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Signaling network response to alpha-particle targeted therapy with actinium-225 labeled minigastrin analogue 225Ac-PP-F11N

ABSTRACT: Alpha-particle emitters have recently been explored as valuable therapeutic radionuclides. Yet, toxicity to healthy organs and cancer radioresistance limit the efficacy of targeted alpha-particle therapy (TAT). Identification of the radiation-activated mechanisms, which drive cancer cell survival, provides opportunities to develop new points for therapeutic interference to improve the efficacy and safety of TAT. Quantitative phosphoproteomics and matching proteomics followed were employed to identify alterations in the signaling networks in response to TAT with actinium-225 labeled minigastrin analogue 225Ac-PP-F11N in A431 cells, which overexpress cholecystokinin B receptor (CCKBR).

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Skin Epidermis, Cell Culture

DISEASE(S): Cancer

SUBMITTER: Michal Grzmil

LAB HEAD: Michal Grzmil

PROVIDER: PXD039033 | Pride | 2023-06-02

REPOSITORIES: Pride

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			Action	DRS
	20190618_002_S198794_Ac_2_enriched.raw	Raw
	20190618_003_S198792_C_3_enriched.raw	Raw
	20190618_004_S198795_Ac_3_enriched.raw	Raw
	20190618_005_S198791_C_2_enriched.raw	Raw
	20190618_007_S198793_Ac_1_enriched.raw	Raw

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