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Journal articles on the topic 'Tumor chemosensitivity'

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Published: 5 June 2025

Last updated: 15 July 2025

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Falkiewicz, B., C. M. Schlotter, U. Bosse, K. Bielawski, and U. Vogt. "c-myc oncogene gene dosage, serum CEA and CA-15.3 antigen levels, and cellular DNA values in relation to ex vivo chemosensitivity of primary human breast cancer." Acta Biochimica Polonica 47, no. 1 (2000): 149–56. http://dx.doi.org/10.18388/abp.2000_4072.

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A pilot study on relationships of selected molecular factors (c-myc oncogene average gene copy numbers (AGCN); serum CEA and CA 15.3 antigen levels; tumor cells' DNA values), to the ex vivo chemosensitivity of primary female human breast cancer in a modified adenosine triphosphate cell viability chemosensitivity assay (ATP-CVA), was performed. Four drug combinations were tested. A group of 75 cases of female primary breast cancer was assessed. Numerous correlations were found among molecular factors tested but none, with the exception of tumor grading, of these reflected ex vivo chemosensitivity of tumors tested. The results suggest that the parameters tested may not be important factors related to adjuvant chemoresponsiveness of primary human breast cancer to tested drug combinations.

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Balmaceda, Casilda. "Advances in brain tumor chemosensitivity." Current Opinion in Oncology 10, no. 3 (1998): 194–200. http://dx.doi.org/10.1097/00001622-199805000-00004.

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Cree, Ian A., and Christian M. Kurbacher. "ATP-based tumor chemosensitivity testing." Anti-Cancer Drugs 10, no. 5 (1999): 431–36. http://dx.doi.org/10.1097/00001813-199906000-00001.

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Cree, Ian A., Russell D. Petty, Christian M. Kurbacher, and Michael Untch. "Tumor chemosensitivity and chemoresistance assays." Cancer 78, no. 9 (1996): 2031–32. http://dx.doi.org/10.1002/(sici)1097-0142(19961101)78:9<2031::aid-cncr27>3.0.co;2-x.

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Kern, David H. "Tumor chemosensitivity and chemoresistance assays." Cancer 79, no. 7 (1997): 1447–49. http://dx.doi.org/10.1002/(sici)1097-0142(19970401)79:7<1447::aid-cncr23>3.0.co;2-z.

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Brown, Elizabeth, and Maurie Markman. "Tumor chemosensitivity and chemoresistance assays." Cancer 77, no. 6 (1996): 1020–25. http://dx.doi.org/10.1002/(sici)1097-0142(19960315)77:6<1020::aid-cncr3>3.0.co;2-l.

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Vogt, U., B. Falkiewicz, K. Bielawski, U. Bosse, and C. M. Schlotter. "Relationship of c-myc and erbB oncogene family gene aberrations and other selected factors to ex vivo chemosensitivity of ovarian cancer in the modified ATP-chemosensitivity assay." Acta Biochimica Polonica 47, no. 1 (2000): 157–64. http://dx.doi.org/10.18388/abp.2000_4073.

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A pilot study on relationships of selected molecular factors [erbB-1, erbB-2, erbB-3, and c-myc oncogene average gene copy numbers (AGCN); steroid receptors and pS2 gene expression; tumor cells' DNA values] to the ex vivo chemosensitivity of ovarian cancer in a modified adenosine triphosphate cell viability chemosensitivity assay (ATP-CVA), was performed. Despite the relatively small number of patients, numerous correlations among the factors tested were found. Nevertheless, only c-myc gene dosage positively affected ex vivo chemosensitivity of tumors tested.

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Ling, Zhi-qiang, Chun-jian Qi, Xiao-xiao Lu, et al. "Heterogeneity of chemosensitivity in esophageal cancer using ATP-tumor chemosensitivity assay." Acta Pharmacologica Sinica 33, no. 3 (2012): 401–6. http://dx.doi.org/10.1038/aps.2011.195.

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Qi, Chun-Jian, Yong-Ling Ning, Yu-Lan Zhu, Hai-Yan Min, Heng Ye, and Ke-Qing Qian. "In vitro chemosensitivity in breast cancer using ATP-tumor chemosensitivity assay." Archives of Pharmacal Research 32, no. 12 (2009): 1737–42. http://dx.doi.org/10.1007/s12272-009-2211-0.

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Kapoor, Shailendra. "Clusterin inhibition to enhance tumor chemosensitivity in systemic tumors." Cancer Chemotherapy and Pharmacology 71, no. 4 (2013): 1101. http://dx.doi.org/10.1007/s00280-013-2072-6.

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Hsieh, Chia-Hsun, Yi-Dao Chen, Shiang-Fu Huang, Hung-Ming Wang, and Min-Hsien Wu. "The Effect of Primary Cancer Cell Culture Models on the Results of Drug Chemosensitivity Assays: The Application of Perfusion Microbioreactor System as Cell Culture Vessel." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/470283.

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To precisely and faithfully perform cell-based drug chemosensitivity assays, a well-defined and biologically relevant culture condition is required. For the former, a perfusion microbioreactor system capable of providing a stable culture condition was adopted. For the latter, however, little is known about the impact of culture models on the physiology and chemosensitivity assay results of primary oral cavity cancer cells. To address the issues, experiments were performed. Results showed that minor environmental pH change could significantly affect the metabolic activity of cells, demonstrating the importance of stable culture condition for such assays. Moreover, the culture models could also significantly influence the metabolic activity and proliferation of cells. Furthermore, the choice of culture models might lead to different outcomes of chemosensitivity assays. Compared with the similar test based on tumor-level assays, the spheroid model could overestimate the drug resistance of cells to cisplatin, whereas the 2D and 3D culture models might overestimate the chemosensitivity of cells to such anticancer drug. In this study, the 3D culture models with same cell density as that in tumor samples showed comparable chemosensitivity assay results as the tumor-level assays. Overall, this study has provided some fundamental information for establishing a precise and faithful drug chemosensitivity assay.

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Wells, Jason D., Jacqueline R. Griffin, and Todd W. Miller. "Pan-Cancer Transcriptional Models Predicting Chemosensitivity in Human Tumors." Cancer Informatics 20 (January 2021): 117693512110024. http://dx.doi.org/10.1177/11769351211002494.

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Motivation: Despite increasing understanding of the molecular characteristics of cancer, chemotherapy success rates remain low for many cancer types. Studies have attempted to identify patient and tumor characteristics that predict sensitivity or resistance to different types of conventional chemotherapies, yet a concise model that predicts chemosensitivity based on gene expression profiles across cancer types remains to be formulated. We attempted to generate pan-cancer models predictive of chemosensitivity and chemoresistance. Such models may increase the likelihood of identifying the type of chemotherapy most likely to be effective for a given patient based on the overall gene expression of their tumor. Results: Gene expression and drug sensitivity data from solid tumor cell lines were used to build predictive models for 11 individual chemotherapy drugs. Models were validated using datasets from solid tumors from patients. For all drug models, accuracy ranged from 0.81 to 0.93 when applied to all relevant cancer types in the testing dataset. When considering how well the models predicted chemosensitivity or chemoresistance within individual cancer types in the testing dataset, accuracy was as high as 0.98. Cell line–derived pan-cancer models were able to statistically significantly predict sensitivity in human tumors in some instances; for example, a pan-cancer model predicting sensitivity in patients with bladder cancer treated with cisplatin was able to significantly segregate sensitive and resistant patients based on recurrence-free survival times ( P = .048) and in patients with pancreatic cancer treated with gemcitabine ( P = .038). These models can predict chemosensitivity and chemoresistance across cancer types with clinically useful levels of accuracy.

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Woltering, Eugene A. "Tumor Chemosensitivity Testing An Evolving Technique." Laboratory Medicine 21, no. 2 (1990): 82–84. http://dx.doi.org/10.1093/labmed/21.2.82.

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DUNN, IAN F., and ROBERT M. FRIEDLANDER. "Inducing Chemosensitivity in Human Tumor Cells." Neurosurgery 53, no. 2 (2003): NA. http://dx.doi.org/10.1227/01.neu.0000309411.45219.73.

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Maurer, R., and S. Casillo. "Tumor cell cultures: Characterization and chemosensitivity." Cytotechnology 2, S3 (1989): 34–40. http://dx.doi.org/10.1007/bf02279722.

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ZHANG, JIN, and HONGXIA LI. "Heterogeneity of tumor chemosensitivity in ovarian epithelial cancer revealed using the adenosine triphosphate-tumor chemosensitivity assay." Oncology Letters 9, no. 5 (2015): 2374–80. http://dx.doi.org/10.3892/ol.2015.3056.

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Nakada, S., D. Aoki, S. Ohie, et al. "Chemosensitivity testing of ovarian cancer using the histoculture drug response assay: sensitivity to cisplatin and clinical response." International Journal of Gynecologic Cancer 15, no. 3 (2005): 445–52. http://dx.doi.org/10.1136/ijgc-00009577-200505000-00006.

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Despite cytoreductive surgery and chemotherapy, the prognosis of advanced ovarian cancer is still poor. Predicting the chemosensitivity of tumors might improve the outcome. Therefore, we investigated the clinical value of the histoculture drug response assay for ovarian cancer. Tumor specimens were cultured for 7 days on collagen gel sponge in medium containing cisplatin, and the 50% inhibitory concentration was determined by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide assay. Then the in vitro sensitivity to cisplatin was compared with the clinical response and survival. Apoptosis of tumor cells was also investigated. Among 173 ovarian cancer patients, 164 were evaluable by the assay, and 29 patients had measurable lesions for which the clinical response could be determined. The 5-year survival rate was significantly higher in patients with chemosensitive tumors than in those with chemoresistant tumors when the cutoff value was set at a 50% inhibitory concentration of 25 μg/mL and the accuracy of the assay was 82.8% (24/29). As chemosensitivity to cisplatin became greater, the number of apoptotic cells also increased. This chemosensitivity assay may help predict the clinical response to cisplatin-based chemotherapy, thus improving the survival of ovarian cancer patients.

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Liu, Siwei, Huajiang Lei, Fangyuan Luo, Yilin Li, and Lan Xie. "The effect of lncRNA HOTAIR on chemoresistance of ovarian cancer through regulation of HOXA7." Biological Chemistry 399, no. 5 (2018): 485–97. http://dx.doi.org/10.1515/hsz-2017-0274.

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AbstractThis study aimed at investigating the biological functions of long non-coding RNAs (lncRNAs) hox transcript antisense intergenic RNA (HOTAIR) in resistant ovarian cancer cells, exploring the regulation effect of HOTAIR onHOXA7, and investigating their influence on the chemosensitivity of ovarian cancer cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied for the verification of HOTAIR expression in resistant and sensitive groups. How HOTAIR downregulation affected cell proliferation, migration and invasion, and apoptosis were determined using the MTT assay and the colony formation assay, the Transwell assay and flow cytometry analysis, respectively. Immunohistochemistry was used to inspect the protein expression of HOXA7 in resistant and sensitive ovarian cancer tissues. The regulation relationship between HOTAIR andHOXA7was investigated by qRT-PCR and Western blot. The effect of HOTAIR andHOXA7on tumor growth was confirmed by the tumor xenograft model of nude mice. By knocking downHOXA7, HOTAIR downregulation restrained the ovarian cancer deterioration in functional experiments. Silencing of HOTAIR andHOXA7could effectively inhibit tumor growth and increase chemosensitivity of ovarian tumors in nude mice. Downregulation of HOTAIR negatively affected the survival and activity of resistant ovarian cancer cells, and suppressed the expression ofHOXA7. Silencing of HOTAIR andHOXA7could increase the chemosensitivity of ovarian cancer cells, thus suppressing tumor development.

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Wang, Qing, and Hsin-Sheng Yang. "The Impact of Pdcd4, a Translation Inhibitor, on Drug Resistance." Pharmaceuticals 17, no. 10 (2024): 1396. http://dx.doi.org/10.3390/ph17101396.

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Programmed cell death 4 (Pdcd4) is a tumor suppressor, which has been demonstrated to efficiently suppress tumorigenesis. Biochemically, Pdcd4 binds with translation initiation factor 4A and represses protein translation. Beyond its role in tumor suppression, growing evidence suggests that Pdcd4 enhances the chemosensitivity of several anticancer drugs. To date, numerous translational targets of Pdcd4 have been identified. These targets govern important signal transduction pathways, and their attenuation may improve chemosensitivity or overcome drug resistance. This review will discuss the signal transduction pathways regulated by Pdcd4 and the potential mechanisms through which Pdcd4 enhances chemosensitivity or counteracts drug resistance.

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Zaffaroni, Nadia, Rosella Silvestrini, Ornella Sanfilippo, Maria Grazia Daidone, Giorgio Bolis, and Patrizia Seminara. "Drug Sensitivity of Different Tumor Lesions from the Same Patient Evaluated by a Short-Term Assay." Tumori Journal 74, no. 2 (1988): 137–44. http://dx.doi.org/10.1177/030089168807400203.

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A short-term antimetabolic assay, which considers the interference with [3H]thymidine incorporation as an indicator of drug effect, has been used to comparatively assess the chemosensitivity of different tumor lesions from the same patient. The analysis was performed on primary tumors and their synchronous metastases from 67 patients with breast, ovarian, gastrointestinal and germ cell testicular tumors. A remarkable difference in sensitivity to cytostatic drugs was observed between the two lesions. In contrast, a strong association in chemosensitivity (81.7% agreement rate; p < 0.01) was observed between two synchronous metastases from 17 patients with breast, ovarian, germ cell testicular tumors or malignant melanoma. In addition, the predictive relevance of the antimetabolic assay on clinical response to chemotherapy was analyzed in relation to the type of tumor lesion tested in vitro in a retrospective correlative study on 57 patients with advanced ovarian and germ cell testicular tumors. The objective clinical response was significantly correlated to the in vitro sensitivity of metastases (83.7% agreement rate; p < 0.01), but not to that of the primary tumor.

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Xie, Jiayin. "Screening of Chemotherapeutic Drugs Against Colorectal Cancer Based on Different Oxygen Environments in Vitro." BIO Web of Conferences 55 (2022): 01026. http://dx.doi.org/10.1051/bioconf/20225501026.

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With the deepening of tumor research, the concept of the tumor microenvironment has gradually come into people’s view. A significant characteristic of the microenvironment is hypoxic. A large number of vitro experiments have confirmed that hypoxic environments can induce angiogenesis, anti-apoptosis, changes in drug sensitivity, and tumor metastasis. Now, chemosensitivity tests are all carried out under normoxic conditions. Therefore, some scholars have pointed out that if it is possible to simulate the hypoxic state of the tumor microenvironment during the chemosensitivity tests in vitro, it may be able to match better the effect of chemotherapeutic drugs on killing tumor cells in vivo. This study clarified the differences in the chemosensitivity for colorectal cancer cells in normoxic and hypoxic environments. The result of CCK-8 detections has shown that the toxicity of drugs to cells is much higher under normoxic conditions. To further figure out the different mechanisms of the chemotherapy drugs under normoxic and hypoxic conditions, we conducted cellular uptake analysis and western blot, which demonstrated that the uptake of Doxorubicin in normoxic cells was significantly higher than that in hypoxic cells. While the result of the western blot has shown that the expression of VDAC (Voltage-dependent anion channel) and cleaved caspase-3 is higher under normoxic conditions. This study provides a specific basis for future research on the chemosensitivity of chemotherapy drugs in hypoxic environments.

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Weinstein, M. Joy, John Berg, Katsuyuki Kusuzaki, Dempsey S. Springfield, Mark C. Gebhardt, and Henry J. Mankin. "In vitro assay of nuclear uptake of doxorubicin hydrochloride in osteosarcoma cells of dogs." American Journal of Veterinary Research 52, no. 12 (1991): 1951–55. http://dx.doi.org/10.2460/ajvr.1991.52.12.1951.

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SUMMARY A rapid, simple chemosensitivity assay, assessing tumor cell nuclear uptake of doxorubicin hydrochloride, was evaluated in 16 dogs with appendicular osteosarcoma. Doxorubicin was administered to dogs in 5 biweekly treatments, and surgical resection was performed after the second or third treatment. The chemosensitivity assay was performed on biopsy specimens from all dogs before chemotherapy. It was repeated on tissue from resected tumors, and tumors were evaluated histologically to determine the degree of necrosis resulting from chemotherapy. Disease-free and total survival time correlated significantly (P < 0.05 in both cases) with the degree of postchemotherapy necrosis of the primary tumors. Significant correlation was not apparent between the percentage of tumor cells with nuclear uptake of doxorubicin (in either biopsy or resection samples) and disease-free or total survival time. The percentage of cells with nuclear uptake of doxorubicin in surgically resected tumors correlated significantly (P < 0.05) with percentage of necrosis.

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Mann, Melissa J., and Linda M. Hendershot. "UPR activation alters chemosensitivity of tumor cells." Cancer Biology & Therapy 5, no. 7 (2006): 736–40. http://dx.doi.org/10.4161/cbt.5.7.2969.

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Han, Chae Young, David A. Patten, Richard B. Richardson, Mary-Ellen Harper, and Benjamin K. Tsang. "Tumor metabolism regulating chemosensitivity in ovarian cancer." Genes & Cancer 9, no. 5-6 (2018): 155–75. http://dx.doi.org/10.18632/genesandcancer.176.

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Blower, Paul E., Ji-Hyun Chung, Joseph S. Verducci, et al. "MicroRNAs modulate the chemosensitivity of tumor cells." Molecular Cancer Therapeutics 7, no. 1 (2008): 1–9. http://dx.doi.org/10.1158/1535-7163.mct-07-0573.

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Epstein, R. J. "Drug-induced DNA damage and tumor chemosensitivity." Journal of Clinical Oncology 8, no. 12 (1990): 2062–84. http://dx.doi.org/10.1200/jco.1990.8.12.2062.

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Cytotoxic drugs act principally by damaging tumor-cell DNA. Quantitative analysis of this interaction provides a basis for understanding the biology of therapeutic cell kill as well as a rational strategy for optimizing and predicting tumor response. Recent advances have made it possible to correlate assayed DNA lesions with cytotoxicity in tumor cell lines, in animal models, and in patients with malignant disease. In addition, many of the complex interrelationships between DNA damage, DNA repair, and alterations of gene expression in response to DNA damage have been defined. Techniques for modulating DNA damage and cytotoxicity using schedule-specific cytotoxic combinations, DNA repair inhibitors, cell-cycle manipulations, and adjunctive noncytotoxic drug therapy are being developed, and critical therapeutic targets have been identified within tumor-cell subpopulations and genomic DNA alike. Most importantly, methods for predicting clinical response to cytotoxic therapy using both in vitro markers of tumor-cell sensitivity and in vivo measurements of drug-induced DNA damage are now becoming a reality. These advances can be expected to provide a strong foundation for the development of innovative cytotoxic drug strategies over the next decade.

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Tsyganov, M. M., I. A. Tsydenova, V. A. Markovich, et al. "Expression heterogeneity of ABC-transporter family genes and chemosensitivity genes in gastric tumor, carcinomatosis and lymph node metastases." Advances in Molecular Oncology 9, no. 4 (2022): 78–88. http://dx.doi.org/10.17650/2313-805x-2022-9-4-78-88.

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Introduction. Metastatic tumors (particularly gastric cancer) have been found to be characterized by heterogeneity between the primary tumor and metastases. This type of heterogeneity comes to the fore when treating primary-metastatic forms of tumor and is an important reason for the low effectiveness of their treatment. In this regard, comparative analysis of ABC-transporter gene expression and chemosensitivity genes will allow to characterize to a certain extent the resistance and sensitivity of primary tumor, carcinomatosis and metastases to therapy and provide the basis for personalized treatment approach.Aim. To evaluate expression heterogeneity of ABC-transporter genes and chemosensitivity genes in gastric tumor, carcinomatosis and lymph node metastases.Materials and methods. Overall 41 patients with disseminated gastric cancer stage IV with carcinomatosis of peritoneum were included in the investigation. All patients underwent surgery according to Roux palliative gastrectomy. After surgery patients underwent chemotherapy depending on indications. RNA was isolated using RNeasy Plus mini kit (Qiagen, Germany). The expression level of ABC transporter genes (ABCB1, ABCC1, ABCC2, ABCC5, ABCG1, ABCG2) and chemosensitivity genes (BRCA1, RRM1, ERCC1, TOP1, TOP2α, TUBβ3, TYMS, GSTP1) was assessed by reverse transcription polymerase chain reaction (RT-PCR) in primary tumor, carcinomatosis and lymph node metastases.Results. The expression levels of the genes under study were shown to vary widely. For ABC transporter genes, ABCG1 (3.1 ± 1.1; max 32.0), ABCG2 (7.9 ± 2.3; max 54.1), ABCG2 (9.6 ± 3.8; max 101.0) were the most expressed genes in gastric tumor tissue, carcinomatosis and lymph node metastasis, respectively. Hyperexpression among chemosensitivity genes at all three sites was characteristic only of TOP2α (17.2 ± 6.0; max. 161.9; 10.8 ± 4.1; max. 105.1; 35.3 ± 0.8; max. 439.6, respectively). We found that TOP2α and BRCA1 gene expression levels were higher in lymph node metastasis compared with gastric tumor tissue and carcinomatosis (at p = 0.005 and p = 0.001). Whereas ABCC1 gene expression was statistically significantly higher in carcinomatosis (p = 0.03).Conclusion. Thus, a high level of expression heterogeneity is observed in gastric cancer, which affects the expression patterns of various genes in different localizations. The expression profile can be used to determine the level of heterogeneity and approach to personalized therapy tactics.

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Liu, Yuanhui, Nancy Azizian, Delaney Sullivan, and Yulin Li. "Abstract 1692: mTOR inhibition attenuates chemosensitivity through induction of a persister state." Cancer Research 83, no. 7_Supplement (2023): 1692. http://dx.doi.org/10.1158/1538-7445.am2023-1692.

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Abstract Effective cancer therapeutics often kill a large fraction of tumor cells, while sparing a small surviving population, which can resurface as future tumor recurrence. Mechanisms of resistance in these residual tumors may involve rare preexisting clones with mutations, as well as de novo development of resistance through various genetic and/or non-genetic processes. In the context of acute stress resulting from cancer therapeutics, the initial adaptation is essential for tumor cell survival and allows for subsequent development of resistance through additional genetic and non-genetic mechanisms. As an integrator of environmental signals and cellular response, the mTOR pathway is a critical driver of cellular adaptation to environmental changes. In particular, mTOR regulates embryonic diapause, a reversible dormancy state in mammalian development in response to unfavorable environments. Analogous to its role in regulating embryonic diapause, mTOR inhibition may induce a diapause-like state in cancer cells, leading to drug tolerance and persistence of residual tumors following therapy. In line with this notion, recent studies have reported markedly reduced mTOR activity in residual tumors. However, the causal relationship between mTOR inhibition and chemosensitivity has not been investigated. Through a genome-wide CRISPR knockout library screen in pancreatic cancer cells treated with chemotherapeutic agents, we have identified the mTOR pathway as a prominent determinant of chemosensitivity. Pharmacological suppression of mTOR activity in cancer cells from diverse tissue origins leads to the persistence of a reversibly resistant population, which is otherwise eliminated by chemotherapeutic agents. Conversely, activation of the mTOR pathway increases chemosensitivity and predicts better survival among various human cancers. Survival of the persisters is dependent on the regulation of autophagy, G2/M checkpoint, and cell death pathways, as revealed by a small-molecule chemical library screen. Thus, mTOR plays a causal yet paradoxical role in regulating chemotherapeutic response; inhibition of the mTOR pathway, while suppressing tumor expansion, facilitates the development of a reversible drug-tolerant persister state. Citation Format: Yuanhui Liu, Nancy Azizian, Delaney Sullivan, Yulin Li. mTOR inhibition attenuates chemosensitivity through induction of a persister state [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 1692.

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Diao, Zhen-bin, Tian-xiao Sun, Yi Zong, Bo-chuan Lin, and Yuan-sheng Xia. "Identification of plasma microRNA-22 as a marker for the diagnosis, prognosis, and chemosensitivity prediction of osteosarcoma." Journal of International Medical Research 48, no. 12 (2020): 030006052096781. http://dx.doi.org/10.1177/0300060520967818.

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Objective MicroRNA (miR)-22 plays crucial roles in malignant tumors and is involved in regulation of chemosensitivity. Additionally, altered expression of circulating miR-22 has been reported in various cancers. This study was designed to investigate plasma miR-22 expression in patients with osteosarcoma (OS) and determine its diagnostic, prognostic, and chemosensitivity prediction value. Methods Plasma miR-22 levels in 120 patients with OS and 120 healthy controls were detected by real-time quantitative reverse transcription PCR. Associations of plasma miR-22 expression with the patients’ clinicopathological features and prognosis were then assessed. Results Plasma miR-22 levels in patients with OS were significantly lower than those in healthy controls. Low plasma miR-22 levels were correlated with large tumor size, advanced clinical stages, positive distant metastasis, and poor tumor response to preoperative chemotherapy. Plasma miR-22 could discriminate OS patients from controls and distinguish patients with a good response to therapy from those with a poor response to therapy. Multivariate analysis revealed that low plasma miR-22 expression was a significant independent predictor of unfavorable prognosis. Conclusions Altered plasma levels of miR-22 might serve as a novel, noninvasive biomarker for OS diagnosis, prognosis, and chemosensitivity prediction.

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Kiran, Sonia, Yu Xue, Drishty B. Sarker, and Qing-Xiang Amy Sang. "Effects of Induced Pluripotent Stem Cell-Derived Astrocytes on Cisplatin Sensitivity in Pediatric Brain Cancer Cells." Cancers 17, no. 6 (2025): 997. https://doi.org/10.3390/cancers17060997.

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Background: ATRTs and DIPGs are deadly pediatric brain tumors with poor prognosis. These tumors can develop resistance to chemotherapies, which may be significantly influenced by their microenvironment. Since astrocytes are the most abundant glial cell type in the brain microenvironment and may support tumor growth and chemoresistance, this study investigated the effects of induced pluripotent stem cell-derived astrocytes (iPSC-astrocytes) on cisplatin sensitivity in CHLA-05-ATRT and SF8628 (DIPG) cells. iPSCs provide an unlimited and standardized source of nascent astrocytes, which enables modeling the interaction between childhood brain tumor cells and iPSC-astrocytes within a controlled coculture system. Methods: To study the effects on tumor growth, the iPSC-astrocytes were cocultured with tumor cells. Additionally, the tumor cells were exposed to various concentrations of cisplatin to evaluate their chemosensitivity in the presence of astrocytes. Results: The paracrine interaction of iPSC-astrocytes with tumor cells upregulated astrocyte activation markers GFAP and STAT3 and promoted tumor cell proliferation. Moreover, the cisplatin treatment significantly decreased the viability of CHLA-05-ATRT and SF8628 cells. However, tumor cells exhibited reduced sensitivity to cisplatin in the coculture with iPSC-astrocytes. During cisplatin treatment, DIPG cells in particular showed upregulation of resistance markers, ERK1, STAT3, and MTDH, which are associated with enhanced proliferation and invasion. They also had increased expression of APEX1, which is involved in the base excision repair pathway following cisplatin-induced DNA damage. Conclusion: These findings underscore the significance of the tumor microenvironment in modulating tumor cell survival and chemosensitivity.

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Cheng, Ching-Yuan, Shur-Hueih Cherng, Wen-Jun Wu, et al. "Reply to: Clusterin inhibition to enhance tumor chemosensitivity in systemic tumors." Cancer Chemotherapy and Pharmacology 71, no. 4 (2013): 1103–4. http://dx.doi.org/10.1007/s00280-013-2085-1.

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Lian, Meng, Jiaming Chen, Xixi Shen, Lizhen Hou, and Jugao Fang. "Pparg may Promote Chemosensitivity of Hypopharyngeal Squamous Cell Carcinoma." PPAR Research 2020 (April 22, 2020): 1–6. http://dx.doi.org/10.1155/2020/6452182.

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The upregulation of peroxisome proliferator-activated receptor gamma (PPARG) has been shown to increase the chemosensitivity of several human cancers. This study is aimed at studying if PPARG sensitizes hypopharyngeal squamous cell carcinoma (HSCC) in chemotherapeutic treatments and at dissecting possible mechanisms of observed effects. We integrated large-scale literature data and HSCC gene expression data to identify regulatory pathways that link PPARG and chemosensitivity in HSCC. Expression levels of molecules within the PPARG regulatory pathways were compared in 21 patients that underwent chemotherapy for primary HSCC, including 12 chemotherapy-sensitive patients (CSP) and 9 chemotherapy-nonsensitive patients (CNSP). In the CPS group, expression levels of PPARG were higher than that in the CNSP group (log‐fold‐change=0.50). Structured text mining identified two chemosensitivity-related regulatory pathways driven by PPARG. In the CSP group, expression levels for 7 chemosensitivity-promoting genes were increased, while for 13 chemosensitivity suppressing the gene expression levels were decreased. Our results support the chemosensitivity-promoting role of PPARG in HSCC tumor cells, most likely by affecting both cell proliferation and cell motility pathways.

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Shin, Dongheon, Chaerin Kim, Yeon Chae, et al. "Successful Management of Incompletely Resected Transitional Cell Carcinoma with Sorafenib Tosylate in a Dog." Journal of the American Animal Hospital Association 60, no. 6 (2024): 275–79. http://dx.doi.org/10.5326/jaaha-ms-7463.

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ABSTRACT Most urinary bladder (UB) tumors are malignant, and transitional cell carcinoma (TCC) is the most common neoplasm affecting the UB in dogs. Sorafenib may be a potential therapeutic agent for canine TCC. A 12 yr old spayed female Maltese dog weighing 3.6 kg and with a history of hematuria was referred for a suspected UB tumor. Abdominal ultrasonography revealed a UB mass attached to the cranioventral wall. The remaining abdominal examinations, including that of the lymph nodes, were unremarkable. Ultrasound-guided traumatic catheterization of the UB mass was performed, and the cytological evaluation of the UB mass indicated TCC. Excision was performed by partial cystectomy, and histopathology confirmed TCC, although the tumor had infiltrated the surgical margins. A chemosensitivity assay was conducted using tissue from the excised tumor. Sorafenib tosylate, a tyrosine kinase inhibitor, showed the greatest effect in the chemosensitivity assay. Therefore, adjuvant chemotherapy with sorafenib tosylate and piroxicam was administered postoperatively. The dog lived without any clinical signs, including hematuria or tumor relapse, for more than 2 yr after the surgery. This is the first report of successful long-term management of TCC with sorafenib tosylate in a dog.

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Liu, Yi, Wei Tang, and Feng Yao. "USP53 Exerts Tumor-Promoting Effects in Triple-Negative Breast Cancer by Deubiquitinating CRKL." Cancers 15, no. 20 (2023): 5033. http://dx.doi.org/10.3390/cancers15205033.

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Breast cancer (BC) ranks in the top five malignant tumors in terms of morbidity and mortality rates. Among BC subtypes, TNBC has a high recurrence rate and metastasis rate and the worst prognosis. However, the exact mechanism by which TNBC develops is unclear. Here, we show that the deubiquitinase USP53 contributes to tumor growth and metastasis in TNBC. USP53 is overexpressed in TNBC, and this phenotype is linked to a poor prognosis. Functionally, USP53 promotes TNBC cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT). More importantly, USP53 decreases the chemosensitivity of BC cells by enhancing v-crk sarcoma virus CT10 oncogene homologue (avian)-like (CRKL) expression. Mechanistically, USP53 directly binds CRKL to stabilize and deubiquitinate it, thereby preventing CRKL degradation. Overall, we discovered that USP53 deubiquitinates CRKL, encourages tumor development and metastasis, and reduces chemosensitivity in TNBC. These findings imply that USP53 might represent a new therapeutic target for the treatment of TNBC.

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Wang, Zhi-Yong, Jun-Ai Zhang, Xian-Jin Wu, et al. "IL-6 Inhibition Reduces STAT3 Activation and Enhances the Antitumor Effect of Carboplatin." Mediators of Inflammation 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/8026494.

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Recent studies suggest that tumor-associated macrophage-produced IL-6 is an important mediator within the tumor microenvironment that promotes tumor growth. The activation of IL-6/STAT3 axis has been associated with chemoresistance and poor prognosis of a variety of cancers including colorectal carcinoma and thus serves as a potential immunotherapeutic target for cancer treatment. However, it is not fully understood whether anticytokine therapy could reverse chemosensitivity and enhance the suppressive effect of chemotherapy on tumor growth. In this study, we aimed to investigate the effect of IL-6 inhibition therapy on the antitumor effect of carboplatin. Enhanced expression of IL-6 and activation of STAT3 were observed in human colorectal carcinoma samples compared to normal colorectal tissue, with higher levels of IL-6/STAT3 in low grade carcinomas. Treatment of carboplatin (CBP) dose-dependently increased IL-6 production and STAT3 activation in human colorectal LoVo cells. Blockade of IL-6 with neutralizing antibody enhanced chemosensitivity of LoVo cells to carboplatin as evidenced by increased cell apoptosis. IL-6 blockade abolished carboplatin-induced STAT3 activation. IL-6 blockade and carboplatin synergistically reduced cyclin D1 expression and enhanced caspase-3 activity in LoVo cells. Our results suggest that inhibition of IL-6 may enhance chemosensitivity of colon cancers with overactive STAT3 to platinum agents.

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O'Toole, S. A., B. L. Sheppard, E. Mcguinness, N. C. Gleeson, and J. Bonnar. "Serous papillary adenocarcinomas of the ovary display heterogeneity in their response to chemotherapy." International Journal of Gynecologic Cancer 11, no. 5 (2001): 365–71. http://dx.doi.org/10.1136/ijgc-00009577-200109000-00005.

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The response of ovarian serous papillary adenocarcinomas to various cytotoxic drugs was examined using the (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt) (MTS) cytotoxicity assay. Thirty tumors were collected and organized into four groups according to histologic grade and FIGO stage: stage III, grade 2; stage III, grade 3; stage IV, grade 2; and stage IV, grade 3. The MTS chemosensitivity assay was performed on each tumor to examine the response to cisplatin, paclitaxel , hycamtin and the combination of cisplatin and paclitaxel. Ovarian adenocarcinomas of similar stage and grade displayed varying responses to the same drug. A lower concentration of the drug was often as effective as the peak plasma concentration. For some specimens combination therapy was more effective for inhibiting tumor growth, and for others single-agent therapy gave a better response. A chemosensitivity/resistance profile is recommended before deciding on appropriate chemotherapy.

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Covell, David G. "Bioinformatic analysis linking genomic defects to chemosensitivity and mechanism of action." PLOS ONE 16, no. 4 (2021): e0243336. http://dx.doi.org/10.1371/journal.pone.0243336.

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A joint analysis of the NCI60 small molecule screening data, their genetically defective genes, and mechanisms of action (MOA) of FDA approved cancer drugs screened in the NCI60 is proposed for identifying links between chemosensitivity, genomic defects and MOA. Self-Organizing-Maps (SOMs) are used to organize the chemosensitivity data. Student’s t-tests are used to identify SOM clusters with enhanced chemosensitivity for tumor cell lines with versus without genetically defective genes. Fisher’s exact and chi-square tests are used to reveal instances where defective gene to chemosensitivity associations have enriched MOAs. The results of this analysis find a relatively small set of defective genes, inclusive of ABL1, AXL, BRAF, CDC25A, CDKN2A, IGF1R, KRAS, MECOM, MMP1, MYC, NOTCH1, NRAS, PIK3CG, PTK2, RPTOR, SPTBN1, STAT2, TNKS and ZHX2, as possible candidates for roles in chemosensitivity for compound MOAs that target primarily, but not exclusively, kinases, nucleic acid synthesis, protein synthesis, apoptosis and tubulin. These results find exploitable instances of enhanced chemosensitivity of compound MOA’s for selected defective genes. Collectively these findings will advance the interpretation of pre-clinical screening data as well as contribute towards the goals of cancer drug discovery, development decision making, and explanation of drug mechanisms.

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Levy, Jean M. Mulcahy, and Andrew Thorburn. "Modulation of pediatric brain tumor autophagy and chemosensitivity." Journal of Neuro-Oncology 106, no. 2 (2011): 281–90. http://dx.doi.org/10.1007/s11060-011-0684-4.

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Testa, U., L. Pasquini, and E. Petrucci. "In vitro assays of tumor chemosensitivity and chemoresistance." Drugs of the Future 29, no. 10 (2004): 1035. http://dx.doi.org/10.1358/dof.2004.029.10.863394.

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Yilmaz, Cengiz, and Demet Kocatepe Cavdar. "Biomarker Discordances and Alterations Observed in Breast Cancer Treated with Neoadjuvant Chemotherapy: Causes, Frequencies, and Clinical Significances." Current Oncology 29, no. 12 (2022): 9695–710. http://dx.doi.org/10.3390/curroncol29120761.

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Purpose: Biomarker discordances and alterations can be encountered between tru-cut biopsy and residual tumor in breast cancer treated with neoadjuvant chemotherapy (NACTx). We aimed to investigate the effect of NACTx on major biomarker expression (ER, PR, HER2, Ki-67) and tumor grade, the frequency and causes of receptor discordances, and the clinical significance of changes in terms of adjuvant therapy need and chemosensitivity. Methods: In this retrospective study, ER, PR, HER2, and Ki-67 expression and tumor grades were compared between pre- and post-NACTx tumor samples using the Wilcoxon signed-rank test. The frequencies of receptor discordances and the need for new adjuvant therapy due to discordances were calculated. The effect of patient and tumor characteristics and NACTx regimens on discordances was investigated using multivariate analysis. Using histopathological examinations, residual tumors were divided into chemotherapy-responsive and chemotherapy-unresponsive tumors. Biomarker changes in both groups were analyzed for predictability of chemosensitivity. Results: Of the 169 patients who received NACTx, 102 patients having enough residual tumors in the surgical pathology specimen were enrolled in the study. Histopathologically, about 70% of tumors were partially responsive to NACTx and 30% were unresponsive (chemo-resistant). The concordance and discordance rates were 95.1% versus 4.9% for ER (p = 0.180), 97.1% versus 2.9% for PR (p = 0.083), and 89.2% versus 10.8% for HER2 (p = 0.763), respectively. In addition, 15% of hormone receptor (HR)-negative patients became HR(+) and 5.7% of HER2(−) patients became HER2(+) in the residual tumors, requiring adjuvant endocrine or anti-HER2 therapy. In particular, 18% of triple-negative patients became HR(+) and 12% became HER2(+). HER2 loss was detected in 40% of HER2(+) patients. Multivariate logistic regression analysis revealed that lower estrogen expression (p = 0.046), a smaller tumor size (p = 0.029), and anti-HER2 therapy (p < 0.001) have independent efficacy on ER discordance, PR discordance, and HER2 discordance, respectively. Ki-67 and PR expression significantly decreased in chemotherapy-responsive tumors (p = 0.001 and p = 0.004), and the tumor grade increased in chemotherapy-unresponsive tumors (p = 0.034). Conclusions: Approximately 3–5% of HR discordance and about 10% of HER2 discordance can be observed in breast cancer after currently used NACTx regimens. Discordances are bi-directional (from positive to negative and vice versa), and their causes are multifactorial; they should be assessed accordingly. The NACTx effect alone cannot explain observed discordances but can cause biomarker alterations. The change in receptor status from positive to negative, especially HER2 loss, is mainly associated with the NACTx effect. However, the shift from negative to positive is thought to be primarily related to intratumoral heterogeneity. Receptor statuses becoming positive are of more clinical importance due to adjuvant therapy requirements. Biomarker alterations in PR, Ki-67, and tumor grade can provide predictive information about tumor chemosensitivity.

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Qiu, Dongjie, Xiaolong Li, Yinfeng Liu, Xiaohuan Bao, and Li Ma. "Tetrahydrocurcumin Chemosensitizes Breast Cancer to Albumin-Bound Paclitaxel by Enhancing SPARC Expression through Demethylation." Journal of Oncology 2022 (September 16, 2022): 1–14. http://dx.doi.org/10.1155/2022/7961537.

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Paclitaxel is an effective chemotherapy drug for breast cancer (BC); however, drug resistance affects long-term clinical applications. In this study, we aimed to explore whether a natural compound, tetrahydrocurcumin (THC), could sensitize BC to albumin-bound paclitaxel (ab-PTX). The in vitro sensitization effect of THC to ab-PTX was evaluated in human BC cell lines, and in vivo chemosensitivity was measured using a xenograft BC tumor model. The expression of secreted protein acidic and rich in cysteine (SPARC), a speculated protein interacting with ab-PTX, was measured. Methylation-specific polymerase chain reaction (MSP) was used to further explore whether demethylation of SPARC by THC contributed to its chemosensitivity capabilities. Higher SPARC expression was correlated with a better prognosis in patients with BC. In vitro analysis showed THC enhanced the inhibitory effect of ab-PTX on BC cells and xenograft tumors and showed significant chemosensitivity. This enhancement mainly relied on upregulating the expression of SPARC through downregulating methylation of the SPARC gene. The demethylating agent, 5-Aza-2 ′ -deoxycytidine (5-Aza-Cdr), decreased THC’s chemosensitivity effect, further confirming this molecular mechanism. THC enhanced the inhibitory effect of ab-PTX in BC by downregulating methylation of the SPARC gene. Further, upregulated SPARC increased the efficacy of ab-PTX.

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Hoare, Owen, Nicolas Fraunhoffer, Abdessamad Elkaoutari, et al. "Exploring the Complementarity of Pancreatic Ductal Adenocarcinoma Preclinical Models." Cancers 13, no. 10 (2021): 2473. http://dx.doi.org/10.3390/cancers13102473.

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Purpose: Compare pancreatic ductal adenocarcinoma (PDAC), preclinical models, by their transcriptome and drug response landscapes to evaluate their complementarity. Experimental Design: Three paired PDAC preclinical models—patient-derived xenografts (PDX), xenograft-derived pancreatic organoids (XDPO) and xenograft-derived primary cell cultures (XDPCC)—were derived from 20 patients and analyzed at the transcriptomic and chemosensitivity level. Transcriptomic characterization was performed using the basal-like/classical subtyping and the PDAC molecular gradient (PAMG). Chemosensitivity for gemcitabine, irinotecan, 5-fluorouracil and oxaliplatin was established and the associated biological pathways were determined using independent component analysis (ICA) on the transcriptome of each model. The selection criteria used to identify the different components was the chemosensitivity score (CSS) found for each drug in each model. Results: PDX was the most dispersed model whereas XDPO and XDPCC were mainly classical and basal-like, respectively. Chemosensitivity scoring determines that PDX and XDPO display a positive correlation for three out of four drugs tested, whereas PDX and XDPCC did not correlate. No match was observed for each tumor chemosensitivity in the different models. Finally, pathway analysis shows a significant association between PDX and XDPO for the chemosensitivity-associated pathways and PDX and XDPCC for the chemoresistance-associated pathways. Conclusions: Each PDAC preclinical model possesses a unique basal-like/classical transcriptomic phenotype that strongly influences their global chemosensitivity. Each preclinical model is imperfect but complementary, suggesting that a more representative approach of the clinical reality could be obtained by combining them. Translational Relevance: The identification of molecular signatures that underpin drug sensitivity to chemotherapy in PDAC remains clinically challenging. Importantly, the vast majority of studies using preclinical in vivo and in vitro models fail when transferred to patients in a clinical setting despite initially promising results. This study presents for the first time a comparison between three preclinical models directly derived from the same patients. We show that their applicability to preclinical studies should be considered with a complementary focus, avoiding tumor-based direct extrapolations, which might generate misleading conclusions and consequently the overlook of clinically relevant features.

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Lucà, Rossella, Giorgia di Blasio, Daniela Gallo, et al. "Estrogens Counteract Platinum-Chemosensitivity by Modifying the Subcellular Localization of MDM4." Cancers 11, no. 9 (2019): 1349. http://dx.doi.org/10.3390/cancers11091349.

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Estrogen activity towards cancer-related pathways can impact therapeutic intervention. Recent omics data suggest possible crosstalk between estrogens/gender and MDM4, a key regulator of p53. Since MDM4 can either promote cell transformation or enhance DNA damage-sensitivity, we analysed in vivo impact of estrogens on both MDM4 activities. In Mdm4 transgenic mouse, Mdm4 accelerates the formation of fibrosarcoma and increases tumor sensitivity to cisplatin as well, thus confirming in vivo Mdm4 dual mode of action. Noteworthy, Mdm4 enhances chemo- and radio-sensitivity in male but not in female animals, whereas its tumor-promoting activity is not affected by mouse gender. Combination therapy of transgenic females with cisplatin and fulvestrant, a selective estrogen receptor degrader, was able to recover tumor cisplatin-sensitivity, demonstrating the relevance of estrogens in the observed sexual dimorphism. Molecularly, estrogen receptor-α alters intracellular localization of MDM4 by increasing its nuclear fraction correlated to decreased cell death, in a p53-independent manner. Importantly, MDM4 nuclear localization and intra-tumor estrogen availability correlate with decreased platinum-sensitivity and apoptosis and predicts poor disease-free survival in high-grade serous ovarian carcinoma. These data demonstrate estrogen ability to modulate chemo-sensitivity of MDM4-expressing tumors and to impinge on intracellular trafficking. They support potential usefulness of combination therapy involving anti-estrogenic drugs.

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Pizon, Monika, Dorothea Zimon, Ulrich A. Pachmann, and Katharina Pachmann. "In vitro chemosensitivity testing of mammospheres cultured from circulating epithelial tumor cells (CETCs) of breast cancer patients: Comparision to chemosensitivity of total CETCs." Journal of Clinical Oncology 32, no. 26_suppl (2014): 50. http://dx.doi.org/10.1200/jco.2014.32.26_suppl.50.

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50 Background: In vitro chemosensitivity testing of circulating epithelial tumor cells (CETCs) provides real-time information about the sensitivity of the tumor cells present in the patient. Nevertheless, a fraction of CETCs can survive after conventional chemotherapy and grow into distant metastasis. This may be a subpopulation of CETCs with proliferation activity which has the ability to form floating spheres in suspension culture. Spheroids exhibit stem cell-like properties and may be responsible for chemotherapeutic resistance. Therefore, the aim of our study was to determine the efficacy of chemotherapeutics on spheroids cultured from CETCs. Methods: The enumeration of CETCs from patients with solid tumors in clinical stage I to IV was performed using the maintrac method. Subsequently, CETCs in the context of the surrounding white blood cells were cultured in a suspension culture allowing for spheroid formation. To evaluate the cytotoxic effect of drugs on CETCs and spheroids we exposed them to anticancer drugs in short time culture in different concentrations and for different periods of time. Results: In contrast to CETCs, spheroids were significantly more chemotherapy resistant. Active drugs led to disintegration of tumor spheres. Interestingly, some cells in the spheres were able to survive. Epirubicin and especially salinomycin, a polyether ionophore antibiotic isolated from Streptomyces albus, showed high efficacy in a high proportion of cells. Furthermore, our data suggested that curcumin, a natural biologically active compound that is extracted from the plant Curcuma longais a promising agent for cancer treatment. Docetaxel, cyclophosphamide, and 5-fluoruracil showed lower cytotoxic effects onto the cells in the spheres. Conclusions: Our results show, for the first time, that stem cells circulating in peripheral blood, capable of forming spheroids are way more resistant to anticancer drugs than the remnant circulating tumor cells. We, furthermore, demonstrate that salinomycin and curcumin efficiently destroy spheroids cultured from CETCs, strengthening their role as promising anticancer therapeutics.

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Filippova, S. Yu, S. V. Timofeeva, T. V. Chembarova, et al. "THREE-DIMENSIONAL IN VITRO MODELS FOR STUDYING THE CHEMOSENSITIVITY OF BREAST CANCER CELLS." CARDIOMETRY, no. 29 (November 1, 2023): 13–14. http://dx.doi.org/10.18137/cardiometry.2023.29.conf.6.

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Scientists agree that three-dimensional tumor cell cultures reflect the in vitro biological features of malignant tumors to a greater extent than it is the case with the conventional monolayer cultures. In particular, the results of assessing the effectiveness of anticancer drugs obtained in three-dimensional cell models are considered as more accurate and consistent with the tumor response in vivo, where sensitivity is usually lower than that found in the in vitro experiments. Some of the most developed cellular models are structures obtained using three-dimensional bioprinting, which include not only malignant cells, but also biogels to imitate the chemical and mechanical properties of the extracellular matrix of the tumor.

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Ávila-López, P. A., G. Guerrero, H. N. Nuñez-Martínez, et al. "H2A.Z overexpression suppresses senescence and chemosensitivity in pancreatic ductal adenocarcinoma." Oncogene 40, no. 11 (2021): 2065–80. http://dx.doi.org/10.1038/s41388-021-01664-1.

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AbstractPancreatic ductal adenocarcinoma (PDAC) is one of the most intractable and devastating malignant tumors. Epigenetic modifications such as DNA methylation and histone modification regulate tumor initiation and progression. However, the contribution of histone variants in PDAC is unknown. Here, we demonstrated that the histone variant H2A.Z is highly expressed in PDAC cell lines and PDAC patients and that its overexpression correlates with poor prognosis. Moreover, all three H2A.Z isoforms (H2A.Z.1, H2A.Z.2.1, and H2A.Z.2.2) are highly expressed in PDAC cell lines and PDAC patients. Knockdown of these H2A.Z isoforms in PDAC cell lines induces a senescent phenotype, cell cycle arrest in phase G2/M, increased expression of cyclin-dependent kinase inhibitor CDKN2A/p16, SA-β-galactosidase activity and interleukin 8 production. Transcriptome analysis of H2A.Z-depleted PDAC cells showed altered gene expression in fatty acid biosynthesis pathways and those that regulate cell cycle and DNA damage repair. Importantly, depletion of H2A.Z isoforms reduces the tumor size in a mouse xenograft model in vivo and sensitizes PDAC cells to gemcitabine. Overexpression of H2A.Z.1 and H2A.Z.2.1 more than H2A.Z.2.2 partially restores the oncogenic phenotype. Therefore, our data suggest that overexpression of H2A.Z isoforms enables cells to overcome the oncoprotective barrier associated with senescence, favoring PDAC tumor grow and chemoresistance. These results make H2A.Z a potential candidate as a diagnostic biomarker and therapeutic target for PDAC.

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Chen, Zhiyao, Shichao Zhang, Sheng Ma, et al. "Evaluation of the in vitro Chemosensitivity and Correlation with Clinical Outcomes in Lung Cancer using the ATP-TCA." Anti-Cancer Agents in Medicinal Chemistry 18, no. 1 (2018): 139–45. http://dx.doi.org/10.2174/1871520617666170419123713.

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Background and Objective: Multiple drug resistance (MDR) to chemotherapeutic agents often leads to a failure to respond to chemotherapy. We utilized an in vitro chemosensitivity test to identify sensitive and effective chemotherapeutic drugs and further elucidated the correlation between the in vivo chemosensitivity and clinical outcomes. Methods: Here, we evaluated the in vitro chemosensitivity and MDR of 120 lung cancer patients to eight singledrug chemotherapies and of 291 lung cancer patients to seven chemotherapy regimens using an ATP-based tumor chemosensitivity assay (ATP-TCA). Additionally, the chemosensitivity profiles of lung adenocarcinoma patients (284 cases) and lung squamous cell carcinoma patients (90 cases) to these single-drug and chemotherapy regimens were compared. Furthermore, the correlations between the chemosensitivity and clinical outcomes were investigated in 16 stage III squamous cell carcinoma patients. Results and Conclusion: PTX (51.7%), TXT (43.3%), GEM (12.5%), PTX+DDP (62.5%), TXT+L-OHP (54.3%) and VP-16+DDP (16.2%) had the highest in vitro chemosensitivity rates. Approximately 31.7% of patients developed resistance to all eight single-drug chemotherapies, and 25.8% of patients displayed resistance to all seven chemotherapy regimens. In addition, lung squamous cell carcinoma was significantly more sensitive to GEM and MTA+DDP than lung adenocarcinoma (P<0.05). Further analysis showed that patients with higher drug sensitivity tended to have longer disease-free survival (18 months vs. 8.5 months) than patients displaying drug resistance (P<0.05). These results suggest that the implementation of in vitro drug susceptibility testing before chemotherapy can effectively prevent the occurrence of primary drug resistance and inappropriate drug treatment.

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Campaner, Elena, Alessandro Zannini, Mariangela Santorsola, et al. "Breast Cancer Organoids Model Patient-Specific Response to Drug Treatment." Cancers 12, no. 12 (2020): 3869. http://dx.doi.org/10.3390/cancers12123869.

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Tumor organoids are tridimensional cell culture systems that are generated in vitro from surgically resected patients’ tumors. They can be propagated in culture maintaining several features of the tumor of origin, including cellular and genetic heterogeneity, thus representing a promising tool for precision cancer medicine. Here, we established patient-derived tumor organoids (PDOs) from different breast cancer subtypes (luminal A, luminal B, human epidermal growth factor receptor 2 (HER2)-enriched, and triple negative). The established model systems showed histological and genomic concordance with parental tumors. However, in PDOs, the ratio of diverse cell populations was frequently different from that originally observed in parental tumors. We showed that tumor organoids represent a valuable system to test the efficacy of standard therapeutic treatments and to identify drug resistant populations within tumors. We also report that inhibitors of mechanosignaling and of Yes-associated protein 1 (YAP) activation can restore chemosensitivity in drug resistant tumor organoids.

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Hamilton, Gerhard, and Barbara Rath. "Applicability of tumor spheroids for in vitro chemosensitivity assays." Expert Opinion on Drug Metabolism & Toxicology 15, no. 1 (2018): 15–23. http://dx.doi.org/10.1080/17425255.2019.1554055.

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Nishiyama, Masahiko, Yoshihiro Noso, Naoki Hirabayashi, et al. "Prediction of individual tumor chemosensitivity in subrenal capsule assay." Japanese Journal of Surgery 16, no. 4 (1986): 257–61. http://dx.doi.org/10.1007/bf02470934.

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