Macrophage-directed immunotherapy as adjuvant to photodynamic therapy of cancer

Korbelik, Mladen; Naraparaju, Venkateswara R.; Yamamoto, Nobuto

doi:10.1038/bjc.1997.34

Cited by 88 publications

(52 citation statements)

References 18 publications

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“…DBP possesses antiangiogenic activity, and cancer cells can inactivate DBP function by deglycosylation (14)(15)(16)(17). Photodynamic therapy with DBP-derived MAF has been shown to have synergistic antitumor effect in squamous cell carcinoma tumor models (18). DBP is inactivated in several other cancers as well (14)(15)(16)(17).…”

Section: Discussionmentioning

confidence: 99%

Comparative Proteomic Profiles of Meningioma Subtypes

Okamoto

Li²,

Vortmeyer³

et al. 2006

Cancer Research

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Meningiomas are classified into three groups (benign, atypical, and anaplastic) based on morphologic characteristics. Atypical meningiomas, which are WHO grade 2 tumors, and anaplastic meningiomas, which are WHO grade 3 tumors, exhibit an increased risk of recurrence and premature death compared with benign WHO grade 1 tumors. Although atypical and anaplastic meningiomas account for <10% of all of meningiomas, it can be difficult to distinguish them from benign meningiomas by morphologic criteria alone. We used selective tissue microdissection to examine 24 human meningiomas and did two-dimensional gel electrophoresis to determine protein expression patterns. Proteins expressed differentially by meningiomas of each WHO grade were identified and sequenced. Proteomic analysis revealed protein expression patterns unique to WHO grade 1, 2, and 3 meningiomas and identified 24 proteins that distinguish each subtype. Fifteen proteins showed significant changes in expression level between benign and atypical meningiomas, whereas nine distinguished atypical from anaplastic meningiomas. Differential protein expression was confirmed by Western blotting and immunohistochemistry. We established differential proteomic profiles that characterize and distinguish meningiomas of increasing grades. The proteins and proteomic profiles enhance understanding of the pathogenesis of meningiomas and have implications for diagnosis, prognosis, and treatment.

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Section: Discussionmentioning

confidence: 99%

Comparative Proteomic Profiles of Meningioma Subtypes

Okamoto

Li²,

Vortmeyer³

et al. 2006

Cancer Research

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“…Consequently, PDT appears to be highly receptive to the adjuvant treatment with the macrophage-activating factors. For example, the effect of PDT treatment of tumours was shown to be enhanced by vitamin D3-binding protein-derived macrophageactivating factor (DBMAF) (Korbelik et al, 1997), glucan SPG (Krosl and Korbelik, 1994) as well as granulocyteÐmacrophage colony-stimulating factor (GM-CSF) . Photodynamic enhancement of macrophage phagocytosis has been reported for HpD (Yamamoto et al, 1991), Photofrin II (Yamamoto et al, 1994) and some cyanine dyes (Yamamoto et al, 1992a;Nakagawa et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Foscan® (mTHPC) photosensitized macrophage activation: enhancement of phagocytosis, nitric oxide release and tumour necrosis factor-α-mediated cytolytic activity

et al. 1999

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Summary Photodynamic activation of macrophage-like cells contributes to an effective outcome of photodynamic therapy (PDT) treatment. The possibility for an enhancement of macrophage activity by photosensitization with meta-tetra(hydroxyphenyl)chlorin (mTHPC) (1 µg ml -1 ) was studied in U937, monocyte cell line differentiated into macrophages (U937Φ cells). Phagocytic activity of U937Φ cells was evaluated by flow-cytometry monitoring of ingestion of fluorescein-labelled Escherichia coli particles. Increase in irradiation fluence up to 3.45 mJ cm -2 (corresponding irradiation time 15 s) resulted in significant increase in fluorescence signal (145%), while at higher light fluences the signal lowered down to the untreated control values. A light energy-dependent production of tumour necrosis factor-alpha (TNF-α) by photosensitized macrophages was further demonstrated using the L929 assay. The maximum TNF-α mediated cytolysis was observed at 28 mJ cm -2 and was 1.7-fold greater than that in control. In addition, we demonstrated a fluence-dependent increase in nitric oxide (NO) production by mTHPC-photosensitized macrophages. NO release increased gradually and reached a plateau after irradiation fluence of 6.9 mJ cm -2 . Cytotoxicity measurements indicated that the observed manifestations of mTHPC-photosensitized macrophage activation took place under the sublethal light doses. The relevance of the present findings to clinical mTHPC-PDT is discussed.

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“…Systemic complement activation with streptokinase treatment had no detectable effect on complement deposition at the tumour site without PDT, but it augmented the complement activity in PDT-treated tumours. Photofrin-mediated PDT was tested against SSCVII tumours in combination with serum vitamin D3 binding protein-derived macrophageactivating factor (DBPMAF) 117 . DBPMAF markedly improved the outcome of PDT, but as a single agent had no significant effect on the growth of SCCVII tumours.…”

Section: Pdt and Microbial Adjuvantsmentioning

confidence: 99%

Photodynamic therapy and anti-tumour immunity

2006

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Photodynamic therapy (PDT) uses non-toxic photosensitizers and harmless visible light in combination with oxygen to produce cytotoxic reactive oxygen species that kill malignant cells by apoptosis and/or necrosis, shut down the tumour microvasculature and stimulate the host immune system. In contrast to surgery, radiotherapy and chemotherapy that are mostly immunosuppressive, PDT causes acute inflammation, expression of heat-shock proteins, invasion and infiltration of the tumour by leukocytes, and might increase the presentation of tumour-derived antigens to T cells.The principle of photodynamic therapy (PDT) was first proposed over 100 years ago 1 . A recent review in Nature Reviews Cancer by Rakesh Jain and colleagues described some of the historical milestones in the development of PDT as a cancer treatment2. Many of the photosensitizers (PSs) that have been studied since PDT was first proposed are based on a porphyrin-like nucleus 3 . PSs function as catalysts when they absorb visible light and then convert molecular oxygen to a range of highly reactive oxygen species (ROS). The ROS that are produced during PDT have been shown to destroy tumours by multifactorial mechanisms4 , 5 (FIG. 1). PDT has a direct affect on cancer cells, producing cell death by necrosis and/or apoptosis 6 . PDT also has an affect on the tumour vasculature, whereby illumination and ROS production causes the shutdown of vessels and subsequently deprives the tumour of oxygen and nutrients 7,8 . Finally, PDT also has a significant effect on the immune system 9-11 , which can be either immunostimulatory or immunosuppressive.Most of the commonly used cancer therapies are immunosuppressive. Chemotherapy and ionizing radiation delivered at doses sufficient to destroy tumours are known to be toxic to the bone marrow, which is the source of all cells of the immune system, and neutropaenia and other forms of myelosuppression are often the dose-limiting toxicity of these therapies. However, it should be noted that low doses of either ionizing radiation12 , 13 or chemotherapy14 can have immunostimulatory effects, including the induction of heat-shock © 2006 Nature Publishing Group Correspondence to M.R.H. Hamblin@helix.mgh.harvard.edu. Competing interests statementThe authors declare no competing financial interests. DATABASES NIH Public Access Author ManuscriptNat Rev Cancer. Author manuscript; available in PMC 2010 September 6. Published in final edited form as:Nat Rev Cancer. 2006 July ; 6(7): 535-545. doi:10.1038/nrc1894. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript proteins 15 . Less well known is the fact that major surgery can also have an immunosuppressive effect that leads to a significant diminution of lymphocyte and natural killer (NK) cell function 16 . The ideal cancer therapy would not only destroy the primary tumour, but at the same time trigger the immune system to recognize, track down and destroy any remaining tumour cells, be they at or near the site of the primary tumour or distant microm...

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Macrophage-directed immunotherapy as adjuvant to photodynamic therapy of cancer

Cited by 88 publications

References 18 publications

Comparative Proteomic Profiles of Meningioma Subtypes

Comparative Proteomic Profiles of Meningioma Subtypes

Foscan® (mTHPC) photosensitized macrophage activation: enhancement of phagocytosis, nitric oxide release and tumour necrosis factor-α-mediated cytolytic activity

Photodynamic therapy and anti-tumour immunity

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