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Clinical Application of Photodynamic Therapy: German Collaborative Studies
Published in Barbara W. Henderson, Thomas J. Dougherty, Photodynamic Therapy, 2020
Dieter Jocham, Reinhold Baumgartner, Wolfgang Beyer, Jens Feyh, Rudolf M. Huber, Alwin E. Goetz, K. Haeussinger
Our clinical experience reveals that tumor recurrences in the bladder cannot be avoided and that, even after an initial complete response to treatment (i.e., with normal findings during follow-up investigations), recurrence of bladder tumors has to be expected. This is probably due to the continuous local onset of carcinogenesis caused by toxic substances in the urine. Dysplasia following treatment has been observed in some of the patients, but its relevance to later tumor recurrence is unclear.
Drug Delivery Intelligent Automation & Soft Computing
Published in Mohammad E. Khosroshahi, Applications of Biophotonics and Nanobiomaterials in Biomedical Engineering, 2017
Neoplasm is an ancient Greek word meaning “New Plasma’’, i.e., formation or creation, which denotes the formation of abnormal growth (i.e., neoplasia) of tissue commonly referred to as a tumor. Usually, but not always, neoplasia forms a mass. According to World Health Organization (WHO) neoplasms is classified into four main groups: (a) benign neoplasms, (b) in situ neoplasms, (c) malignant neoplasms (or cancers), and (d) neoplasms of uncertain or unknown behaviour. Prior to the abnormal growth of tissue, as neoplasia, cells often undergo an abnormal pattern of growth, such as metaplasia or dysplasia. However, metaplasia or dysplasia does not always progress to neoplasia (Birbrair et al. 2014). Tumor cells consist of various structures and areas, of which the actual cancer cells occupy less than 50%, the vasculature 1–10%. The remaining structure consists of a collagen-rich matrix. As it was mentioned in §5.5, tumors develop a chaotic capillary network that distinguishes them from normal vasculature and they follow a branching pattern. The capillary vasculature in tumors is normally accompanied by occlusions caused by rapidly proliferating cancer cells. Hypoxia is produced as a result of compression of vasculature and finally necrosis of viable tumor cells occurs. Unlike normal tissue, tumors often lack a functional lymphatic system. Another characteristic of tumor is the high proportion of proliferating endothelial cells and aberrant basement membranes of tumor vasculature. Tumor blood vessels are up to 3–10 times more permeable to counterbalance the high oxygen and nutrient requirements of the growing tumor (Weindel et al. 1994, Olesen 1986). The interstitial compartment of tumor contains a network of collagen and elastic fibre, which is immersed by hyaluronate and proteoglycan-containing fluid. The interstitial pressure and rapid aberrant cell growth are thought to be the main reasons for the compression and occlusion of blood and lymphatic vessels in solid tumors (Murray and Carmichael 1995). It is crucial to appreciate the fact that any transport of drug into the tumor is dependent on the interstitial pressure as well as on its composition, charge, and the characteristic of the drug. Also, the dense packing of tumor cells limits the movement of molecules from the vessel into the interstitial compartment. Macromolecules and drugs are transported into the tumor cells through interendothelial junctions and vesicular vacuolar organelles. The range of pore cut-off size in tumor tissue has been reported between 100–780 nm (Hobbs et al. 1998, Yuan et al. 1995) and can be increased up to 800 nm, for example in human colon tumors by perfusion with low dosage (10 μg/mL) of vascular endothelial growth factor (VEGF) (Monsky et al. 1999). The process of entering colloidal NPs into interstitial compartment through leaky vessels and accumulation in tumor due to poor lymphatic drainage system is called “Enhanced Permeability Enhancement-EPR” effect.
Bioimpedance spectroscopy and spectral camera techniques in detection of oral mucosal diseases: a narrative review of the state-of-the-art
Published in Journal of Medical Engineering & Technology, 2019
Shekh Emran, Miia Hurskainen, Laura Tomppo, Reijo Lappalainen, Arja M. Kullaa, Sami Myllymaa
Fournier and Darier first introduced the name erythroplasia to describe a malignant dyskeratosis with the obscure aetiology in 1893 and termed it as épithéliome papillaire [15]. This rare lesion is typically asymptomatic, but a few patients may complain of a burning sensation in the mouth [15]. The most common locations of oral erythroplakia are the lateral surface of the tongue, the retromolar area, and the soft palate [17]. On biopsy and histopathologic assessment, oral erythroplakia regularly displays signs of severe epithelial dysplasia, carcinoma in situ, or micro invasive carcinoma [15]. Oral erythroplakia carries the greatest potential for malignant transformation of all the OPMDs with a malignant transformation rate ranging from 14 to 50% [18] and thus early diagnosis and treatment of oral erythroplakia is crucial.
Understanding the complex microenvironment in oral cancer: the contribution of the Faculty of Dentistry, University of Otago over the last 100 years
Published in Journal of the Royal Society of New Zealand, 2020
Alison Mary Rich, Haizal Mohd Hussaini, Benedict Seo, Rosnah Bt Zain
How Tregs modulate the immune system is not fully understood but one way might be through TLR. TLR were first recognised on the surface of inflammatory cells, especially macrophages where they alert the body to external pathogens, particularly bacteria, and set off an immune response, but it is now well known that they recognise endogenous damage as well. Danger signals arising from injured or altered cells are known as damage–associated molecular patterns (DAMPS) and these are recognised by certain TLRs. Perhaps cancer cells and/or potentially malignant cells release DAMPS? Our group assessed 50 cases each of inflamed irritative hyperplasia (IH), epithelial dysplasia (ED) and OSCC and found that more inflammatory cells expressed TLR2 in the stroma of OSCC than in hyperplastic tissue (Figure 4A,B). No hyperplastic samples showed TLR2+ keratinocytes but keratinocytes in 64% of cases of OSCC were TLR2+. Positive TLR2 expression in the TME suggests that immune surveillance is activated against the altered epithelial cells while TLR2 expression by malignant keratinocytes may correlate with apoptosis resistance and hence the survival of tumour cells (Ng et al. 2011). Double immunofluoresence studies showed that TLR2+FoxP3+ Tregs were present in the OSCC microenvironment (Figure 5) with apparent cell-to-cell contact between TLR2+ and FoxP3+ cells. The presence of FoxP3+TLR2+ cells may represent a dendritic cell-dependent pathway capable of inhibiting Treg suppressive activity, potentially beneficial to the anti-tumour response (Hussaini et al. 2017).
Chemoprotection by Kolaviron of Garcinia kola in Benzene-induced leukemogenesis in Wistar rats
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Olaniyi Solomon Ola, Esther Oladayo Ogunkanmbi, Emmanuel Babatife Opeodu
Most cancer chemotherapy regimens and even the remission-induction therapy for the treatment of leukemia are accompanied by severe side effects besides their chemotherapeutic efficacy [8,9]. There is a need for modified treatment and intensive assessment of cytotoxic agents in the field of oncology [10] because many cytotoxic agents conferred severe side effects during the course of treatment [11,12]. Most commonly, some cancer chemotherapeutic agents are radiomimetic in nature especially alkylating agents affecting hematology, bone marrow cellularity and effective dysplasia formation in myeloid tissue, which may ultimately result in therapy-related myelodysplasia or acute myelogenous leukemia [13]. Therefore, leukemia burden has led to increased research in isolation and identification of more cytotoxic agents [14,15]. Considerably, herbal medicine that presents natural compounds of sufficient chemotherapeutic effect with little or no side effects may be investigated for cancer chemotherapy. One such natural compound is kolaviron, which is a biflavonoid isolate of the seed of Garcinia kola extract. It is a defatted fraction of Garcinia kola seed with valuable major constituents such as Garcinia biflavonoids GB1 and GB2 and kolaflavone [16,17]. It has organ protective capability [18], improved hematological indices and offered immunity boosting effects [19]. The safety profile of kolaviron, its antioxidant properties and antiproliferative capacity have been extensively studied in vitro and in vivo [20–21]. Moreover, it is known to offer protection against xenobiotic and chemical-induced oxidative stress-mediated toxicities in experimental murine models [22,23]. Therefore, the present work investigated the myeloprotective effect of kolaviron on benzene-induced bone marrow dysplasia in Wistar rats.