Journal: British Journal of Cancer

Article Title: Combined treatment of the experimental human papilloma virus-16-positive cervical and head and neck cancers with cisplatin and radioimmunotherapy targeting viral E6 oncoprotein

doi: 10.1038/bjc.2013.43

Figure Lengend Snippet: Lactate dehydrogenase assay of CasKi and 2A3 cells treated in vitro with various concentrations of cisplatin.

Article Snippet: The HPV16+ 2A3 cell line was produced by stably transfecting the FaDu cell line from the American Type Culture Collection with the LXSN 16E6/E7 as described in Harris et al (2011) .

Techniques: Lactate Dehydrogenase Assay, In Vitro

Journal: British Journal of Cancer

Article Title: Combined treatment of the experimental human papilloma virus-16-positive cervical and head and neck cancers with cisplatin and radioimmunotherapy targeting viral E6 oncoprotein

doi: 10.1038/bjc.2013.43

Figure Lengend Snippet: Tumour uptake of E6-binding mAb 188 Re-C1P5 in nude mice-bearing CasKi and 2A3 tumours post treatment with cisplatin. Mice were treated with various doses of cisplatin for 3 days, 188 Re-C1P5 mAb was administered 24 h after the last dose of cisplatin, and the tumour uptake was assessed 24 h post 188 Re-C1P5 administration: ( A ) CasKi; ( B ) 2A3; ( C , D ) TUNEL staining of the untreated and cisplatin-treated tumours. Apoptotic cells stained brown. Original magnification × 400: ( C ) CasKi tumours—untreated (left panel) and treated with 5 mg kg −1 cisplatin (right panel); ( D ) 2A3 tumours—untreated (left panel) and treated with 5 mg kg −1 cisplatin (right panel).

Article Snippet: The HPV16+ 2A3 cell line was produced by stably transfecting the FaDu cell line from the American Type Culture Collection with the LXSN 16E6/E7 as described in Harris et al (2011) .

Techniques: Binding Assay, TUNEL Assay, Staining

Journal: British Journal of Cancer

Article Title: Combined treatment of the experimental human papilloma virus-16-positive cervical and head and neck cancers with cisplatin and radioimmunotherapy targeting viral E6 oncoprotein

doi: 10.1038/bjc.2013.43

Figure Lengend Snippet: Therapy with cisplatin and RIT with E6-binding mAb 188 Re-C1P5 of nude mice-bearing 2A3 ( A ) and CasKi ( B ) tumours. T n—tumour volume on the day of measurement; T 0 —tumour volume on day 0. The mice with 2A3 HNSCC tumours were treated IP with: 400 μ Ci 188 Re-C1P5 mAb on day 0; or 5 mg kg −1 per day cisplatin on days 0, 1, 2 followed by 400 μ Ci 188 Re-C1P5 mAb on day 3; or 5 mg kg −1 cisplatin alone on days 0, 1, 2; or left untreated. The mice with CasKi cervical tumours were treated IP with: 200 μ Ci 188 Re-C1P5 mAb on day 0; or 5 mg kg −1 per day cisplatin on days 0, 1, 2 followed by 200 μ Ci 188 Re-C1P5 mAb on day 3; or 5 mg kg −1 cisplatin alone on days 0. 1, 2; or left untreated.

Article Snippet: The HPV16+ 2A3 cell line was produced by stably transfecting the FaDu cell line from the American Type Culture Collection with the LXSN 16E6/E7 as described in Harris et al (2011) .

Techniques: Binding Assay

Journal: British Journal of Cancer

Article Title: Combined treatment of the experimental human papilloma virus-16-positive cervical and head and neck cancers with cisplatin and radioimmunotherapy targeting viral E6 oncoprotein

doi: 10.1038/bjc.2013.43

Figure Lengend Snippet: 18 F-FDG microPET/CT images of 2A3 tumour-bearing on day 15 post treatment: left panel—untreated mouse, middle panel—the mouse treated with cisplatin alone, right panel—the mouse treated with cisplatin and RIT. Green arrows are pointing to the tumours.

Article Snippet: The HPV16+ 2A3 cell line was produced by stably transfecting the FaDu cell line from the American Type Culture Collection with the LXSN 16E6/E7 as described in Harris et al (2011) .

Techniques:

Journal: British Journal of Cancer

Article Title: Combined treatment of the experimental human papilloma virus-16-positive cervical and head and neck cancers with cisplatin and radioimmunotherapy targeting viral E6 oncoprotein

doi: 10.1038/bjc.2013.43

Figure Lengend Snippet: Immunohistochemical evaluation of E6 and E7 oncogenes expression in RIT-treated CasKi and 2A3 cells. ( A ) E6 in CasKi cells, ( B ) E7 in CasKi cells; ( C ) E6 in 2A3 cells; ( D ) E7 in 2A3 cells. Left panels show untreated cells and right panels RIT-treated cells. Cells positive for E6 and E7 oncogenes stained brown. Original magnification × 400.

Article Snippet: The HPV16+ 2A3 cell line was produced by stably transfecting the FaDu cell line from the American Type Culture Collection with the LXSN 16E6/E7 as described in Harris et al (2011) .

Techniques: Immunohistochemical staining, Expressing, Staining

Journal: Oncoimmunology

Article Title: ERAP1 overexpression in HPV-induced malignancies: A possible novel immune evasion mechanism

doi: 10.1080/2162402X.2017.1336594

Figure Lengend Snippet: (A) Constitutive expression of the APM in keratinocyte cell lines on the mRNA level. Total RNA was purified from cells, reverse transcribed to cDNA and analyzed for APM component expression by qRT-PCR. PCR reactions were run in triplicates. The geometric mean of at least three of the following genes was used as internal reference: GAPDH, PGK1, PPIA and IPO8. Gene expression was calibrated to the NOK cell line. All quantitative qRT-PCR data were processed by LinRegPCR and data management was done by qbasePLUS 2. Log10 data were plotted as a heatmap using R. Expression of 20 APM components is shown. Each column represents a single gene and each row represents one cell line. Increased expression is shown in green and decreased expression is shown in red (see scale bar in the bottom right corner). HNSCC = head and neck squamous cell carcinoma. (B) APM components that showed a significantly elevated expression in HPV16-positive tumor cell lines compared to HPV-negative cells. Log10 expression data is plotted for each cell line, mean ± SD of each group is shown. *p ≤ 0.05, **p ≤ 0.01 (unpaired t-test).

Article Snippet: This study included 3 HPV-negative keratinocyte lines (NOK, HaCat, C33A [ATCC HTB-31]) and HPV-negative primary human keratinocytes [pHK] and primary human foreskin keratinocytes [pHFK]), 12 HPV16-positive cervical cancer cell lines (866, 915, Goe, Mar, CaSki [ATCC CRL-1550], SiHa [ATCC HTB-35], MRI-H196, SNU17, SNU703, SNU1000, SNU1005, SNU1299), 6 HPV16-positive head and neck squamous cell carcinoma (HNSCC) cell lines (SCC090, SCC152, SCC154, UDSCC2, UMSCC47, 93VU147T) and 5 cell lines transfected with the HPV16 genome (HPK1A, FK16A, C66-3, C66-7 and 2A3).

Techniques: Expressing, Purification, Quantitative RT-PCR

Journal: Oncoimmunology

Article Title: ERAP1 overexpression in HPV-induced malignancies: A possible novel immune evasion mechanism

doi: 10.1080/2162402X.2017.1336594

Figure Lengend Snippet: The effect of ERAP1 attenuation in target cells on cytotoxicity mediated by HPV16 E781–91-specific CD8+ T-cells. Vital-FR assay using HPV16 E781–91-specific CD8+ effector T-cells from a HLA-A2-positive donor. The HLA-A2-positive and HPV16-positive cell lines CaSki (A) and 866 (B) were used as target cells, whereas the HLA-matched HPV16-negative cell line C33A (HPV16- control cell line) served as background control. 24 h after siRNA transfection, target cells and titrated numbers of effector cells were incubated for 48 h and were then analyzed by flow cytometry. One representative experiment of two independent experiments is shown. The results are plotted as mean ± SD from at least duplicates.

Article Snippet: This study included 3 HPV-negative keratinocyte lines (NOK, HaCat, C33A [ATCC HTB-31]) and HPV-negative primary human keratinocytes [pHK] and primary human foreskin keratinocytes [pHFK]), 12 HPV16-positive cervical cancer cell lines (866, 915, Goe, Mar, CaSki [ATCC CRL-1550], SiHa [ATCC HTB-35], MRI-H196, SNU17, SNU703, SNU1000, SNU1005, SNU1299), 6 HPV16-positive head and neck squamous cell carcinoma (HNSCC) cell lines (SCC090, SCC152, SCC154, UDSCC2, UMSCC47, 93VU147T) and 5 cell lines transfected with the HPV16 genome (HPK1A, FK16A, C66-3, C66-7 and 2A3).

Techniques: Transfection, Incubation, Flow Cytometry