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This PDF file contains the front matter associated with SPIE
Proceedings Volume 6857, including the Title Page, Copyright
information, Table of Contents, and the
Conference Committee listing.
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Phototherapy and Immune Activities I: Clinical Studies
Currently there are no truly effective treatments for advanced melanoma (surgically unresectable stage III
and IV). In situ photoimmunotherapy (ISPI) is a recently developed therapy based on physical and
immunological principles that uses lasers in combination with immunostimulants to achieve clinically
significant responses in advanced melanoma patients. Results from an ongoing phase I clinical trial suggest
that this form of therapy has the highest response rate of any treatment known for advanced melanoma, and
in a significant number of subjects, periods of prolonged remissions from the disease can be achieved. ISPI
is therefore clearly one of the most promising forms of therapy for this disease and better understanding of
the immunological and physical parameters of this treatment will lead to even better clinical results.
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Photodynamic therapy (PDT) is a promising treatment modality. It offers alternative options in the treatment of cancer and vascular diseases. In cancer treatment, PDT has been used primarily for localized superficial or endoluminal malignant and premalignant conditions. More recently, its application has also been expanded to solid tumors. However, its antitumor efficacy remains debatable and its acceptance still variable. Pre-clinical studies demonstrate that, in addition to the primary local cytotoxicity, PDT might induce secondary host immune responses, which may further enhance PDT's therapeutic effects on primary tumor as well as metastasis. Therefore, PDT-induced local and systemic antitumor immune response might play an important role in successful control of malignant diseases. Furthermore, PDT's antitumor efficacy might also be enhanced through an effective immunoadjuvant or immunomodulator. Our recent clinical data also indicate that improved clinical outcomes can be obtained by a combination of PDT and immunomodulation therapy for the treatment of pre-malignant skin diseases. For instance, the combination of topical ALA-PDT and Imiquimod is effective for the treatment of genital bowenoid papulosis. This presentation will also report our preliminary data in developing combination approaches of PDT and immunotherapy for actinic keratosis (AK), basal cell carcinomas (BCCs) and Bowen's disease.
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Phototherapy and Immune Activities II: Pre-Clinical Studies
The involvement of adrenal glucocorticoid hormones in the response of the treatment of solid tumors by photodynamic
therapy (PDT) comes from the induction of acute phase response by this modality. This adrenal gland activity is
orchestrated through the engagement of the
hypothalamic-pituitary-adrenal hormonal axis incited by stress signals
emanating from the PDT-treated tumor. Glucocorticoid hormone activity engendered within the context of PDT-induced
acute phase response performs multiple important functions; among other involvements they beget acute phase reactant
production, systemic neutrophil mobilization, and control the production of inflammation-modulating and
immunoregulatory proteins.
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Photodynamic therapy (PDT) involves the IV administration of photosensitizers followed by illumination of the tumor with red light producing reactive oxygen species that eventually cause vascular shutdown and tumor cell apoptosis. Anti-tumor immunity is stimulated after PDT due to the acute inflammatory response, recognition of tumor-specific antigens, and induction of heat-shock proteins, while the three commonest cancer therapies (surgery, chemotherapy and radiotherapy) all tend to suppress the immune system. Like many other immunotherapies, the extent of the immune response after PDT tends to depend on the antigenicity of the particular tumor, or in other words, whether the tumor contains proteins with the correct characteristics to provide peptides that can bind to MHC class I molecules and provide a target for cytolytic T lymphocytes. We have described certain mouse tumors containing defined or naturally occurring tumor associated antigens that respond particularly well to PDT, and potent immune responses capable of destroying distant untreated tumors can be induced. In this report we address the induction of immunity after PDT of the DBA2 mastocytoma known as P815. This tumor was the first mouse tumor to be shown to possess a tumor-rejection antigen capable of being recognized by cytotoxic T-cells.
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Combination therapy using laser photothermal interaction and immunological stimulation has demonstrated
its ability to induce immunological responses. Glycated chitosan (GC), an immunological stimulant, and
imiquimod, a new type of immune response modifier (IRM), when used in conjunction with laser
phototherapy, have shown to have a great immunological stimulation function. Specifically, imiquimod can
help release cytokines from immunocompetent cells, stimulate TH1 lymphocyte responses (CD8+ T-cells),
and recruit additional dendritic cells. To study the effects of immunoadjuvnats in combination of laser
photo-irradiation, we treated animal tumors with laser-ICG-GC combination and late-stage melanoma
patients with laser-ICG-imiquimod combination. At designated times, tumors, blood, and spleens in both
treated and untreated animals were colleted for analysis. The major immunological indicators, such as IL-6,
IL-12, IFN-gamma, CD4, and CD8 were analyzed. The same immunological analysis was also performed
for melanoma patients treated by the laser-imiquimod combination.
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Introduction. The whole mechanism of the cellular level of tumor destruction by photodynamic therapy (PDT) is still
unknown. Despite necrotic and apoptotic ways of cell death, there is a variety of events leading to and magnifying the
inactivation of tumor cells. Material and methods. J-774A.1 were incubated with δ-aminolevulinic acid (ALA) at different concentrations (125, 250, 500, 1000 μM) and then irradiated with VIS (400 - 750 nm) at the dose of 5,10 and 30 J/cm2 delivered from the incoherent light source. The effects of the application of ALA-PDT were evaluated on the basis of cell viability,
nitric oxide (NO), tumor necrosis factor α- (TNF-α) and interleukin-1β (IL-1β) produced by the J-774A.1 cells. Results. The cell viability (assessed using MTT test) was comparable with control group at 5,10 and 30 J/cm2. At these doses of
energy using different concentrations of ALA we have observed that at the higher energy doses, the greater increase of TNF-α release, lowering of the level of IL-1β production and decrease of NO release were observed. There was also observed the dependence of the secretional activity of the cells on the ALA concentrations. Conclusion. The cell viability and production of cytokines depended on ALA concentrations and energy doses of the light. The higher some cytokines' release after PDT could be an additional factor for the complete eradication of tumor.
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Chemotherapies currently constitute one main venue of cancer treatment. For a large number of adult and elderly
patients, however, treatment options are poor. These patients may suffer from disease that is resistant to conventional
chemotherapy or may not be candidates for curative therapies because of advanced age or poor medical conditions. To
control disease in these patients, new therapies must be developed that are selectively targeted to unique characteristics
of tumor cell growth and metastasis. A reliable early evaluation and prediction of response to the chemotherapy is
critical to its success. Chemotherapies induce apoptosis in tumor cells and a portion of such apoptotic cancer cells may
be present in the circulation. However, the fate of circulating tumor cells is difficult to assess with conventional methods
that require blood sampling. We report the in situ measurement of circulating apoptotic cells in live animals using in
vivo flow cytometry, a novel method that enables real-time detection and quantification of circulating cells without blood
extraction. Apoptotic cells are rapidly cleared from the circulation with a half-life of ~10 minutes. Real-time monitoring
of circulating apoptotic cells can be useful for detecting early changes in disease processes, as well as for monitoring
response to therapeutic intervention.
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High fluence low-power laser irradiation (LPLI) can induce cell apoptosis which is mediated by a high level of mitochondrial reactive oxygen species (ROS) production; however the mechanism is still unclear. Here, we further studied the mitochondrial signaling pathways involved in the apoptotic process. Activation of caspase-9 indicated an apoptotic process occurred under the high fluence LPLI treatment. Increasing of dichlorodihydrofluorescein diacetate (H2DCFDA) fluorescence products showed a high level of mitochondrial ROS generation after irradiation. Cyclosporine A (CsA) has been reported to inhibit some kinds of apoptosis, which are especially mediated by ROS. The question is whether CsA has some effect on high fluence LPLI induced apoptosis. Results showed that CsA significantly delayed mitochondria depolarization, observably delayed cell death in response to high fluence LPLI treatment demonstrating a significant protective role of CsA on the apoptotic process. These results suggest that high fluence LPLI induced cell apoptosis via some CsA-sensitive mitochondrial signal pathways.
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Photodynamic therapy (PDT) functions as a cancer therapy through two major cell death mechanisms: apoptosis and
necrosis. Immunological responses induced by PDT has been mainly associated with necrosis while apoptosis
associated immune responses have not fully investigated. Heat shock proteins (HSPs) play an important role in
regulating immune responses. In present study, we studied whether apoptotic tumor cells could induce immune response
and how the HSP70 regulates immune response. The endocytosis of tumor cells by the activated macrophages was
observed at single cell level by LSM. The TNF-α release of macrophages induced by co-incubated with PDT-apoptotic
tumor cells was detected by ELISA. We found that apoptotic tumor cells treated by PDT could activate the macrophages,
and the immune effect decreased evidently when HSP70 was blocked. These findings not only show that apoptosis can
induce immunological responses, but also show HSP70 may serves as a danger signal for immune cells and induce
immune responses to regulate the efficacy of PDT.
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Photodynamic therapy (PDT) employing photosensiter N-aspartyl chlorin e6 (NPe6) can induce lysosome disruption and
initiate the intrinsic apoptotic pathway. Bax, a member of the Bcl-2 family of proteins, is an essential regulator of
apoptosis. Bax is normally found in the cytosol of healthy cells, and translocates to mitochondria in response to many
apoptotic stimuli. In this study, using real-time single-cell analysis, we have investigated the kinetics of Bax
distribution during NPe6-induced apoptosis in ASTC-a-1 cells. In order to monitor Bax subcellular distribution, cells
were stained with GFP-Bax and Mito Tracker Red. The results show that Bax redistribution occurred at about 170 min
after treated with NPe6-PDT, and then sequestered into clusters associated with the mitochondira within 30 min. Our
data clearly showed the spatial and temporal changes in Bax distribution in living cells during NPe6-induced apoptosis.
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The 3-D, in vivo temperature distributions within tumor-bearing rats were measured using Magnetic
Resonance Imaging (MRI) technique. The in vivo thermal distributions of rats were measured using MRI
chemical shift of water proton density. DMBA-4 tumor bearing rats are treated using laser photothermal
therapy combined with immunoadjuvant under the observation of MRI. The thermal images and the
immunological responses were studied and their relationships were investigated. The study of thermal
distribution and correlation with the immunological response under laser treatment provided rich information
with potential guidance for thermal-immunological therapy.
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Scanning of microscope slides is an important part of cytogenetic diagnosis. Metaphase chromosomes arranged
in a karyotype reveal the nature and severity of cancer and other diseases. Searching for metaphases spreads is a lengthy
and tedious process that can benefit from computer aided systems. When slides are searched by such systems in
continuous motion, the image quality is reduced. The motion blur is a function of the scan speed, the camera frame rate
and sample time, and the level of magnification. In this study, normalized contrast transfer function (CTF) is used to
define the amount of image degradation.
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A high spatial resolution computed radiography (CR) detector was used to develop a phase contrast x-ray imaging prototype with a microfocus x-ray source. The phase contrast imaging was realized with appropriate magnifications. Meanwhile, the basic system parameters, such as the modulation transfer function (MTF) and detective quantum efficiency (DQE) were measured with and without phase contrast effect. The experimental results indicated that the phase contrast can enhance the detectability of the imaging system.
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ChanSu(CS), a traditional Chinese medicine, is composed of many chemical compoments. It is isolated
from the dried white secretion of the auricular and skin glands of toads, and it has been widely used for treating
the heart diseases and other systemic illnesses. However, it is difficult to judge antitumor effect of agents
derived from ChanSu and the underlying mechanism of ChanSu inducing cell apoptosis is still unclear. This
report was performed to explore the inhibitory effect and mechanism of ChanSu on human lung
adenocarcinoma cells (ASTC-a-1). Fluorescence emission spectra and fluorescence resonance energy transfer
(FRET) were used to study the caspase-3 activation during the
ChanSu-induced human lung adenocarcinoma
(ASTC-a-1) cell apoptosis. CCK-8 was used to assay the inhibition of ChanSu on the cell viability. The cells
expressing stably with SCAT3 was used to examine if caspase-3 was activated by ChanSu using acceptor
photobleaching technique. Our data showed that treatment of ASTC-a-1 cell with ChanSu resulted in the
inhibition of viability and induction of apoptosis in a dose-dependent manner and the SCAT3 was almost
cleaved 24 h after ChanSu treatment, implying that ChanSu induced cell apoptosis via a caspase-3-dependent
death pathway. Our findings extend the knowledge about the cellular signaling mechanisms mediating
ChanSu-induced apoptosis.
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Caspase-3 is a key activated death protease, which catalyzes the specific cleavage of many cellular proteins and induces
DNA cleavage eventually. In this report, cells were treated with mitomycin C (MMC) at different concentration and its
activity was detected by cell counting kit (CCK-8). Based on results of CCK-8, cells were treated with 10μg/mL MMC
and Hoechst 33258 has been used to observe cell apoptosis. Fluorescence resonance energy transfer (FRET) and
confocal microscopy have been used to the effect of MMC on the caspase3 activation in living cells. Human lung
adenocarcinoma cells (ASTC-a-1) was transfected with plasmid SCAT3 (pSCAT3)/CKAR FRET receptor. Acceptor
photobleaching techniques of FRET plasmid has been used to destruct fluorophore of cells stably expressing SCAT3
reporter on a fluorescence confocal microscope. The activity of caspase3 can be analyzed by FRET dynamics of SCAT3
in living cells. Our results show that MM C can induce ASTC-a-1 cell apoptosis through activation of caspase3.
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Taxol (Paclitaxel), an isolated component from the bark of the Pacific yew Taxus brevifolia, exhibits a broad spectrum of
clinical activity against human cancers. Taxol can promote microtubule (MT) assembly, inhibit depolymerization, and
change MT dynamics, resulting in disruption of the normal reorganization of the microtubule network required for
mitosis and cell proliferation. However, the molecular mechanism of taxol-induced cell death is still unclear. In this
report, CCK-8 was used to assay the inhibition of taxol on the human lung adenocarcinoma (ASTC-a-1) cells viability, confocal fluorescence microscope was used to monitor the morphology changes of cells with taxol treatment. We for the
first time describe the characteristics of taxol-induced cells swelling, cytoplasmic vacuolization and cell death. Taxol
induced swelling, cytoplasmatic vacuolization and cell death without cell shrinkage and membrane rupture. These
features differ from those of apoptosis and resemble the paraptosis, a novel nonapoptotic PCD.
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Ultraviolet (UV) irradiation can induce apoptosis through both the membrane death receptor and the intrinsic apoptotic
signaling pathways as DNA-damaging agents. PUMA, a BH3-only Bcl-2 family protein, plays an essential role in
DNA damage-induced apoptosis. Bax, also a Bcl-2 family member, translocates from the cytosol to the mitochondrial
membrane during UV-induced apoptosis. However, the regulation of Bax activation induced by UV irradiation remains
poorly understood. In this study, the FRET (fluorescence resonance energy transfer) technique was used to study the
interactions of Bax, Bcl-Xl, and PUMA in ASTC-a-1 cells. The results show that Bax translocated from the cytosol to the
mitochondrial membrane at about 7 h after UV irradiation, and the translocation can not be blocked completely when
overexpressed Bcl-xl. Moreover, The interaction of Bax and Bcl-Xl weakened markedly. In addition,
Co-immunoprecipitation shows that PUMA released Bax by directly binding to Bcl-XL after UV irradiation in
ASTC-a-1 cells. Taken together, these results indicated that PUMA can promote Bax translocation by binding to
Bcl-Xl during UV-induced apoptosis.
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The selective photothermal-tissue interaction using dye enhancement has been proven to be effective in
minimizing the peripheral normal tissue damage during cancer treatment. It is important that the tissue-thermal
damage be analyzed and the damage rate process be estimated before the photothermal-immunotherapy
for cancer treatment. In this study, we have used the EMT6 mouse tumor model for the
laser-tumor treatment with a simultaneous surface temperature measurement using infrared thermography.
The images acquired were processed to obtain the temperature profiles. The saturation temperature and
corresponding time of irradiation from the temporal profiles were used to calculate the damage parameter
using Arrhenius rate process equation. The damage parameters obtained from six mice were compared. Our
results of in vivo study show that the damage analyses agree with the previous in vitro study on skins.
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Laser energy can induce acute photothermal tissue damage, but without systemic effect in the treatment of
tumors. However, it could serve as a precursor of immune responses if its photothermal actions could be
used effectively as a means of producing tumor-specific antigens and other immunological stimulation
elements. When used in a combination with immunoadjuvants, laser photothermal energy had been
successfully applied in the treatment of metastatic tumors.
Pre-clinical and preliminary clinical studies have
demonstrated the systemic and immunological effects of the combination of laser irradiation and
immunological stimulation through eradication of primary and secondary tumors, and through molecular and
cellular anti-tumor immune activities. This study focuses on the histological and morphological aspects of
laser immunotherapy induced immune responses, using glycated chitosan as the adjuvant and an 805-nm
laser as the source of photothermal energy source. Cellular activities, such as tumor destruction and
lymphocyte infiltration after the laser immunotherapy treatment were observed and analyzed. These cellular
activities further support the hypothesis that induced immune activities are crucial outcome of laser
immunotherapy.
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Caspase-2 is an initiating caspase required for stress-induced apoptosis in various human cancer cells. Activation of
caspase-9, a key event in stress-mediated apoptosis, also has been shown to be an initiator caspase. However, the timing
or activation sequence of these initiator caspases, which trigger apoptotic pathway, is unclear. Here we report caspase-2
and caspase-9 dynamics during cisplatin-induced HeLa apoptosis using Double Fluorescence Resonance Energy
Transfer (FRET) technique. Two FRET probes were constructed that each encoded a CRS (caspase-2 or caspase-9
recognition Site) fused with a cyan/yellow fluorescent protein (CFP/YFP) and a red fluorescent protein (DsRed)
(CFP/YFP-CRS-DsRed). By using two probes, CFP-C2-DsRed and
YFP-C9-DsRed, we carried out simultaneous
double-FRET analysis and revealed that activation of caspase-2 had the same time course with caspase-9. These data
suggest parallel activation of initiator caspase-2 and caspase-9 in cisplatin-induced cell death.
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