EVIDENCE OF A BIOCHEMICAL LESION STAGE IN ADVANCE OF FROG TUMOR FORMATION*

2006 ◽  
Vol 126 (1) ◽  
pp. 222-236
Author(s):  
Gladys S. King
2020 ◽  
Vol 13 (3) ◽  
pp. 585-591
Author(s):  
Luana Melo ◽  
Isabel Velasco ◽  
Julia Aquino ◽  
Rosangela Rodrigues ◽  
Edris Lopes ◽  
...  

Fibropapillomatosis is a neoplastic disease that affects sea turtles. It is characterized by multiple papillomas, fibropapillomas and cutaneous and/or visceral fibromas. Although its etiology has not been fully elucidated, it is known that there is a strong involvement of an alpha - herpesvirus, but the influence of other factors such as parasites, genetics, chemical carcinogens, contaminants, immunosuppression and ultraviolet radiation may be important in the disease, being pointed out as one of the main causes of a reduction in the green turtle population. Thus, the objective of this article was to describe the morphology of cutaneous fibropapillomas found in specimens of the green turtle (Chelonia mydas), using light and scanning electron microscopy in order to contribute to the mechanism of tumor formation. Microscopically, it presented hyperplastic stromal proliferation and epidermal proliferation with hyperkeratosis. The bulky mass was coated with keratin, with some keratinocyte invaginations, that allowed the keratin to infiltrate from the epidermis into the dermis, forming large keratinized circular spirals. Another fact that we observed was the influence of the inflammation of the tumors caused by ectoparasites.


2020 ◽  
Vol 15 (6) ◽  
pp. 482-491 ◽  
Author(s):  
Milena Kostadinova ◽  
Milena Mourdjeva

Mesenchymal stem/stromal cells (MSCs) are localized throughout the adult body as a small population in the stroma of the tissue concerned. In injury, tissue damage, or tumor formation, they are activated and leave their niche to migrate to the site of injury, where they release a plethora of growth factors, cytokines, and other bioactive molecules. With the accumulation of data about the interaction between MSCs and tumor cells, the dualistic role of MSCs remains unclear. However, a large number of studies have demonstrated the natural anti-tumor properties inherent in MSCs, so this is the basis for intensive research for new methods using MSCs as a tool to suppress cancer cell development. This review focuses specifically on advanced approaches in modifying MSCs to become a powerful, precision- targeted tool for killing cancer cells, but not normal healthy cells. Suppression of tumor growth by MSCs can be accomplished by inducing apoptosis or cell cycle arrest, suppressing tumor angiogenesis, or blocking mechanisms mediating metastasis. In addition, the chemosensitivity of cancer cells may be increased so that the dose of the chemotherapeutic agent used could be significantly reduced.


Author(s):  
Merve Erkisa ◽  
Nazlihan Aztopal ◽  
Elif Erturk ◽  
Engin Ulukaya ◽  
Veysel T. Yilmaz ◽  
...  

Background: Cancer stem cells (CSC) are subpopulation within the tumor that acts a part in the initiation, progression, recurrence, resistance to drugs and metastasis of cancer. It is well known that epigenetic changes lead to tumor formation in cancer stem cells and show drug resistance. Epigenetic modulators and /or their combination with different agents have been used in cancer therapy. Objective: In our study we scope out the effects of combination of a histone deacetylases inhibitor, valproic acid (VPA), and Cu(II) complex [Cu(barb-κN)(barb-κ2N,O)(phen-κN,N’)]·H2O] on cytotoxicity/apoptosis in a stem-cell enriched population (MCF-7s) obtained from parental breast cancer cell line (MCF-7). Methods: Viability of the cells was measured by the ATP assay. Apoptosis was elucidated via the assessment of caspase-cleaved cytokeratin 18 (M30 ELISA) and a group of flow cytometry analysis (caspase 3/7 activity, phosphatidylserine translocation by annexin V-FITC assay, DNA damage and oxidative stress) and 2ˈ,7ˈ–dichlorofluorescein diacetate staining. Results: The VPA combined with Cu(II) complex showed anti proliferative activity on MCF-7s cells in a dose- and time-dependently. Treatment with combination of 2.5 mM VPA and 3.12 μM Cu(II) complex induces oxidative stress in a time-dependent manner, as well as apoptosis that is evidenced by the increase in caspase 3/7 activity, positive annexin-V-FITC, and increase in M30 levels. Conclusion: The results suggest that the combination therapy induces apoptosis following increased oxidative stress, thereby making it a possible promising therapeutic strategy that further analysis is required.


1964 ◽  
Vol 40 (6) ◽  
pp. 445-447 ◽  
Author(s):  
Ryoichi MORI ◽  
Kikuo NOMOTO ◽  
Kenji TAKEYA

1984 ◽  
Vol 49 (2) ◽  
pp. 325-332 ◽  
Author(s):  
F Poirier ◽  
P Jullien ◽  
P Dezelee ◽  
G Dambrine ◽  
E Esnault ◽  
...  

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