Mixed Response to Cancer Immunotherapy is Driven by Intratumor Heterogeneity and Differential Interlesion Immune Infiltration

Takao Morinaga(Chiba Cancer Center), Takashi Inozume(Chiba University), Masahito Kawazu(Chiba Cancer Center), Youki Ueda(Okayama University), Nicolas Sax(Raptamer Discovery Group (United States)), Kazuo Yamashita(Raptamer Discovery Group (United States)), Shusuke Kawashima(Chiba University), Joji Nagasaki(Okayama University), Toshihide Ueno(National Cancer Research Institute), Jason Lin(Chiba Cancer Center), Yuuki Ohara(National Cancer Center Hospital East), Takeshi Kuwata(National Cancer Center Hospital East), Hiroki Yukami(National Cancer Center Hospital East), Akihito Kawazoe(National Cancer Center Hospital East), Kohei Shitara(National Cancer Center Hospital East), Akiko Honobe‐Tabuchi(University of Yamanashi), Takehiro Ohnuma(University of Yamanashi), Tatsuyoshi Kawamura(University of Yamanashi), Yoshiyasu Umeda(Saitama International Medical Center), Yu Kawahara(Saitama International Medical Center), Yasuhiro Nakamura(Saitama International Medical Center), Yukiko Kiniwa(Shinshu University), Ayako Morita(Okayama University Hospital), Eiki Ichihara(Okayama University Hospital), Katsuyuki Kiura(Okayama University Hospital), Tomohiro Enokida(National Cancer Center Hospital East), Makoto Tahara(National Cancer Center Hospital East), Yoshinori Hasegawa(Kazusa DNA Research Institute), Hiroyuki Mano(National Cancer Research Institute), Yutaka Suzuki(Chiba University), Hiroyoshi Nishikawa(National Cancer Research Institute), Yosuke Togashi(Okayama University)
Cancer Research Communications
July 11, 2022
Cited by 17Open Access
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Abstract

Some patients experience mixed response to immunotherapy, whose biological mechanisms and clinical impact have been obscure. We obtained two tumor samples from lymph node (LN) metastatic lesions in a same patient. Whole exome sequencing for the both tumors and single-cell sequencing for the both tumor-infiltrating lymphocytes (TIL) demonstrated a significant difference in tumor clonality and TILs’ characteristics, especially exhausted T-cell clonotypes, although a close relationship between the tumor cell and T-cell clones were observed as a response of an overlapped exhausted T-cell clone to an overlapped neoantigen. To mimic the clinical setting, we generated a mouse model of several clones from a same tumor cell line. Similarly, differential tumor clones harbored distinct TILs, and one responded to programmed cell death protein 1 (PD-1) blockade but the other did not in this model. We further conducted cohort study (n = 503) treated with PD-1 blockade monotherapies to investigate the outcome of mixed response. Patients with mixed responses to PD-1 blockade had a poor prognosis in our cohort. Particularly, there were significant differences in both tumor and T-cell clones between the primary and LN lesions in a patient who experienced tumor response to anti–PD-1 mAb followed by disease progression in only LN metastasis. Our results underscore that intertumoral heterogeneity alters characteristics of TILs even in the same patient, leading to mixed response to immunotherapy and significant difference in the outcome. Significance: Several patients experience mixed responses to immunotherapies, but the biological mechanisms and clinical significance remain unclear. Our results from clinical and mouse studies underscore that intertumoral heterogeneity alters characteristics of TILs even in the same patient, leading to mixed response to immunotherapy and significant difference in the outcome.


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