cell line generation human prostate cancer 22rv1 Search Results


99
ATCC human prostate carcinoma cell line 22rv1
FIGURE 5 APR‐246 preferentially inhibits tumor growth of <t>22Rv1</t> TP53 R175H mutant prostate cancer cells in vivo. (A) Representative images of 22Rv1 TP53 WT and R175H tumor treated with control vehicle, 25, and 80 mg/kg/day APR‐246 dosage. (B) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 WT tumor. (C) APR‐246 significantly inhibited 22Rv1 TP53 WT tumor growth. Control versus 25 mg/ kg, p = 0.0411. Control versus 80 mg/kg, p = 0.0134. 25 mg/kg/day versus 80 mg/kg/day p = 0.5611 (ns). (D) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 WT tumors. Control versus 25 mg/kg: HR = 2.422, 95% CI: 0.625–39.383, p = 0.0619(ns). Control versus 80 mg/ kg: HR = 7, 95% CI: 1.269–38.62, p = 0.0255. 25 versus 80 mg/kg/day: HR = 4.912, 95% CI: 1.001–24.10, p = 0.0498. (E) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 R175H tumors. (F) APR‐246 significantly inhibited 22Rv1 TP53 R175H tumor growth. Control versus 25 mg/kg, p = 0.0038. Control versus 80 mg/kg, p < 0.0001. 25 versus 80 mg/kg/day, p = 0.0368. (G) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 R175H tumors. Control versus 25 mg/kg: HR = 7.645, 95% CI: 1.473–39.68, p = 0.0155. Control versus 80 mg/kg: HR = 20.36, 95% CI: 3.389–122.4, p = 0.0016. 25 versus 80 mg/kg/day: HR = 13.24, 95% CI: 2.462–71.2, p = 0.0026. There were three male mice and three female mice in each treatment condition. [Color figure can be viewed at wileyonlinelibrary.com]
Human Prostate Carcinoma Cell Line 22rv1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC human prostate cancer cells
FIGURE 5 APR‐246 preferentially inhibits tumor growth of <t>22Rv1</t> TP53 R175H mutant prostate cancer cells in vivo. (A) Representative images of 22Rv1 TP53 WT and R175H tumor treated with control vehicle, 25, and 80 mg/kg/day APR‐246 dosage. (B) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 WT tumor. (C) APR‐246 significantly inhibited 22Rv1 TP53 WT tumor growth. Control versus 25 mg/ kg, p = 0.0411. Control versus 80 mg/kg, p = 0.0134. 25 mg/kg/day versus 80 mg/kg/day p = 0.5611 (ns). (D) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 WT tumors. Control versus 25 mg/kg: HR = 2.422, 95% CI: 0.625–39.383, p = 0.0619(ns). Control versus 80 mg/ kg: HR = 7, 95% CI: 1.269–38.62, p = 0.0255. 25 versus 80 mg/kg/day: HR = 4.912, 95% CI: 1.001–24.10, p = 0.0498. (E) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 R175H tumors. (F) APR‐246 significantly inhibited 22Rv1 TP53 R175H tumor growth. Control versus 25 mg/kg, p = 0.0038. Control versus 80 mg/kg, p < 0.0001. 25 versus 80 mg/kg/day, p = 0.0368. (G) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 R175H tumors. Control versus 25 mg/kg: HR = 7.645, 95% CI: 1.473–39.68, p = 0.0155. Control versus 80 mg/kg: HR = 20.36, 95% CI: 3.389–122.4, p = 0.0016. 25 versus 80 mg/kg/day: HR = 13.24, 95% CI: 2.462–71.2, p = 0.0026. There were three male mice and three female mice in each treatment condition. [Color figure can be viewed at wileyonlinelibrary.com]
Human Prostate Cancer Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC human prostate cell lines
FIGURE 5 APR‐246 preferentially inhibits tumor growth of <t>22Rv1</t> TP53 R175H mutant prostate cancer cells in vivo. (A) Representative images of 22Rv1 TP53 WT and R175H tumor treated with control vehicle, 25, and 80 mg/kg/day APR‐246 dosage. (B) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 WT tumor. (C) APR‐246 significantly inhibited 22Rv1 TP53 WT tumor growth. Control versus 25 mg/ kg, p = 0.0411. Control versus 80 mg/kg, p = 0.0134. 25 mg/kg/day versus 80 mg/kg/day p = 0.5611 (ns). (D) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 WT tumors. Control versus 25 mg/kg: HR = 2.422, 95% CI: 0.625–39.383, p = 0.0619(ns). Control versus 80 mg/ kg: HR = 7, 95% CI: 1.269–38.62, p = 0.0255. 25 versus 80 mg/kg/day: HR = 4.912, 95% CI: 1.001–24.10, p = 0.0498. (E) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 R175H tumors. (F) APR‐246 significantly inhibited 22Rv1 TP53 R175H tumor growth. Control versus 25 mg/kg, p = 0.0038. Control versus 80 mg/kg, p < 0.0001. 25 versus 80 mg/kg/day, p = 0.0368. (G) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 R175H tumors. Control versus 25 mg/kg: HR = 7.645, 95% CI: 1.473–39.68, p = 0.0155. Control versus 80 mg/kg: HR = 20.36, 95% CI: 3.389–122.4, p = 0.0016. 25 versus 80 mg/kg/day: HR = 13.24, 95% CI: 2.462–71.2, p = 0.0026. There were three male mice and three female mice in each treatment condition. [Color figure can be viewed at wileyonlinelibrary.com]
Human Prostate Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC crl 1978 22rv1 prostate atcc crl 2505 du 145 prostate atcc htb 81 lncap
FIGURE 5 APR‐246 preferentially inhibits tumor growth of <t>22Rv1</t> TP53 R175H mutant prostate cancer cells in vivo. (A) Representative images of 22Rv1 TP53 WT and R175H tumor treated with control vehicle, 25, and 80 mg/kg/day APR‐246 dosage. (B) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 WT tumor. (C) APR‐246 significantly inhibited 22Rv1 TP53 WT tumor growth. Control versus 25 mg/ kg, p = 0.0411. Control versus 80 mg/kg, p = 0.0134. 25 mg/kg/day versus 80 mg/kg/day p = 0.5611 (ns). (D) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 WT tumors. Control versus 25 mg/kg: HR = 2.422, 95% CI: 0.625–39.383, p = 0.0619(ns). Control versus 80 mg/ kg: HR = 7, 95% CI: 1.269–38.62, p = 0.0255. 25 versus 80 mg/kg/day: HR = 4.912, 95% CI: 1.001–24.10, p = 0.0498. (E) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 R175H tumors. (F) APR‐246 significantly inhibited 22Rv1 TP53 R175H tumor growth. Control versus 25 mg/kg, p = 0.0038. Control versus 80 mg/kg, p < 0.0001. 25 versus 80 mg/kg/day, p = 0.0368. (G) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 R175H tumors. Control versus 25 mg/kg: HR = 7.645, 95% CI: 1.473–39.68, p = 0.0155. Control versus 80 mg/kg: HR = 20.36, 95% CI: 3.389–122.4, p = 0.0016. 25 versus 80 mg/kg/day: HR = 13.24, 95% CI: 2.462–71.2, p = 0.0026. There were three male mice and three female mice in each treatment condition. [Color figure can be viewed at wileyonlinelibrary.com]
Crl 1978 22rv1 Prostate Atcc Crl 2505 Du 145 Prostate Atcc Htb 81 Lncap, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
ATCC prostate cancer cell line
FIGURE 5 APR‐246 preferentially inhibits tumor growth of <t>22Rv1</t> TP53 R175H mutant prostate cancer cells in vivo. (A) Representative images of 22Rv1 TP53 WT and R175H tumor treated with control vehicle, 25, and 80 mg/kg/day APR‐246 dosage. (B) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 WT tumor. (C) APR‐246 significantly inhibited 22Rv1 TP53 WT tumor growth. Control versus 25 mg/ kg, p = 0.0411. Control versus 80 mg/kg, p = 0.0134. 25 mg/kg/day versus 80 mg/kg/day p = 0.5611 (ns). (D) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 WT tumors. Control versus 25 mg/kg: HR = 2.422, 95% CI: 0.625–39.383, p = 0.0619(ns). Control versus 80 mg/ kg: HR = 7, 95% CI: 1.269–38.62, p = 0.0255. 25 versus 80 mg/kg/day: HR = 4.912, 95% CI: 1.001–24.10, p = 0.0498. (E) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 R175H tumors. (F) APR‐246 significantly inhibited 22Rv1 TP53 R175H tumor growth. Control versus 25 mg/kg, p = 0.0038. Control versus 80 mg/kg, p < 0.0001. 25 versus 80 mg/kg/day, p = 0.0368. (G) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 R175H tumors. Control versus 25 mg/kg: HR = 7.645, 95% CI: 1.473–39.68, p = 0.0155. Control versus 80 mg/kg: HR = 20.36, 95% CI: 3.389–122.4, p = 0.0016. 25 versus 80 mg/kg/day: HR = 13.24, 95% CI: 2.462–71.2, p = 0.0026. There were three male mice and three female mice in each treatment condition. [Color figure can be viewed at wileyonlinelibrary.com]
Prostate Cancer Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC lncap atcc human prostate cancer
FIGURE 5 APR‐246 preferentially inhibits tumor growth of <t>22Rv1</t> TP53 R175H mutant prostate cancer cells in vivo. (A) Representative images of 22Rv1 TP53 WT and R175H tumor treated with control vehicle, 25, and 80 mg/kg/day APR‐246 dosage. (B) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 WT tumor. (C) APR‐246 significantly inhibited 22Rv1 TP53 WT tumor growth. Control versus 25 mg/ kg, p = 0.0411. Control versus 80 mg/kg, p = 0.0134. 25 mg/kg/day versus 80 mg/kg/day p = 0.5611 (ns). (D) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 WT tumors. Control versus 25 mg/kg: HR = 2.422, 95% CI: 0.625–39.383, p = 0.0619(ns). Control versus 80 mg/ kg: HR = 7, 95% CI: 1.269–38.62, p = 0.0255. 25 versus 80 mg/kg/day: HR = 4.912, 95% CI: 1.001–24.10, p = 0.0498. (E) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 R175H tumors. (F) APR‐246 significantly inhibited 22Rv1 TP53 R175H tumor growth. Control versus 25 mg/kg, p = 0.0038. Control versus 80 mg/kg, p < 0.0001. 25 versus 80 mg/kg/day, p = 0.0368. (G) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 R175H tumors. Control versus 25 mg/kg: HR = 7.645, 95% CI: 1.473–39.68, p = 0.0155. Control versus 80 mg/kg: HR = 20.36, 95% CI: 3.389–122.4, p = 0.0016. 25 versus 80 mg/kg/day: HR = 13.24, 95% CI: 2.462–71.2, p = 0.0026. There were three male mice and three female mice in each treatment condition. [Color figure can be viewed at wileyonlinelibrary.com]
Lncap Atcc Human Prostate Cancer, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC human prostate cancer cell lines
FIGURE 5 APR‐246 preferentially inhibits tumor growth of <t>22Rv1</t> TP53 R175H mutant prostate cancer cells in vivo. (A) Representative images of 22Rv1 TP53 WT and R175H tumor treated with control vehicle, 25, and 80 mg/kg/day APR‐246 dosage. (B) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 WT tumor. (C) APR‐246 significantly inhibited 22Rv1 TP53 WT tumor growth. Control versus 25 mg/ kg, p = 0.0411. Control versus 80 mg/kg, p = 0.0134. 25 mg/kg/day versus 80 mg/kg/day p = 0.5611 (ns). (D) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 WT tumors. Control versus 25 mg/kg: HR = 2.422, 95% CI: 0.625–39.383, p = 0.0619(ns). Control versus 80 mg/ kg: HR = 7, 95% CI: 1.269–38.62, p = 0.0255. 25 versus 80 mg/kg/day: HR = 4.912, 95% CI: 1.001–24.10, p = 0.0498. (E) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 R175H tumors. (F) APR‐246 significantly inhibited 22Rv1 TP53 R175H tumor growth. Control versus 25 mg/kg, p = 0.0038. Control versus 80 mg/kg, p < 0.0001. 25 versus 80 mg/kg/day, p = 0.0368. (G) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 R175H tumors. Control versus 25 mg/kg: HR = 7.645, 95% CI: 1.473–39.68, p = 0.0155. Control versus 80 mg/kg: HR = 20.36, 95% CI: 3.389–122.4, p = 0.0016. 25 versus 80 mg/kg/day: HR = 13.24, 95% CI: 2.462–71.2, p = 0.0026. There were three male mice and three female mice in each treatment condition. [Color figure can be viewed at wileyonlinelibrary.com]
Human Prostate Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC human prostate adenocarcinoma cell lines
Fig. 1. Expression Analysis of Vav3 in Prostate Cancer Cells and in Human Prostate Cancer Specimens A, Vav3 expression in prostate cancer cell lines. Cell extracts (100 g) were used for Western blot analysis of Vav3 expression in LNCaP and LNCaP-AI cells, as well as PC3, <t>DU145,</t> and <t>22RV1</t> cells. -Actin is served as loading control. B, IHC analysis of Vav3 expression in human prostate cancer specimens. I, The normal prostate tissues are shown an area of unremarkable prostate glands and stroma with negative immunoreactivity for Vav3. II, An area of prostatic <t>adenocarcinoma</t> Gleason score 6 (33) with moderate to intense diffuse immunoreactivity for Vav3. III, An area of prostatic adenocarcinoma Gleason score 8 (44) with intense diffuse immunoreactivity for Vav3. The microphotographs of immunohistochemical staining are shown at original magnification of 400.
Human Prostate Adenocarcinoma Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC human prostate adenocarcinoma
Fig. 1. Expression Analysis of Vav3 in Prostate Cancer Cells and in Human Prostate Cancer Specimens A, Vav3 expression in prostate cancer cell lines. Cell extracts (100 g) were used for Western blot analysis of Vav3 expression in LNCaP and LNCaP-AI cells, as well as PC3, <t>DU145,</t> and <t>22RV1</t> cells. -Actin is served as loading control. B, IHC analysis of Vav3 expression in human prostate cancer specimens. I, The normal prostate tissues are shown an area of unremarkable prostate glands and stroma with negative immunoreactivity for Vav3. II, An area of prostatic <t>adenocarcinoma</t> Gleason score 6 (33) with moderate to intense diffuse immunoreactivity for Vav3. III, An area of prostatic adenocarcinoma Gleason score 8 (44) with intense diffuse immunoreactivity for Vav3. The microphotographs of immunohistochemical staining are shown at original magnification of 400.
Human Prostate Adenocarcinoma, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC prostate cancer cell lines
Fig. 1. Expression Analysis of Vav3 in Prostate Cancer Cells and in Human Prostate Cancer Specimens A, Vav3 expression in prostate cancer cell lines. Cell extracts (100 g) were used for Western blot analysis of Vav3 expression in LNCaP and LNCaP-AI cells, as well as PC3, <t>DU145,</t> and <t>22RV1</t> cells. -Actin is served as loading control. B, IHC analysis of Vav3 expression in human prostate cancer specimens. I, The normal prostate tissues are shown an area of unremarkable prostate glands and stroma with negative immunoreactivity for Vav3. II, An area of prostatic <t>adenocarcinoma</t> Gleason score 6 (33) with moderate to intense diffuse immunoreactivity for Vav3. III, An area of prostatic adenocarcinoma Gleason score 8 (44) with intense diffuse immunoreactivity for Vav3. The microphotographs of immunohistochemical staining are shown at original magnification of 400.
Prostate Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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DSMZ prostate
Fig. 1. Expression Analysis of Vav3 in Prostate Cancer Cells and in Human Prostate Cancer Specimens A, Vav3 expression in prostate cancer cell lines. Cell extracts (100 g) were used for Western blot analysis of Vav3 expression in LNCaP and LNCaP-AI cells, as well as PC3, <t>DU145,</t> and <t>22RV1</t> cells. -Actin is served as loading control. B, IHC analysis of Vav3 expression in human prostate cancer specimens. I, The normal prostate tissues are shown an area of unremarkable prostate glands and stroma with negative immunoreactivity for Vav3. II, An area of prostatic <t>adenocarcinoma</t> Gleason score 6 (33) with moderate to intense diffuse immunoreactivity for Vav3. III, An area of prostatic adenocarcinoma Gleason score 8 (44) with intense diffuse immunoreactivity for Vav3. The microphotographs of immunohistochemical staining are shown at original magnification of 400.
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BioResource International Inc human prostate cancer cell lines lncap
Fig. 1. Expression Analysis of Vav3 in Prostate Cancer Cells and in Human Prostate Cancer Specimens A, Vav3 expression in prostate cancer cell lines. Cell extracts (100 g) were used for Western blot analysis of Vav3 expression in LNCaP and LNCaP-AI cells, as well as PC3, <t>DU145,</t> and <t>22RV1</t> cells. -Actin is served as loading control. B, IHC analysis of Vav3 expression in human prostate cancer specimens. I, The normal prostate tissues are shown an area of unremarkable prostate glands and stroma with negative immunoreactivity for Vav3. II, An area of prostatic <t>adenocarcinoma</t> Gleason score 6 (33) with moderate to intense diffuse immunoreactivity for Vav3. III, An area of prostatic adenocarcinoma Gleason score 8 (44) with intense diffuse immunoreactivity for Vav3. The microphotographs of immunohistochemical staining are shown at original magnification of 400.
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FIGURE 5 APR‐246 preferentially inhibits tumor growth of 22Rv1 TP53 R175H mutant prostate cancer cells in vivo. (A) Representative images of 22Rv1 TP53 WT and R175H tumor treated with control vehicle, 25, and 80 mg/kg/day APR‐246 dosage. (B) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 WT tumor. (C) APR‐246 significantly inhibited 22Rv1 TP53 WT tumor growth. Control versus 25 mg/ kg, p = 0.0411. Control versus 80 mg/kg, p = 0.0134. 25 mg/kg/day versus 80 mg/kg/day p = 0.5611 (ns). (D) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 WT tumors. Control versus 25 mg/kg: HR = 2.422, 95% CI: 0.625–39.383, p = 0.0619(ns). Control versus 80 mg/ kg: HR = 7, 95% CI: 1.269–38.62, p = 0.0255. 25 versus 80 mg/kg/day: HR = 4.912, 95% CI: 1.001–24.10, p = 0.0498. (E) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 R175H tumors. (F) APR‐246 significantly inhibited 22Rv1 TP53 R175H tumor growth. Control versus 25 mg/kg, p = 0.0038. Control versus 80 mg/kg, p < 0.0001. 25 versus 80 mg/kg/day, p = 0.0368. (G) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 R175H tumors. Control versus 25 mg/kg: HR = 7.645, 95% CI: 1.473–39.68, p = 0.0155. Control versus 80 mg/kg: HR = 20.36, 95% CI: 3.389–122.4, p = 0.0016. 25 versus 80 mg/kg/day: HR = 13.24, 95% CI: 2.462–71.2, p = 0.0026. There were three male mice and three female mice in each treatment condition. [Color figure can be viewed at wileyonlinelibrary.com]

Journal: The Prostate

Article Title: TP53 structure-function relationships in metastatic castrate-sensitive prostate cancer and the impact of APR-246 treatment.

doi: 10.1002/pros.24629

Figure Lengend Snippet: FIGURE 5 APR‐246 preferentially inhibits tumor growth of 22Rv1 TP53 R175H mutant prostate cancer cells in vivo. (A) Representative images of 22Rv1 TP53 WT and R175H tumor treated with control vehicle, 25, and 80 mg/kg/day APR‐246 dosage. (B) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 WT tumor. (C) APR‐246 significantly inhibited 22Rv1 TP53 WT tumor growth. Control versus 25 mg/ kg, p = 0.0411. Control versus 80 mg/kg, p = 0.0134. 25 mg/kg/day versus 80 mg/kg/day p = 0.5611 (ns). (D) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 WT tumors. Control versus 25 mg/kg: HR = 2.422, 95% CI: 0.625–39.383, p = 0.0619(ns). Control versus 80 mg/ kg: HR = 7, 95% CI: 1.269–38.62, p = 0.0255. 25 versus 80 mg/kg/day: HR = 4.912, 95% CI: 1.001–24.10, p = 0.0498. (E) APR‐246 treatment did not cause changes in the body weight of mice carrying 22Rv1 TP53 R175H tumors. (F) APR‐246 significantly inhibited 22Rv1 TP53 R175H tumor growth. Control versus 25 mg/kg, p = 0.0038. Control versus 80 mg/kg, p < 0.0001. 25 versus 80 mg/kg/day, p = 0.0368. (G) APR‐246 treatment significantly prevented the development of large 22Rv1 TP53 R175H tumors. Control versus 25 mg/kg: HR = 7.645, 95% CI: 1.473–39.68, p = 0.0155. Control versus 80 mg/kg: HR = 20.36, 95% CI: 3.389–122.4, p = 0.0016. 25 versus 80 mg/kg/day: HR = 13.24, 95% CI: 2.462–71.2, p = 0.0026. There were three male mice and three female mice in each treatment condition. [Color figure can be viewed at wileyonlinelibrary.com]

Article Snippet: Human prostate carcinoma cell line 22Rv1, human prostate carcinoma cell line DU145, and immortalized human prostate RWPE‐1 prostate cancer cell lines were purchased from ATCC.

Techniques: Mutagenesis, In Vivo, Control

Fig. 1. Expression Analysis of Vav3 in Prostate Cancer Cells and in Human Prostate Cancer Specimens A, Vav3 expression in prostate cancer cell lines. Cell extracts (100 g) were used for Western blot analysis of Vav3 expression in LNCaP and LNCaP-AI cells, as well as PC3, DU145, and 22RV1 cells. -Actin is served as loading control. B, IHC analysis of Vav3 expression in human prostate cancer specimens. I, The normal prostate tissues are shown an area of unremarkable prostate glands and stroma with negative immunoreactivity for Vav3. II, An area of prostatic adenocarcinoma Gleason score 6 (33) with moderate to intense diffuse immunoreactivity for Vav3. III, An area of prostatic adenocarcinoma Gleason score 8 (44) with intense diffuse immunoreactivity for Vav3. The microphotographs of immunohistochemical staining are shown at original magnification of 400.

Journal: Molecular endocrinology (Baltimore, Md.)

Article Title: Vav3 oncogene is overexpressed and regulates cell growth and androgen receptor activity in human prostate cancer.

doi: 10.1210/me.2006-0048

Figure Lengend Snippet: Fig. 1. Expression Analysis of Vav3 in Prostate Cancer Cells and in Human Prostate Cancer Specimens A, Vav3 expression in prostate cancer cell lines. Cell extracts (100 g) were used for Western blot analysis of Vav3 expression in LNCaP and LNCaP-AI cells, as well as PC3, DU145, and 22RV1 cells. -Actin is served as loading control. B, IHC analysis of Vav3 expression in human prostate cancer specimens. I, The normal prostate tissues are shown an area of unremarkable prostate glands and stroma with negative immunoreactivity for Vav3. II, An area of prostatic adenocarcinoma Gleason score 6 (33) with moderate to intense diffuse immunoreactivity for Vav3. III, An area of prostatic adenocarcinoma Gleason score 8 (44) with intense diffuse immunoreactivity for Vav3. The microphotographs of immunohistochemical staining are shown at original magnification of 400.

Article Snippet: The human prostate adenocarcinoma cell lines (LNCaP, PC-3, DU145, and 22Rv1) and cervical carcinoma cell line Hela were obtained from ATCC (Manassas, VA) and maintained in RPMI 1640 medium supplemented with 10% FBS (complete medium) at 37 C in 5% CO2.

Techniques: Expressing, Western Blot, Control, Immunohistochemical staining, Staining