Macrophage-tumor cell interaction promotes ATRT progression and chemoresistance
Standard
Macrophage-tumor cell interaction promotes ATRT progression and chemoresistance. / Melcher, Viktoria; Graf, Monika; Interlandi, Marta; Moreno, Natalia; de Faria, Flavia W; Kim, Su Na; Kastrati, Dennis; Korbanka, Sonja; Alfert, Amelie; Gerß, Joachim; Meyer Zu Hörste, Gerd; Hartmann, Wolfgang; Frühwald, Michael C; Dugas, Martin; Schüller, Ulrich; Hasselblatt, Martin; Albert, Thomas K; Kerl, Kornelius.
In: ACTA NEUROPATHOL, Vol. 139, No. 5, 05.2020, p. 913-936.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Macrophage-tumor cell interaction promotes ATRT progression and chemoresistance
AU - Melcher, Viktoria
AU - Graf, Monika
AU - Interlandi, Marta
AU - Moreno, Natalia
AU - de Faria, Flavia W
AU - Kim, Su Na
AU - Kastrati, Dennis
AU - Korbanka, Sonja
AU - Alfert, Amelie
AU - Gerß, Joachim
AU - Meyer Zu Hörste, Gerd
AU - Hartmann, Wolfgang
AU - Frühwald, Michael C
AU - Dugas, Martin
AU - Schüller, Ulrich
AU - Hasselblatt, Martin
AU - Albert, Thomas K
AU - Kerl, Kornelius
PY - 2020/5
Y1 - 2020/5
N2 - Atypical teratoid/rhabdoid tumors (ATRT) are known for their heterogeneity concerning pathophysiology and outcome. However, predictive factors within distinct subgroups still need to be uncovered. Using multiplex immunofluorescent staining and single-cell RNA sequencing we unraveled distinct compositions of the immunological tumor microenvironment (TME) across ATRT subgroups. CD68+ cells predominantly infiltrate ATRT-SHH and ATRT-MYC and are a negative prognostic factor for patients' survival. Within the murine ATRT-MYC and ATRT-SHH TME, Cd68+ macrophages are core to intercellular communication with tumor cells. In ATRT-MYC distinct tumor cell phenotypes express macrophage marker genes. These cells are involved in the acquisition of chemotherapy resistance in our relapse xenograft mouse model. In conclusion, the tumor cell-macrophage interaction contributes to ATRT-MYC heterogeneity and potentially to tumor recurrence.
AB - Atypical teratoid/rhabdoid tumors (ATRT) are known for their heterogeneity concerning pathophysiology and outcome. However, predictive factors within distinct subgroups still need to be uncovered. Using multiplex immunofluorescent staining and single-cell RNA sequencing we unraveled distinct compositions of the immunological tumor microenvironment (TME) across ATRT subgroups. CD68+ cells predominantly infiltrate ATRT-SHH and ATRT-MYC and are a negative prognostic factor for patients' survival. Within the murine ATRT-MYC and ATRT-SHH TME, Cd68+ macrophages are core to intercellular communication with tumor cells. In ATRT-MYC distinct tumor cell phenotypes express macrophage marker genes. These cells are involved in the acquisition of chemotherapy resistance in our relapse xenograft mouse model. In conclusion, the tumor cell-macrophage interaction contributes to ATRT-MYC heterogeneity and potentially to tumor recurrence.
U2 - 10.1007/s00401-019-02116-7
DO - 10.1007/s00401-019-02116-7
M3 - SCORING: Journal article
C2 - 31848709
VL - 139
SP - 913
EP - 936
JO - ACTA NEUROPATHOL
JF - ACTA NEUROPATHOL
SN - 0001-6322
IS - 5
ER -