4 research outputs found
Oral squamous cell carcinoma proliferative phenotype is modulated by proanthocyanidins: a potential prevention and treatment alternative for oral cancer-1
<p><b>Copyright information:</b></p><p>Taken from "Oral squamous cell carcinoma proliferative phenotype is modulated by proanthocyanidins: a potential prevention and treatment alternative for oral cancer"</p><p>http://www.biomedcentral.com/1472-6882/7/22</p><p>BMC Complementary and Alternative Medicine 2007;7():22-22.</p><p>Published online 19 Jun 2007</p><p>PMCID:PMC1914364.</p><p></p> 20 μg/mL, and the lower row (K-O) under PAC administration at 50 μg/mL. All cell lines exhibited a dose-dependent response to PAC administration, with higher doses resulting in fewer cells at day 4. Ca Ski (A), CAL 27 (C), CAL 27-TF16 (D) and Hs27 (E) cells were reduced in number with PAC at 20 μg/mL (F, H, I, J), unlike GH354 cells (B), which experienced a reduction in proliferation, and morphological changes indicative of apoptosis (G). Cellular proliferation was reduced by PAC in all cell lines (K-O) at 50 μg/mL; all cell lines exhibited altered morphology, except Hs27 (O) cells which appeared normal, although fewer in number
Oral squamous cell carcinoma proliferative phenotype is modulated by proanthocyanidins: a potential prevention and treatment alternative for oral cancer-2
<p><b>Copyright information:</b></p><p>Taken from "Oral squamous cell carcinoma proliferative phenotype is modulated by proanthocyanidins: a potential prevention and treatment alternative for oral cancer"</p><p>http://www.biomedcentral.com/1472-6882/7/22</p><p>BMC Complementary and Alternative Medicine 2007;7():22-22.</p><p>Published online 19 Jun 2007</p><p>PMCID:PMC1914364.</p><p></p>Lane 2) also did not express HPV. HPV 16-transfected cells (A: Lane 3) expressed HPV 16; specific primers were tested using PCR and the full-length HPV 16-DNA template (A: Lane 4). Total DNA isolated from CAL 27 cells (B: Lane 1) and CAL 27-TF16 cells (B: Lane 3) demonstrated DNA alterations following PAC treatment (50 μg/mL), including a more diffuse banding pattern and lower molecular weight, possibly indicating the onset of DNA fragmentation among the treated cells (B: Lane 2, 4)
Oral squamous cell carcinoma proliferative phenotype is modulated by proanthocyanidins: a potential prevention and treatment alternative for oral cancer-3
<p><b>Copyright information:</b></p><p>Taken from "Oral squamous cell carcinoma proliferative phenotype is modulated by proanthocyanidins: a potential prevention and treatment alternative for oral cancer"</p><p>http://www.biomedcentral.com/1472-6882/7/22</p><p>BMC Complementary and Alternative Medicine 2007;7():22-22.</p><p>Published online 19 Jun 2007</p><p>PMCID:PMC1914364.</p><p></p>umber and ratio of cell spreading without PAC (A,B) but displayed morphological features characteristic of apoptosis under PAC treatment (F,G). CAL 27 (C,H) and HPV 16-transfected CAL 27 cells (D,I) also grew in the absence of PAC (C,D), but demonstrated surface blebbing activity and morphological changes similar to cervical cells under PAC treatment (H, I). Hs27 normal fibroblast controls (E,J) grew in the absence of PAC (E) and less rapidly in the presence of PAC (J), without demonstrable microscopic evidence of apoptotic cellular features
Oral squamous cell carcinoma proliferative phenotype is modulated by proanthocyanidins: a potential prevention and treatment alternative for oral cancer-0
<p><b>Copyright information:</b></p><p>Taken from "Oral squamous cell carcinoma proliferative phenotype is modulated by proanthocyanidins: a potential prevention and treatment alternative for oral cancer"</p><p>http://www.biomedcentral.com/1472-6882/7/22</p><p>BMC Complementary and Alternative Medicine 2007;7():22-22.</p><p>Published online 19 Jun 2007</p><p>PMCID:PMC1914364.</p><p></p>umber and ratio of cell spreading without PAC (A,B) but displayed morphological features characteristic of apoptosis under PAC treatment (F,G). CAL 27 (C,H) and HPV 16-transfected CAL 27 cells (D,I) also grew in the absence of PAC (C,D), but demonstrated surface blebbing activity and morphological changes similar to cervical cells under PAC treatment (H, I). Hs27 normal fibroblast controls (E,J) grew in the absence of PAC (E) and less rapidly in the presence of PAC (J), without demonstrable microscopic evidence of apoptotic cellular features