A83–01, SB202190, PGE2 | NM | The individualized patient-specific genomic and proteomic profiles of CRC PDOs may help the disease diagnosis | [27] |
CRC | NM | 91 | Wnt-3A, Noggin, R-spondin-1, EGF, Gastrin, A83–01, SB202190 | NM | The therapeutic responses and inhibitor effects on the oncogene related signal pathways to the CRC PDOs were widely variable. | [28] |
mCRC | Biopsy | 14 | Noggin, R-Spondin, EGF, Gastrin, A83–01, SB202190, PGE2 | 71% | Nearly 90% of somatic mutations are shared between PDOs and matched tumors. None of the mutations that were found in either CRC tissues or CRC PDOs were genes amenable for drug targeting or in tumor driver genes. | [29] |
mCRC | Surgery | 3 | Noggin, EGF, Gastrin, A83–01, SB202190 | NM | To test the efficacy of PARP inhibitors in mCRC patients who carry HR deficient tumors and have experienced tumor shrinkage upon induction of FOLFOX-chemotherapy. | [30] |
mCRC | Biopsy | 40 | Wnt-3A, Noggin, R-spondin-1, EGF, Gastrin, A83–01, SB202190 | 63% | CRC PDOs can be applied to predict the drug response of corresponding CRC patients to CPT-11-based chemotherapy. | [31] |
RC | NM | 65 | Wnt-3A, R-spondin-1, EGF, Gastrin I, A83–01, SB202190. | 77% | RC PDOs retain molecular features of the original tumors. | [32] |
RC | Biopsy | 96 | Noggin, R-spondin 1, EGF, Gastrin, A83–01, SB202190, PGE2 | 86% | A living biobank was generated from advanced RC patients treated with neoadjuvant chemoradiotherapy in a phase III clinical trial. | [33] |
PC | Biopsy and surgery | 8 | Wnt-3A, Noggin, R-spondin1, EGF, Gastrin, FGF10 | 80% | The tumor development progress from early-grade tumor formation to locally invasive carcinomas and even metastatic carcinomas is reappeared in the PC PDO-X model. | [20] |
PC | Biopsy and surgery | 101 | Wnt-3A, Noggin, R-spondin-1, EGF, Gastrin I, FGF10, PGE2 | 73% | The gene mutational spectrum and transcriptional subtypes of PC PDOs are largely the same as those of human PC tissues. Novel driver oncogenes and unique clusters are identified based on PC PDOs. | [34] |
PC | Biopsy and surgery | 52 | Noggin, R-spondin, EGF, Gastrin, A83–01, PGE2, FGF10 | 63% | The PC PDOs copy the histology and typical genetic alterations of human PC tissues. Drug screening of 76 new drugs provides evidence for the drug’s effectiveness in the clinic. | [35] |
PC | Surgery and biopsy | 44 | Wnt-3A, Noggin, R-spondin1, EGF, Gastrin, FGF10 | NM | The PDO-based prediction model successfully predicts the response in treatment-naive patients for front-line regimens but fails to predict the response in pretreated patients. | [36] |
PC | Biopsy | 10 | Wnt-3A, Noggin, R-spondin1, EGF, Gastrin, A83–01, Y-27632, FGF10 | NM | The mutational spectrum in PC PDO supernatants recapitulates this in the human PC tissues, which facilitates drug screening of PC PDOs in a shortened time frame. | [37] |
PDAC | Surgery | 17 | Y-27632, FGF2, hydrocortisone, all-trans retinoic acid, Ascorbic acid, Insulin | 85% | PDAC PDOs recapitulate the differentiation status, histology, phenotypic heterogeneity patient-specific physiologic changes of parental tumors. | [38] |
PDAC | Biopsy and surgery | 39 | Wnt-3A, Noggin, Rspondin-1, Gastrin, FGF10 | 80% | Three functional subtypes based on the dependencies on R-spondin and Wnt are confirmed. The heterogeneity of Wnt niche independency of PDAC forms in tumor progression. | [21] |
PDAC | Biopsy | 25 | Wnt-3A, Noggin, R-spondin1, EGF, Gastrin I, A83–01, PGE2, FGF10 | 67% | PDCA PDOs were successfully established using EUS-FNB at the time of initial diagnosis. | [39] |
PDAC | Biopsy | 18 | Wnt-3A, Noggin, R-spondin1, EGF, Gastrin I, A83–01, Y-27632, FGF-10 | 83% | The drug screening of PDAC PDOs can inform therapeutic selection and patient stratification for PDAC patients, and identify gene signatures associated with new therapeutic response combined with omics data. | [40] |
PDAC | Surgery | 6 | Wnt-3A, R-spondin1, EGF, Gastrin I, A83–01, Y-27632, FGF-10 | NM | Nine metabolites in early recurrent PDAC PDOs are increased when compared with late recurrent PDOs, indicating that an increased anaplerotic metabolism and energy metabolism fasten the PDAC recurrence. | [41] |
GC | Biopsy and surgery | 15 | Wnt-3A, Noggin, R-spondin-1, EGF, Gastrin, FGF10 | NM | The genomic profiling of paired human GC tissues and GC PDOs is largely the same, including the similar KRAS alterations. | [42] |
GC | NM | 37 | Wnt-3A, Noggin, R-spondin1, EGF, A83–01, FGF10, Nutlin-3 | NM | Generation and analysis of GC PDOs reveal molecular signatures underlying distinct histopathological subtypes and independence of Wnt signaling. | [43] |
GC | NM | 46 | Wnt-3A, Noggin, R-spondin-1, EGF, FGF10, Gastrin, A83–01, Y-27632 | > 50% | A biobank of GC PDOs with distinct subtypes is established and the PDOs maintain similarity to the parental tumors for long. | [44] |
GC | Surgery | 24 | Wnt, Noggin, R-spondin-1, EGF, Gastrin, FGF10, A83–01, Y-27632 | NM | The living bank of GC PDOs may predict therapy response for individual patients. | [45] |
GC | Surgery | 7 | Wnt, Noggin, R-spondin-1, EGF, Gastrin, FGF10, Y-27632 | NM | RNA sequencing reveals that the PDOs closely resemble the primary tumor tissue. | [46] |
GC | MA | 11 | Wnt-3A, Noggin, R-spondin1, EGF, Gastrin, A83–01, Y-27632, FGF10 | 92% | GC MADOs copy the histology, and genomic feature of the original MA cancer cells. | [47] |
PLC | Surgery | 8 | EGF, Gastrin I, A83–01, FGF10, HGF, FSK, Y-27632, dexamethasone | 47% | PDOs of PLC (including HCC, CAC, and CHC) copy the histology and gene signature of the parental human PLC tissues. | [25] |
PLC | Surgery and biopsy | 27 | Wnt-3A, Noggin, R-spondin, EGF, Gastrin, A83–01, FGF-10, HGF, FSK | NM | Drug screening of 129 drugs was performed using PLC PDO model. | [48] |
HCC | Biopsy | 10 | Wnt-3A, Rspondin-1, Gastrin, EGF, A83–01 FGF10, HGF, FSK | 26% | HCC PDOs maintain the morphology, HCC tumor markers and genetic heterogeneity of the original human HCC tissues. | [49] |
EADC | Surgery | 10 | Wnt-3A, Noggin, R-Spondin-1, EGF, A83–01, SB202190, FGF10 | 31% | EADC PDOs maintain the morphology and molecular signature of the primary human EADC tissues. EADC PDOs and the original tumor tissues have the same clonal architecture. | [50] |
ESCC | Biopsy | 11 | Wnt-3A, Noggin, R-Spondin, EGF, Gastrin, A83–01, SB202190 | 69% | ESCC PDOs recapitulate the histopathologic features of the original tumor tissues. Successful ESCC PDO generation is positively connected with poor response to radiation, chemotherapy and neoadjuvant chemotherapy. | [51] |
BC | Surgery | 6 | R-spondin-1, EGF, Gastrin, A83–01, FSK, Y-27632 | NM | The long-term cultured BC PDOs recapitulate the histopathology, gene signature of the original BC tissues. | [52] |