4.6 Review

Sensitive Photodynamic Detection of Adult T-cell Leukemia/Lymphoma and Specific Leukemic Cell Death Induced by Photodynamic Therapy: Current Status in Hematopoietic Malignancies

Journal

CANCERS
Volume 12, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/cancers12020335

Keywords

ATL; HTLV-1; PDT; PDD; chemotherapy; allogeneic hematopoietic cell transplantation; immunotherapy; GVHD; ALA-PDT/PDD

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Funding

  1. Japan Society for the Promotion of Science (JSPS) [22590312, 25460437]
  2. Japan Agency for Medical Research and Development (AMED) (A.U.) [19ck0106254h0003]
  3. Grants-in-Aid for Scientific Research [22590312, 25460437] Funding Source: KAKEN

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Adult T-cell leukemia/lymphoma (ATL), an aggressive type of T-cell malignancy, is caused by the human T-cell leukemia virus type I (HTLV-1) infections. The outcomes, following therapeutic interventions for ATL, have not been satisfactory. Photodynamic therapy (PDT) exerts selective cytotoxic activity against malignant cells, as it is considered a minimally invasive therapeutic procedure. In PDT, photosensitizing agent administration is followed by irradiation at an absorbance wavelength of the sensitizer in the presence of oxygen, with ultimate direct tumor cell death, microvasculature injury, and induced local inflammatory reaction. This review provides an overview of the present status and state-of-the-art ATL treatments. It also focuses on the photodynamic detection (PDD) of hematopoietic malignancies and the recent progress of 5-Aminolevulinic acid (ALA)-PDT/PDD, which can efficiently induce ATL leukemic cell-specific death with minor influence on normal lymphocytes. Further consideration of the ALA-PDT/PDD system along with the circulatory system regarding the clinical application in ATL and others will be discussed. ALA-PDT/PDD can be promising as a novel treatment modality that overcomes unmet medical needs with the optimization of PDT parameters to increase the effectiveness of the tumor-killing activity and enhance the innate and adaptive anti-tumor immune responses by the optimized immunogenic cell death.

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