Table 5 Several types of synthetic chemotherapeutic agents inducing ICD

Alkylating agents

Cyclophosphamide

↑ Type-I interferons,

Stimulating T and NK cell expansion, IL-17, and Th17 cells production

[174,175,176,177]

Oxaliplatin

↑ ER stress and CRT exposure, activate cytotoxic T lymphocytes

[58, 178]

Melphalan

HSP90 exposure

IL-1β, IL-8, and IL-6 production, DCs activation and maturation

[179]

Antimetabolites

Gemcitabine

↓ Tumor growth by ICD induction with hypoxia-inducible factor-1 (HIF-1) inhibitor PX-478 combination

[180]

5-fluorouracil (5-FU)

HMGB1 and ATP release, ↑ CRT, recruiting DCs, production of IL-1

[18, 181, 182]

trifluridine/tipiracil

CRT exposure, HMGB1 and ATP release, A synergistic effect in ICD was achieved by combining trifluridine/tipiracil with OXP.

[183]

Anthracyclines

doxorubicin

Induced apoptosis in a caspase-dependent manner in many cancers cell line

[144]

mitoxantrone

Promoting CRT exposure in colorectal cancer cells, induces autophagy by releasing HMGB1 and ATP in pancreatic and breast cancer cells

[184]

Daunorubicin

Induced CRT surface expression and release of HSP70/HSP90 and IFN in AML treatment.

[63]

idarubicin (IDA)

HMGB1, HSP70/90, and CRT exposure were detected in response to IDA treatment in several cancer cell lines.

[13]

Bleomycin

Translocation of CRT or ERp57. HMGB1 and ATP were released from dying cancer cells as a result of bleomycin-induced autophagy

[185]

Microtubular inhibitors

paclitaxel

CRT expression in ovarian tumors

[186]

docetaxel (on its own does not appear to be a particularly effective ICD inducer)

NSCLC cell lines exhibited the greatest levels of ATP, CRT, and HMGB1 when was combined with carboplatin or cisplatin.

↑ CTLs and ↓ Tregs in patients with breast cancer and NSCLC treated with Co-administration of vinorelbine and cisplatin with docetaxel

[187]

Other chemo-therapeutics

bortezomib

Appearance of HSP90 on tumor cells

[188]

crizotinib

High-dose could induce ICD in cancer cells

[189]

Other drugs

colchicine

HSP70, HSP90, and HMGB1, without affecting the expression of CRT

[107]

Cetuximab (combined with FOLFIRI)

Letting DCs phagocytose tumor-dying cells and triggering an immune response by CD8 + T cells.

Panitumumab or cetuximab alone induces ICD in DiFi cells

[190]