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CDK4/6 Inhibition Augments Antitumor Immunity by Enhancing T-cell Activation
Open accessPublished version of a preprint
Abstract
Immune checkpoint blockade, exemplified by antibodies targeting the PD-1 receptor, can induce durable tumor regressions in some patients. To enhance the efficacy of existing immunotherapies, we screened for small molecules capable of increasing the activity of T cells suppressed by PD-1. Here, we show that short-term exposure to small-molecule inhibitors of cyclin-dependent kinases 4 and 6 (CDK4/6) significantly enhances T-cell activation, contributing to antitumor effects in vivo, due in part to the derepression of NFAT family proteins and their target genes, critical regulators of T-cell function. Although CDK4/6 inhibitors decrease T-cell proliferation, they increase tumor infiltration and activation of effector T cells. Moreover, CDK4/6 inhibition augments the response to PD-1 blockade in a novel ex vivo organotypic tumor spheroid culture system and in multiple in vivo murine syngeneic models, thereby providing a rationale for combining CDK4/6 inhibitors and immunotherapies. Significance: Our results define previously unrecognized immunomodulatory functions of CDK4/6 and suggest that combining CDK4/6 inhibitors with immune checkpoint blockade may increase treatment efficacy in patients. Furthermore, our study highlights the critical importance of identifying complementary strategies to improve the efficacy of immunotherapy for patients with cancer. Cancer Discov; 8(2); 216–33. ©2017 AACR. See related commentary by Balko and Sosman, p. 143. See related article by Jenkins et al., p. 196. This article is highlighted in the In This Issue feature, p. 127
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In the citing paper
“cyclin-dependent kinase inhibitors 4 and 6 (CDK4/6) facilitate T cell activation, resulting in a higher number of tumour-infiltrating T cells in PDOs, cultivated over several days in a microfluidic 3D chip setup.”
From Human disease models in drug development (2023) · cites this paper as [129]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“CDK4/6 inhibition also showed high in vitro and in vivo activity and synergy with anti-PD-1 blocking antibodies129.”
From Human disease models in drug development (2023) · cites this paper as [129]
In the citing paper
“activation of effector T (TEFF) cells upon nuclear factor of activated T cells 1 (NFATC1, best known as NFAT) signaling and interleukin-2 (IL2) secretion (Deng et al., 2018)”
From Immunomodulation by targeted anticancer agents (2021) · cites this paper as Deng et al., 2018
In the citing paper
“CDK4/6 inhibition is also able to stimulate PD-1 expressing T-cells in vitro and enhance T cell infiltration (Deng et al., 2017).”
From CDK4/6 Inhibitors: The Mechanism of Action May Not Be as Simple as Once Thought (2018) · cites this paper as Deng et al., 2017
In the citing paper
“This enhancement is driven at least in part by CDK6-induced phosphorylation of NFAT4.”
From CDK4/6 Inhibitors: The Mechanism of Action May Not Be as Simple as Once Thought (2018) · cites this paper as Deng et al., 2017
In the citing paper
“Combining palbociclib with a PD-1 blockade enhanced tumor regression and improved overall survival in mouse xenograft models of colon adenocarcinoma (Deng et al., 2017; Zhang et al., 2018).”
From CDK4/6 Inhibitors: The Mechanism of Action May Not Be as Simple as Once Thought (2018) · cites this paper as Deng et al., 2017
In the citing paper
“CDK4/6 inhibitors improved the efficacy of α-PD-1 in murine models by enhancing lymphocyte infiltration and TIL activities [245–248].”
From Combination strategies with PD-1/PD-L1 blockade: current advances and future directions (2022) · cites this paper as [248]
In the citing paper
“We also recently demonstrated that CDK6, but not CDK4, phosphorylates NFAT family transcription factors to promote T cell activation and enhance the anti-tumor immune response[7].”
From Development of dual and selective degraders of cyclin-dependent kinases 4 and 6 (2019) · cites this paper as [7]
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Citations
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“As Kras mutant GEMMs are not responsive to checkpoint blockade (3,44), in part due to a low levels of somatic mutations (45), we utilized the murine syngeneic colon adenocarcinoma model MC38.”
BackgroundMethodInfluential
Cited by
Sorted by citations
Items 401–500 of 776
Development of Dual and Selective Degraders of Cyclin‐Dependent Kinases 4 and 6
Jiang, B., Wang, E. S., Donovan, K. A., Liang, Y., Fischer, E. S., Zhang, T., & Gray, N. S. (2019) · Angewandte Chemie · doi:10.1002/ange.201901336 · Cited by 14
Self-citationDevelopment and Strategies of CDK4/6 Inhibitors
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“Combination of CDK4/6 inhibitors and anti-PD-1 antibody showed a synergistic effects on antitumor immunity, which is mediated by enhancement of T cell activation (116).”
BackgroundSelf-citationEmerging Therapies for Breast CancerPreprint
Goel, S., & Chandarlapaty, S. (2022) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a041333 · Cited by 15
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“CDK4/6 inhibition was also shown to be able to block the PDL1 degradation mediated by the proteasome and to enhance PD-1 expressing T cell [72].”
BackgroundTahir, I. M., Rauf, A., Mehboob, H., Sadaf, S., Alam, M. S., Kalsoom, F., Bouyahya, A., Allam, A. E., Omari, N. E., Bakrim, S., et al. (2022) · Human Antibodies · doi:10.3233/hab-220001 · Cited by 12
Emerging target discovery and drug repurposing opportunities in chordoma
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“Notably, CDK4/6 inhibition has been reported to potentiate T cell immunity in several contexts (66, 67), and we discuss opportunities for evaluating CDK4/6 inhibitor combinations in this context further below.”
BackgroundSamnani, S., Sachedina, F., Gupta, M., Guo, E., & Navani, V. (2023) · Cancer Drug Resistance · doi:10.20517/cdr.2023.02 · Cited by 12
PKCα inhibitors promote breast cancer immune evasion by maintaining PD-L1 stability
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“The combination of small-molecule kinase inhibitors with anti-PD-1/PD-L1 antibodies provides attractive therapeutic strategies against many different cancers 38,72,73 .”
Macy, M. E., Mody, R. J., Reid, J. M., Piao, J., Saguilig, L., Alonzo, T. A., Berg, S. L., Fox, E., Weigel, B. J., Hawkins, D. S., et al. (2024) · JCO Precision Oncology · doi:10.1200/po-24-00418 · Cited by 15
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Chronic cutaneous lupus erythematosus (discoid lupus) induced by palbociclib
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“Indeed, treatment with a CDK inhibitor appears to synergize well with checkpoint blockade therapy, as CDK4/6 inhibitors have been shown to significantly enhance T cell activation and augment the response to PD1 blockade in preclinical models of breast and lung cancers [111,112].”
BackgroundMasuda, N., Chen, Y., Kawaguchi, T., Dozono, K., & Toi, M. (2022) · Cancer Management and Research · doi:10.2147/cmar.s348591 · Cited by 14
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“In vivo models confirm enhanced tumor regression when an immune checkpoint blockade with an anti-PD-L1 antibody is added to CDK4/6 inhibition.(24,25) Of interest, researchers are currently recruiting for a multicenter phase II study to evaluate the combination of LET, palbociclib, and pembrolizumab in postmenopausal w…”
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“In both studies, e authors demonstrated that the combination of CDK4/6 nhibitors with immune checkpoint antibodies had a strong r effect that each treatme t alone [107,108].”
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“Both RT and CDK4/6 inhibitors have been recognized for their immunomodulatory effects [43–45], prompting investigations to determine whether their combination can enhance the efficacy of anti-PD-L1 therapy.”
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CDK4/6 inhibition mitigates chemotherapy-induced expansion of TP53-mutant clonal hematopoiesis
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“However, although CDK inhibitors could inflame cold tumors (45), we recommend caution with this strategy because they can stimulate oxidative stress in cancer cells (46, 47) due to glucose, glutamine, and lipid competition with immune cells (48–50) and increase the antioxidant network (51).”
BackgroundImmunotherapy for Liposarcoma: Emerging Opportunities and Challenges
Song, Z., Lu, L., Gao, Z., Zhou, Q., Wang, Z., Sun, L., & Zhou, Y. (2022) · Future Oncology · doi:10.2217/fon-2021-1549 · Cited by 13
Vitiligo-like lesions associated with ribociclib in a woman with metastatic breast cancer
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“23 Vitiligo-like lesions are not a life-threatening side effect.”
Tailoring therapies to counter the divergent immune landscapes of breast cancer
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“Some studies have indicated that CDK4/6 inhibitors exert long-term anti-T-cell immunity and increase immunogenicity, which may provide a rationale for new combination strategies combining CDK4/6 inhibitors and immunotherapies for cancer treatment [28].”
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“Preclinical studies have shown that palbociclib also increases tumor antigen presentation and enhances cytotoxic T-cell activity.(6,7) A similar phenomenon has been described with cyclophosphamide; at low doses, it preferentially depletes T regulatory cells and increases cytotoxic T-cell activity, leading to enhanced…”
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Human Colon Organoids and Other Laboratory Strategies to Enhance Patient Treatment Selection
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Tumor immune organoids in immunotherapy resistance and drug screening
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“Another study also showed enhanced proportions of CD4+ and CD8+ T cells in lung tumors of genetically engineered mice after treatment with palbociclib or trilaciclib (Deng et al., 2018).”
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“An additional investigation confirmed the exceptional anti-cancer effectiveness of combination treatment using CDK4/6 inhibitors and anti-PDL1 antibody (Deng et al., 2018).”
BackgroundLenz, H., Liu, T., Chen, E. Y.-S., Horváth, Z., Bondarenko, I., Danielewicz, I., Ghidini, M., Alfonso, P. G., Jones, R., Aapro, M., et al. (2024) · JNCI Cancer Spectrum · doi:10.1093/jncics/pkae116 · Cited by 10
“22,23 Although the “immune-cold” nature of pMMR/MSS mCRC tumors could explain a lack of antitumor efficacy in this patient population, 24 it does not account for the low antitumor response rates observed in this study.”
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“Notably, CDK4/6 inhibitors can modulate the tumor immune microenvironment favorably through direct effects on T cells, including suppression of regulatory T cells (33, 34), direct stimulation of cytotoxic T-cell activity (35), and induction of T-cell memory (36, 37).”
Cutting‐Edge Therapy and Immune Escape Mechanisms in EBV‐Associated Tumors
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Patient-Derived In Vitro and In Vivo Models of Cancer
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“…of CDK4/6 has been shown to favour the elimination of tumour cells by the adaptive immune system through various mechanisms including enhanced antigen presentation by cancer cells, increased infiltration and activation of T cells; and inhibition of regulatory T cells proliferation [29,30,128 – 130].”
BackgroundTargeting protein tyrosine phosphatases for CDK6-induced immunotherapy resistance
Gao, X., Wu, Y., Chick, J. M., Abbott, A., Jiang, B., Wang, J., Comte‐Walters, S., Johnson, R. H., Oberholtzer, N. P., Nishimura, M. I., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.112314 · Cited by 11
“…inhibitors showed that targeting CDK4/6 suppresses CD4 + FOXP3 + regulatory T cell proliferation and numbers to promote effector T cell activity, 67 increases T cell activity by suppressing the NFAT protein family and enhances T cell tumor infiltration, 68 and promotes CD8 T cell memory formation.”
Pita, J. M. G., Raspé, E., Coulonval, K., Decaussin‐Petrucci, M., Tarabichi, M., Dom, G., Libert, F., Craciun, L., Andry, G., Wicquart, L., et al. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1247542 · Cited by 12
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“Taken together with previous studies, this inhibition rate was not low in the mouse model [11, 18].”
Pyo, D. H., Hong, H. K., Lee, W. Y., & Cho, Y. B. (2020) · Cancer Biology & Therapy · doi:10.1080/15384047.2020.1738907 · Cited by 13
“Deng and colleagues have used the OTS model in support of beneficial effects of CDK4/6 inhibition on tumor immunity.(64) The authors were able to reveal that CDK4/6 inhibition in combination with an anti-PD-1 antibody could increase tumor cell deaths and reduce chemokines.”
MethodEnhancing Adoptive Cell Transfer with Combination BRAF-MEK and CDK4/6 Inhibitors in Melanoma
Lau, P. K. H., Cullinane, C. M., Jackson, S., Walker, R., Smith, L. K., Slater, A. A., Kirby, L., Patel, R. P., von Scheidt, B., Slaney, C. Y., et al. (2021) · Cancers · doi:10.3390/cancers13246342 · Cited by 10
“Palbociclib treatment is associated with upregulation of nuclear factor of activated T-cells (NFAT) in Jurkat cells with subsequent higher IL-2 and GM-CSF production [18].”
BackgroundAssociating Immunotherapy and Targeted Therapies: Facts and Hopes
Ladoire, S., Rébé, C., & Ghiringhelli, F. (2022) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-22-1184 · Cited by 10
Evaluation of PD-1 blockade using a multicellular tumor spheroid model.
Zhou, S., Zhu, M., Meng, F., Shao, J., Xu, Q., Wei, J., & Liu, B. (2019) · Europe PMC (PubMed Central) · Cited by 10
ESCO2’s oncogenic role in human tumors: a pan-cancer analysis and experimental validation
Huang, Y., Chen, D., Bai, Y., Zhang, Y., Zheng, Z., Fu, Q., Yi, B., Jiang, Y., Zhang, Z., & Zhu, J. (2024) · BMC Cancer · doi:10.1186/s12885-024-12213-w · Cited by 10
“Meanwhile, CDK4/6 inhibitors substantially reduce the proliferation of regulatory T cells and encourage cytotoxic T cells to eliminate tumor cells [33].”
BackgroundSelf-citationDemirsoy, Ş., Tran, H., Liu, J. N., Li, Y., Yang, S., Aregawi, D. G., Glantz, M. J., Jacob, N. K., Walter, V., Schell, T. D., et al. (2024) · Cancers · doi:10.3390/cancers16122253 · Cited by 9
“Recent studies suggest that CDK4/6 inhibition stimulates the anti-tumor immune response [28,29].”
BackgroundThe role of targeting CDK4/6 in cancer immunotherapy
Sun, M., Dong, L., Wang, Y., Liu, C., Du, J., Wang, B., Xing, B., Yao, X., Ren, Y. Y., & Zhou, X. (2024) · Holistic Integrative Oncology · doi:10.1007/s44178-024-00100-0 · Cited by 9
“Finally, inhibition of CDK6 results in high activation of NFAT4 signaling in relation to IL-2 secretion and upregulation of activation markers of T-cells, such as 4-1BB (Tnfrsf9), Icosl, GITR (Tnfrsf18), CD40, and CD86 [59].”
A patent review of small molecule CDK4/6 inhibitors in the treatment of cancer: 2020–present
Huang, X., Xu, S., Duan, L., Xu, S., & Zhu, W. (2024) · Expert Opinion on Therapeutic Patents · doi:10.1080/13543776.2024.2379926 · Cited by 9
“PD-1 serves as an immune checkpoint in immunotherapy, and anti-PD-1 or PD-L1 antibodies has played a very good role in the treatment of many cancers [101,102].”
Lizana‐Vasquez, G. D., Ramasubramanian, S., Davarzani, A., Cappabianca, D., Saha, K., Karumbaiah, L., & Torres‐Lugo, M. (2024) · Journal of Biomedical Materials Research Part A · doi:10.1002/jbm.a.37823 · Cited by 11
Research progress in bifunctional small molecules for cancer immunotherapy
Cheng, B., Li, H., Hong, Y., Zhou, Y., Chen, J., Shao, C., & Kong, Z. (2025) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2025.117289 · Cited by 9
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Unraveling the regulatory role of endoplasmic-reticulum-associated degradation in tumor immunity
Qin, X., Denton, W. D., Huiting, L. N., Smith, K. S., & Feng, H. (2020) · Critical Reviews in Biochemistry and Molecular Biology · doi:10.1080/10409238.2020.1784085 · Cited by 9
“Abemaciclib enhances antigen presentation in tumor cells and suppresses Treg functions, while palbociclib activates effector T cells (Goel et al. 2017; Deng et al. 2018; Schaer et al. 2018).”
BackgroundLi, W., Wang, D., Yue, R., Chen, X., Liu, A.-X., Xu, H., Teng, P., Wang, Z., Zou, Y. F., Xu, X., et al. (2021) · The Journal of Heart and Lung Transplantation · doi:10.1016/j.healun.2021.08.008 · Cited by 9
Zhao, Y., Xu, B., Wang, F., Jiang, F., Xu, J., & Yu, D. (2022) · Cancer Medicine · doi:10.1002/cam4.5260 · Cited by 9
Tian, Y., Zhou, J., Qiao, J., Liu, Z., Gu, L., Zhang, B., Lu, Y., Xing, R., & Deng, D. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.1038380 · Cited by 9
CDK4/6i enhances the antitumor effect of PD1 antibody by promoting TLS formation in ovarian cancer
Feng, W., Jiang, D., Xu, Y., Li, Y., Chen, L., Zhao, M., Shen, Y., Liao, W., Yang, H., & Li, J. (2023) · Heliyon · doi:10.1016/j.heliyon.2023.e19760 · Cited by 9
Lao, C., Moon, J., Ma, V. T.-L., Fruehauf, J. P., Flaherty, L. E., Bury, M. J., Martin, W. G., Gross, H. M., Akerley, W., Hopkins, J. O., et al. (2024) · Cancer · doi:10.1002/cncr.35587 · Cited by 9
[Research Progress of CDK4/6 Inhibitors in Non-small Cell Lung Cancer].
Qin, Q., Ren, Y., & Zhong, D. (2020) · PubMed Central · doi:10.3779/j.issn.1009-3419.2020.03.07 · Cited by 9
The antiviral immune forces awaken in the cancer wars
Pyeon, D., Vu, L., Giacobbi, N. S., & Westrich, J. A. (2020) · PLoS Pathogens · doi:10.1371/journal.ppat.1008814 · Cited by 9
Zhu, W., & Jin, X. (2021) · Annals of Palliative Medicine · doi:10.21037/apm-21-2062 · Cited by 8
“In addition, CDK4/6i inhibited T cell proliferation, but enhanced the activation of effective T cells, and in part modulated NFAT family proteins and their target genes (24).”
BackgroundConstruction of a ceRNA network in glioma and analysis of its clinical significance
Liu, G., Li, H., Ji, W., Gong, H., Jiang, Y., Ji, G., & Liu, G. (2021) · BMC Genomics · doi:10.1186/s12864-021-08035-w · Cited by 9
Oualla, K., Kassem, L. M. H., Nouiakh, L., Amaadour, L., Benbrahim, Z., Arifi, S., & Mellas, N. (2020) · International Journal of Breast Cancer · doi:10.1155/2020/8209173 · Cited by 8
“effector T lymphocytes and reduction of proliferation of immunosuppressive Treg cells [46, 47].”
BackgroundTan, A. R., O’Shaughnessy, J., Cao, S., Ahn, S., & Yi, J. S. (2023) · Breast Cancer Research and Treatment · doi:10.1007/s10549-023-07009-8 · Cited by 8
“Specifically, trilaciclib has been shown to enhance T-cell activation and the production of cytokines and chemokines [15, 20], to promote a favorable tumor immune microenvironment by increasing the intratumoral ratio of effector T cells to regulatory T cells (Tregs) and the number of activated T cells in the periphery…”
BackgroundInfluentialAlbert, V., Bruß, C., Tümen, D., Piendl, G., Weber, F., Dahl, E., Seitz, S., Ortmann, O., Wege, A. K., & Brockhoff, G. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25137475 · Cited by 9
“Notably, other researchers who used mouse BC models also reported a reduced expression of checkpoint molecules on immune cells upon CDK4/6 inhibitor therapy [66,67]; however, they associated this finding with less T cell exhaustion.”
BackgroundTorrisi, R., Gerosa, R., Miggiano, C., Saltalamacchia, G., Benvenuti, C., & Santoro, A. (2025) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2025.104634 · Cited by 8
Deciphering Breast Tumor Heterogeneity Through Patient-Derived Organoids and Circulating Tumor Cells
Policastro, B., Nissen, N., & Alves, C. L. (2025) · Journal of Personalized Medicine · doi:10.3390/jpm15070271 · Cited by 8
“…cells, retaining both the heterogeneity of cell populations, such as cancer-associated fibroblasts (CAFs), cytotoxic T lymphocytes (CTLs), T-helper cells, tumor-associated macrophages (TAMs), NK cells, and B cells and the tumor architecture and spatial arrangement of its components [42,43,60].”
Organoid: a promising solution to current challenges in cancer immunotherapy
Kang, X., Cheemalamarri, S. K., & Yin, Q. (2025) · npj Biomedical Innovations. · doi:10.1038/s44385-025-00051-9 · Cited by 9
“PDOs derived from NSCLC patients showed that combined inhibition of CDK4/6 enhances ICB response by promoting T cell activation 183 .”
About Face: Molecular Aberrations in Head and Neck Mucosal Melanomas
Shoushtari, A. N. (2019) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-0658 · Cited by 8
“Recent work also links CDK4 expression with reduced effector function of tumor-infiltrating CD8þ T cells exposed to PD-1, which is ameliorated by short-term CDK4 inhibition in murine models of non–small cell lung cancer (5).”
BackgroundBeddok, A., Mouren, V., Cottu, P. H., Laki, F., Fourquet, A., & Kirova, Y. (2023) · International Journal of Cancer · doi:10.1002/ijc.34562 · Cited by 8
“In addition, preclinical research has shown that CDK4/6i can induce antitumor immune responses due to interferon production, reduction of Treg proliferation and stimulation of effector T cells, which enhances the effect of immune checkpoint inhibitors.(39,40) These effects may provide a rationale for developing new co…”
BackgroundPawar, V. A., Tyagi, A., Verma, C., Sharma, K. P., Ansari, S., Mani, I., Srivastva, S. K., Shukla, P. K., Kumar, A., & Kumar, V. (2023) · PubMed Central · Cited by 8
Wang, Y., Chen, J., Gao, Y., Chai, K. X. Y., Hong, J. H., Wang, P., Chen, J., Yu, Z., Liu, L., Huang, C., et al. (2024) · Cancer Letters · doi:10.1016/j.canlet.2024.217080 · Cited by 8
CDK4/6 inhibitors as neoadjuvant treatment in breast cancer—what can we learn?
Brandão, M., & Ignatiadis, M. (2018) · Annals of Oncology · doi:10.1093/annonc/mdy456 · Cited by 8
Parkin, A., Man, J., Chou, A. S. Y., Nagrial, A. M., Samra, J. S., Gill, A. J., Timpson, P., & Pajic, M. (2018) · Diseases · doi:10.3390/diseases6040103 · Cited by 8
“Moreover, recent studies in PDAC and other cancers, suggest a considerably more complex mechanism of action for CDK4/6 inhibitors that includes multifaceted global inhibitory effects on tumour cells, stromal cells and extracellular matrix (ECM) organisation at different stages of PDAC progression [78], inhibition of e…”
BackgroundSmall Molecular Immune Modulators as Anticancer Agents
Han, Y., Zhu, L., Wu, W., Zhang, H., Hu, W., Dai, L., & Yang, Y. (2020) · Advances in experimental medicine and biology · doi:10.1007/978-981-15-3266-5_22 · Cited by 8
Self-citationAn overview of immune checkpoint inhibitors in breast cancer
Miglietta, F., Cona, M. S., Dieci, M. V., Guarneri, V., & Verde, N. M. L. (2020) · Exploration of Targeted Anti-tumor Therapy · doi:10.37349/etat.2020.00029 · Cited by 8
“Preclinical evidence suggests that CDK 4/6 blockade may boost anti-tumor immune response by enhancing tumor antigen presentation (mediated by the activation of tumor cell expression of endogenous retroviral elements) as well as suppressing regulatory T-cell proliferation [57, 58].”
BackgroundZhu, M., Wang, H., Zhou, S., Wei, J., Ding, N., Shao, J., Yu, L., Feng, Z., & Liu, B. (2021) · OncoTargets and Therapy · doi:10.2147/ott.s291086 · Cited by 8
Reddy, S., Barkhane, Z., Elmadi, J., Kumar, L. S., Pugalenthi, L. S., & Ahmad, M. (2022) · Cureus · doi:10.7759/cureus.23901 · Cited by 8
Guo, X., Chen, H., Zhou, Y., Shen, L., Wu, S., & Chen, Y. (2022) · Expert Opinion on Investigational Drugs · doi:10.1080/13543784.2022.2097067 · Cited by 7
“by cell-cycle arrest in abemaciclib-sensitive cells and is characterized by recruitment of immune cells and promotion of the secretion of pro-inflammatory cytokines such as IL-1, IL-6, and IL-8 (Figure 2) [7,117,118].”
BackgroundZhang, T., Zhang, C., Fu, Z., & Gao, Q. (2022) · Pharmaceutics · doi:10.3390/pharmaceutics14091768 · Cited by 8
“The immunostimulatory activity of CDK4/6 inhibition can be achieved by interacting with T cells via the depression of the nuclear factor of the activated T cell (NFATC) family [18].”
BackgroundTrilaciclib: A First-in-class Therapy to Reduce Chemotherapy-induced Myelosuppression
Young, J. A., & Tan, A. R. (2022) · touchREVIEWS in Oncology & Haematology · doi:10.17925/ohr.2022.18.2.152 · Cited by 8
“Trilaciclib has been shown to enhance antitumour immune response through the direct stimulation of T-cell and suppression of regulatory T-cell growth.(52,53) When given before chemotherapy infusions, trilaciclib may prevent chemotherapy-induced T-cell apoptosis and bone marrow myeloid skewing and preserve intratumoura…”
BackgroundWang, H., Yu, M., Yang, C., & Li, Q. (2023) · Journal of Cancer · doi:10.7150/jca.84579 · Cited by 7
“Deng et al. suggested that CDK4/6 enhanced T cell activation and augmented antitumor immunity in lymphoma [49].”
BackgroundFraire, C. R., Desai, K. K., Jagadeeswaran, I., Obalapuram, U. A., Mendyka, L. K., Rajaram, V., Sebastian, T., Wang, Y., Onel, K., Lee, J., et al. (2025) · Genes & Development · doi:10.1101/gad.352485.124 · Cited by 8
“S10D; Goel et al. 2017; Deng et al. 2018; Schaer et al. 2018; Zhang et al. 2018).”
ROS, Redox Regulation, and Anticancer Therapy
Bansal, M. P. (2023) · Springer eBooks · doi:10.1007/978-981-99-7342-2_9 · Cited by 7
Tzetzo, S. L., Schultz, E., Wang, J., Rosenheck, H. R., Mahan, S., Knudsen, E. S., & Witkiewicz, A. K. (2025) · npj Breast Cancer · doi:10.1038/s41523-025-00767-2 · Cited by 7
“CD8 + T cells are instrumental for antitumor activity and evidence demonstrates that CDK4/6i-based therapy may activate CD8 + T cells while reducing immunosuppressive Tregs 15,16,19 .”
Novel Therapeutic Development for Nasopharyngeal Carcinoma
Kim, J., Lee, Y., Kim, S., & Park, J. C. (2025) · Current Oncology · doi:10.3390/curroncol32090479 · Cited by 7
“Other Targets CDK4/6 inhibitors, such as dalpiciclib, not only suppress tumor proliferation through G1-phase arrest but also enhance tumor immunogenicity by upregulating MHC class I and interferon signaling, supporting their use in combination with immunotherapy [96].”
Organoid-based precision cancer modeling: New frontier in lung cancer research
Terai, H., Yasuda, H., & Sato, T. (2025) · Cell Reports · doi:10.1016/j.celrep.2025.116595 · Cited by 9
Scordamaglia, D., Talia, M., Zicarelli, A., Mondino, A. A., Rosis, S. D., Dio, M. D., Silvestri, F., Meliti, C., Cirillo, F., Francesco, E. M. D., et al. (2025) · Cancer and Metastasis Reviews · doi:10.1007/s10555-025-10307-w · Cited by 9
“…nd ac ti v a ti on v i a t h e S T I N G p a t h w a y [ 129 ] N F A T - d e p e nd e n t C D 8 ⁺ T ce ll r ec r u it m e n t a nd ac ti v a ti on [ 134 ] C D 8 ⁺ T a nd NK ce ll r ec r u it m e n t a nd ac ti v a ti on v i a t h e c GA S / S T I NG s i gn a lli ng [ 38 ] M xd4 / M y c - d e p e…”
The evolving landscape of CDK inhibitor use in breast cancer therapy and beyond
Knudsen, E. S., Witkiewicz, A. K., & Kabraji, S. K. (2026) · Nature Reviews Drug Discovery · doi:10.1038/s41573-026-01431-5 · Cited by 8
“CDK4/6 inhibitors singly and in combination with other therapies can stimulate an interferon-like response or senescence-associated secretory phenotype that is accompanied by the upregulation of genes that are associated with response to immune checkpoint inhibitors 43–45 .”
Song, F., Lu, Y.-J., Sun, H., Cheng, J.-W., Li, W., Liu, Z., Li, R., Wang, P.-X., Zheng, W.-J., Zhong, Y.-C., et al. (2026) · Journal for ImmunoTherapy of Cancer · doi:10.1136/jitc-2025-014555 · Cited by 7
Metadata
- Authors
- Deng, J., Wang, E. S., Jenkins, R. W., Li, S., Dries, R., Yates, K., Chhabra, S., Huang, W., Liu, H., Aref, A. R., Ivanova, E., Paweletz, C. P., Bowden, M., Zhou, C. W., Herter-Sprie, G. S., Sorrentino, J. A., Bisi, J. E., Lizotte, P. H., Merlino, A. A., Quinn, M. M., Bufe, L. E., Yang, A., Zhang, Y., Zhang, H., Gao, P., Chen, T., Cavanaugh, M. E., Rode, A. J., Haines, E., Roberts, P. J., Strum, J. C., Richards, W. G., Lorch, J. H., Parangi, S., Gunda, V., Boland, G. M., Bueno, R., Palakurthi, S., Freeman, G. J., Ritz, J., Haining, W. N., Sharpless, N. E., Arthanari, H., Shapiro, G. I., Barbie, D. A., Gray, N. S., & Wong, K.-K.
- Affiliations
- NYU Langone Health (US)
- Harvard University (US)
- Dana-Farber Cancer Institute (US)
- 9G1 Therapeutics, Research Triangle Park, North Carolina.
- Brigham and Women's Hospital (US)
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Barbie, David A.
- Gray, Nathanael S.
- Wong, Kwok-Kin
- ORCID
- Deng, Jiehui
- Wang, Eric S.
- Jenkins, Russell W.
- Li, Shuai
- Dries, Ruben
- Yates, Kathleen
- Chhabra, Sandeep
- Huang, Wei
- Liu, Hongye
- Aref, Amir R.
- Ivanova, Elena
- Paweletz, Cloud P.
- Bowden, Michaela
- Zhou, Chensheng W.
- Herter-Sprie, Grit S.
- Sorrentino, Jessica A.
- Bisi, John E.
- Lizotte, Patrick H.
- Yang, Annan
- Zhang, Hua
- Gao, Peng
- Chen, Ting
- Haines, Eric
- Roberts, Patrick J.
- Strum, Jay C.
- Richards, William G.
- Lorch, Jochen H.
- Parangi, Sareh
- Boland, Genevieve M.
- Bueno, Raphael
- Palakurthi, Sangeetha
- Freeman, Gordon J.
- Ritz, Jerome
- Haining, W. Nicholas
- Sharpless, Norman E.
- Arthanari, Haribabu
- Shapiro, Geoffrey I.
- Barbie, David A.
- Gray, Nathanael S.
- Wong, Kwok-Kin
- Venue
- Cancer Discovery
- Published
- 2018-02-01
- Volume
- 8
- Issue
- 2
- Pages
- 216-233
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC5809273
- OpenAlex
- W2766016994
- Cited by
- 770
- References
- 63
- Citations by year
- 2026: 62 · 2025: 111 · 2024: 83 · 2023: 109 · 2022: 115 · 2021: 104 · 2020: 96 · 2019: 61 · 2018: 29
- FWCI
- 22.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Damon Runyon Cancer Research Foundation (Damon Runyon) (DRG-2270-16)
- HHS | NIH | National Cancer Institute (NCI) (CA154303-05, CA179483-03, P01CA120964, 5R01CA163896-04, 5R01CA140594-07, 5R01CA122794-10, 5R01CA166480-04)
- Dana-Farber Cancer Institute (DFCI) (Medical Oncology Discovery Grant)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- CDK4/6 inhibitors, antitumor immunity, T cell activation, anti-PD-1 therapy, immune checkpoint blockade, combination immunotherapy, tumor-infiltrating T cells, small-molecule immunomodulators
- MeSH terms
- Antineoplastic Agents, Immunological, Animals, Antineoplastic Agents, Humans, Lymphocyte Activation, Neoplasms, T-Lymphocytes, Lymphocytes, Tumor-Infiltrating, Xenograft Model Antitumor Assays, Cell Line, Tumor, Protein Kinase Inhibitors, Cyclin-Dependent Kinase 4, Cyclin-Dependent Kinase 6, Mice
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