TY - JOUR
T1 - Rethinking the chemokine cascade in brain metastasis
T2 - Preventive and therapeutic implications
AU - Maurya, Shailendra Kumar
AU - Khan, Parvez
AU - Rehman, Asad Ur
AU - Kanchan, Ranjana K.
AU - Perumal, Naveenkumar
AU - Mahapatra, Sidharth
AU - Chand, Hitendra S.
AU - Santamaria-Barria, Juan A.
AU - Batra, Surinder K.
AU - Nasser, Mohd Wasim
N1 - Publisher Copyright:
© 2021 Elsevier Ltd
PY - 2022/11
Y1 - 2022/11
N2 - Brain metastasis (BrM) is one of the major causes of death in cancer patients and is associated with an estimated 10–40 % of total cancer cases. The survival rate of brain metastatic patients has not improved due to intratumor heterogeneity, the survival adaptations of brain homing metastatic cells, and the lack of understanding of underlying molecular mechanisms that limit the availability of effective therapies. The heterogeneous population of immune cells and tumor-initiating cells or cancer stem cells in the tumor microenvironment (TME) release various factors, such as chemokines that upon binding to their cognate receptors enhance tumor growth at primary sites and help tumor cells metastasize to the brain. Furthermore, brain metastatic sites have unique heterogeneous microenvironment that fuels cancer cells in establishing BrM. This review explores the crosstalk of chemokines with the heterogeneous TME during the progression of BrM and recognizes potential therapeutic approaches. We also discuss and summarize different targeted, immunotherapeutic, chemotherapeutic, and combinatorial strategies (with chemo-/immune- or targeted-therapies) to attenuate chemokines mediated BrM.
AB - Brain metastasis (BrM) is one of the major causes of death in cancer patients and is associated with an estimated 10–40 % of total cancer cases. The survival rate of brain metastatic patients has not improved due to intratumor heterogeneity, the survival adaptations of brain homing metastatic cells, and the lack of understanding of underlying molecular mechanisms that limit the availability of effective therapies. The heterogeneous population of immune cells and tumor-initiating cells or cancer stem cells in the tumor microenvironment (TME) release various factors, such as chemokines that upon binding to their cognate receptors enhance tumor growth at primary sites and help tumor cells metastasize to the brain. Furthermore, brain metastatic sites have unique heterogeneous microenvironment that fuels cancer cells in establishing BrM. This review explores the crosstalk of chemokines with the heterogeneous TME during the progression of BrM and recognizes potential therapeutic approaches. We also discuss and summarize different targeted, immunotherapeutic, chemotherapeutic, and combinatorial strategies (with chemo-/immune- or targeted-therapies) to attenuate chemokines mediated BrM.
KW - Brain metastasis
KW - Brain microenvironment
KW - Chemokines
KW - Heterogeneity
KW - Immune cells
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U2 - 10.1016/j.semcancer.2021.12.009
DO - 10.1016/j.semcancer.2021.12.009
M3 - Review article
C2 - 34968667
AN - SCOPUS:85122142123
SN - 1044-579X
VL - 86
SP - 914
EP - 930
JO - Seminars in Cancer Biology
JF - Seminars in Cancer Biology
ER -