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mesothelioma  (Novus Biologicals)


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    Novus Biologicals mesothelioma
    Representative immunofluorescent staining of cultured <t>mesothelioma</t> cells using AX10 antibody (a), immunohistochemical staining (b), and secondary antibody‐drug conjugate assay in vitro (c). (a) AX10 immunoreactivity in MPM‐1, −2, and −3 cells, representing sarcomatoid, epithelioid, and biphasic type mesothelioma, respectively. All MPM‐1, −2, and −3 cells exhibited AX10 antibody immunoreactivity at the cell surface. The staining was analyzed using a Guava easyCyte cell analyzer and accompanying software to obtain a one‐parameter log histogram. (b) AX10 immunoreactivity in various mesothelioma tissue specimens. Weak or no AX10 immunoreactivity was detected in five out of 10 epithelioid mesothelioma tissues (a). One out of five biphasic mesotheliomas exhibited AX10 immunoreactivity in spindle sarcomatoid components (arrow) but weak immunoreactivity in epithelioid components (arrowhead) (b). Five out of six sarcomatoid mesothelioma tissues exhibited strong AX10 immunoreactivity (c). Little AX10 immunoreactivity was detected in normal human tissues. No significant AX10 immunoreactivity was detected in the lung (d) (pleural mesothelial cells; insert) tissue specimens. Weak AX10 immunoreactivity was detected in myofibrous cells in the uterus (e). We did not detect any significant AX10 immunoreactivity in the brain, liver, or kidney, whereas strong AX10 immunoreactivity was observed in a nonmelanocytic (hypomelanocytic) melanoma tissue sample that was supplementally included in the microarray (f) (staining without AX10 antibody; insert). (c) MPM‐1 sarcomatoid mesothelioma cells were incubated with AX10 at 10, 100, and 1000 ng/mL followed by incubation with anti‐murine IgG (Fc) antibody conjugated to duocarmycin. Representative staining with Annexin V‐PI is presented. Note the dose‐dependent Annexin V‐positive and PI‐negative apoptotic MPM‐1 cells in the presence of AX10 antibody
    Mesothelioma, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tissue+microarray/pmc09475231-47-4-27?v=Novus+Biologicals
    Average 93 stars, based on 2 article reviews
    mesothelioma - by Bioz Stars, 2026-07
    93/100 stars

    Images

    1) Product Images from "Tumor suppressor effect of an antibody on xenotransplanted sarcomatoid mesothelioma cells"

    Article Title: Tumor suppressor effect of an antibody on xenotransplanted sarcomatoid mesothelioma cells

    Journal: Thoracic Cancer

    doi: 10.1111/1759-7714.14591

    Representative immunofluorescent staining of cultured mesothelioma cells using AX10 antibody (a), immunohistochemical staining (b), and secondary antibody‐drug conjugate assay in vitro (c). (a) AX10 immunoreactivity in MPM‐1, −2, and −3 cells, representing sarcomatoid, epithelioid, and biphasic type mesothelioma, respectively. All MPM‐1, −2, and −3 cells exhibited AX10 antibody immunoreactivity at the cell surface. The staining was analyzed using a Guava easyCyte cell analyzer and accompanying software to obtain a one‐parameter log histogram. (b) AX10 immunoreactivity in various mesothelioma tissue specimens. Weak or no AX10 immunoreactivity was detected in five out of 10 epithelioid mesothelioma tissues (a). One out of five biphasic mesotheliomas exhibited AX10 immunoreactivity in spindle sarcomatoid components (arrow) but weak immunoreactivity in epithelioid components (arrowhead) (b). Five out of six sarcomatoid mesothelioma tissues exhibited strong AX10 immunoreactivity (c). Little AX10 immunoreactivity was detected in normal human tissues. No significant AX10 immunoreactivity was detected in the lung (d) (pleural mesothelial cells; insert) tissue specimens. Weak AX10 immunoreactivity was detected in myofibrous cells in the uterus (e). We did not detect any significant AX10 immunoreactivity in the brain, liver, or kidney, whereas strong AX10 immunoreactivity was observed in a nonmelanocytic (hypomelanocytic) melanoma tissue sample that was supplementally included in the microarray (f) (staining without AX10 antibody; insert). (c) MPM‐1 sarcomatoid mesothelioma cells were incubated with AX10 at 10, 100, and 1000 ng/mL followed by incubation with anti‐murine IgG (Fc) antibody conjugated to duocarmycin. Representative staining with Annexin V‐PI is presented. Note the dose‐dependent Annexin V‐positive and PI‐negative apoptotic MPM‐1 cells in the presence of AX10 antibody
    Figure Legend Snippet: Representative immunofluorescent staining of cultured mesothelioma cells using AX10 antibody (a), immunohistochemical staining (b), and secondary antibody‐drug conjugate assay in vitro (c). (a) AX10 immunoreactivity in MPM‐1, −2, and −3 cells, representing sarcomatoid, epithelioid, and biphasic type mesothelioma, respectively. All MPM‐1, −2, and −3 cells exhibited AX10 antibody immunoreactivity at the cell surface. The staining was analyzed using a Guava easyCyte cell analyzer and accompanying software to obtain a one‐parameter log histogram. (b) AX10 immunoreactivity in various mesothelioma tissue specimens. Weak or no AX10 immunoreactivity was detected in five out of 10 epithelioid mesothelioma tissues (a). One out of five biphasic mesotheliomas exhibited AX10 immunoreactivity in spindle sarcomatoid components (arrow) but weak immunoreactivity in epithelioid components (arrowhead) (b). Five out of six sarcomatoid mesothelioma tissues exhibited strong AX10 immunoreactivity (c). Little AX10 immunoreactivity was detected in normal human tissues. No significant AX10 immunoreactivity was detected in the lung (d) (pleural mesothelial cells; insert) tissue specimens. Weak AX10 immunoreactivity was detected in myofibrous cells in the uterus (e). We did not detect any significant AX10 immunoreactivity in the brain, liver, or kidney, whereas strong AX10 immunoreactivity was observed in a nonmelanocytic (hypomelanocytic) melanoma tissue sample that was supplementally included in the microarray (f) (staining without AX10 antibody; insert). (c) MPM‐1 sarcomatoid mesothelioma cells were incubated with AX10 at 10, 100, and 1000 ng/mL followed by incubation with anti‐murine IgG (Fc) antibody conjugated to duocarmycin. Representative staining with Annexin V‐PI is presented. Note the dose‐dependent Annexin V‐positive and PI‐negative apoptotic MPM‐1 cells in the presence of AX10 antibody

    Techniques Used: Staining, Cell Culture, Immunohistochemical staining, In Vitro, Software, Microarray, Incubation

    AX10 does not affect cell proliferation, but significantly decreases Matrigel invasion activity of MPM‐1 sarcomatoid mesothelioma cells in vitro. (a) Representative cell proliferation assay. At 24 h, the cell number was 1.80 ± 0.10 (mock) and 1.77 ± 0.06 (AX10). Respective numbers at 48 h were 2.40 ± 0.10 (mock) and 2.37 ± 0.12 (AX10), while at 72 h they were 3.90 ± 0.20 (mock) and 4.20 ± 0.61 (AX10). The data represent means ± SD from triplicate assays (Student's t ‐test, p > 0.5). (b) AX10 significantly reduced Matrigel invasion activity of MPM‐1 cells (Student's t ‐test, p < 0.01). The number of invading cells was 59.7 ± 7.02 (mock) and 10.3 ± 1.52 (AX10) at 24 h, and 210.7 ± 11.4 (mock) and 15.0 ± 3.00 (AX10) at 48 h. Data from triplicate assays are expressed as means ± SD ( n = 3). (c) Cells that migrated to the lower surface of the membrane are shown (48 h). Original magnification, ×100
    Figure Legend Snippet: AX10 does not affect cell proliferation, but significantly decreases Matrigel invasion activity of MPM‐1 sarcomatoid mesothelioma cells in vitro. (a) Representative cell proliferation assay. At 24 h, the cell number was 1.80 ± 0.10 (mock) and 1.77 ± 0.06 (AX10). Respective numbers at 48 h were 2.40 ± 0.10 (mock) and 2.37 ± 0.12 (AX10), while at 72 h they were 3.90 ± 0.20 (mock) and 4.20 ± 0.61 (AX10). The data represent means ± SD from triplicate assays (Student's t ‐test, p > 0.5). (b) AX10 significantly reduced Matrigel invasion activity of MPM‐1 cells (Student's t ‐test, p < 0.01). The number of invading cells was 59.7 ± 7.02 (mock) and 10.3 ± 1.52 (AX10) at 24 h, and 210.7 ± 11.4 (mock) and 15.0 ± 3.00 (AX10) at 48 h. Data from triplicate assays are expressed as means ± SD ( n = 3). (c) Cells that migrated to the lower surface of the membrane are shown (48 h). Original magnification, ×100

    Techniques Used: Activity Assay, In Vitro, Proliferation Assay, Membrane

    Inhibitory effect of AX10 on MPM‐1 xenotransplanted sarcomatoid mesothelioma cell proliferation. (a) Inoculation of AX10 antibody delayed the growth of xenotransplanted MPM‐1 sarcomatoid mesothelioma tumors. On day 0, SCID‐NOD mice were subcutaneously implanted with MPM‐1 cells. The following day, day 3, the mice were administered AX10 antibody or vehicle only by intraperitoneal injection and weekly thereafter as indicated by arrows. Values are represented as means ± standard error for n = 5 mice. Statistical significance was measured by a two‐sided unpaired Student's t ‐test (* p < 0.01). (b) On day 42, the xenotransplanted tumors were excised to determine their weight. Total tumor weights are represented as means ± standard error for n = 5 mice. Statistical significance was measured by a two‐sided unpaired Student's t ‐test ( p < 0.01). (c) Gross and histological appearance of a representative xenotransplanted tumor. Arrowhead indicates the tumor without AX10 antibody, while the arrow indicates the small tumor remaining following weekly AX10 injection. Note the elimination of tumor cells, which were histologically replaced by regenerative muscle in mice inoculated with AX10 antibody. Scale bar indicates 100 μm
    Figure Legend Snippet: Inhibitory effect of AX10 on MPM‐1 xenotransplanted sarcomatoid mesothelioma cell proliferation. (a) Inoculation of AX10 antibody delayed the growth of xenotransplanted MPM‐1 sarcomatoid mesothelioma tumors. On day 0, SCID‐NOD mice were subcutaneously implanted with MPM‐1 cells. The following day, day 3, the mice were administered AX10 antibody or vehicle only by intraperitoneal injection and weekly thereafter as indicated by arrows. Values are represented as means ± standard error for n = 5 mice. Statistical significance was measured by a two‐sided unpaired Student's t ‐test (* p < 0.01). (b) On day 42, the xenotransplanted tumors were excised to determine their weight. Total tumor weights are represented as means ± standard error for n = 5 mice. Statistical significance was measured by a two‐sided unpaired Student's t ‐test ( p < 0.01). (c) Gross and histological appearance of a representative xenotransplanted tumor. Arrowhead indicates the tumor without AX10 antibody, while the arrow indicates the small tumor remaining following weekly AX10 injection. Note the elimination of tumor cells, which were histologically replaced by regenerative muscle in mice inoculated with AX10 antibody. Scale bar indicates 100 μm

    Techniques Used: Injection



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    Image Search Results


    Overexpression of DNPH1 in human breast tumors (A) DNPH1 mRNA expression in various breast cancer subtypes was analyzed in published microarray data. Mean with standard deviation and statistical significance compared to normal breast tissue are indicated; ∗∗∗∗, p < 0.0001 (one-way ANOVA, Tukey’s multiple comparisons test). (B) High (top quartile) DNPH1 mRNA levels predict reduced survival. Data derived from published microarray experiments ; p < 0.0001 (log rank test). (C) DNPH1 protein expression in human breast cell lines assayed by Western blotting. (D) Examples of immunohistochemical staining with DNPH1 antibodies on matching normal and cancerous breast tissue. Scale bars, 0.1 mm. (E) DNPH1 protein expression was measured by immunohistochemistry in 20 matching normal and cancerous human breast tissues; two-tailed, paired t test.

    Journal: iScience

    Article Title: Promotion of breast cancer by the DNPH1 enzyme

    doi: 10.1016/j.isci.2026.115227

    Figure Lengend Snippet: Overexpression of DNPH1 in human breast tumors (A) DNPH1 mRNA expression in various breast cancer subtypes was analyzed in published microarray data. Mean with standard deviation and statistical significance compared to normal breast tissue are indicated; ∗∗∗∗, p < 0.0001 (one-way ANOVA, Tukey’s multiple comparisons test). (B) High (top quartile) DNPH1 mRNA levels predict reduced survival. Data derived from published microarray experiments ; p < 0.0001 (log rank test). (C) DNPH1 protein expression in human breast cell lines assayed by Western blotting. (D) Examples of immunohistochemical staining with DNPH1 antibodies on matching normal and cancerous breast tissue. Scale bars, 0.1 mm. (E) DNPH1 protein expression was measured by immunohistochemistry in 20 matching normal and cancerous human breast tissues; two-tailed, paired t test.

    Article Snippet: Human breast tissue microarray , ISU Abxis , A312.

    Techniques: Over Expression, Expressing, Microarray, Standard Deviation, Derivative Assay, Western Blot, Immunohistochemical staining, Staining, Immunohistochemistry, Two Tailed Test

    Cell surface GRP78 colocalizes with ROR1, Cripto, and PD-L1 on late-stage patient GBM tissues but not on normal brain cerebrum tissues. A, three brain tissue microarrays with patient core tissue samples of GBM and normal tissues (#T174T from Biomax.us.) were stained for GBM markers. B, one microarray was stained with 4′,6-diamidino-2-phenylindole (DAPI) ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), ROR1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B2 (stage 4 GBM) and C7 (normal cerebrum) are pictured. C, a second microarray was stained with DAPI ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), PD-L1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B6 (stage 4 GBM) and C5 (normal cerebrum) are pictured. D, a third microarray was stained with DAPI ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), PD-L1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B6 (stage 4 GBM) and C5 (normal cerebrum) are pictured. Scale bars represent 400 μm (10×). All images are from the same magnification of (10×) 400 μm. GBM, glioblastoma multiforme; GRP78, glucose-regulated protein 78; PD-L1, programed death-ligand 1; ROR1, receptor tyrosine kinase–like orphan receptor-1.

    Journal: The Journal of Biological Chemistry

    Article Title: Inhibition of cell surface GRP78 on brain tumors reverses drug resistance and stops cancer stem cell expansion

    doi: 10.1016/j.jbc.2026.111146

    Figure Lengend Snippet: Cell surface GRP78 colocalizes with ROR1, Cripto, and PD-L1 on late-stage patient GBM tissues but not on normal brain cerebrum tissues. A, three brain tissue microarrays with patient core tissue samples of GBM and normal tissues (#T174T from Biomax.us.) were stained for GBM markers. B, one microarray was stained with 4′,6-diamidino-2-phenylindole (DAPI) ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), ROR1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B2 (stage 4 GBM) and C7 (normal cerebrum) are pictured. C, a second microarray was stained with DAPI ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), PD-L1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B6 (stage 4 GBM) and C5 (normal cerebrum) are pictured. D, a third microarray was stained with DAPI ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), PD-L1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B6 (stage 4 GBM) and C5 (normal cerebrum) are pictured. Scale bars represent 400 μm (10×). All images are from the same magnification of (10×) 400 μm. GBM, glioblastoma multiforme; GRP78, glucose-regulated protein 78; PD-L1, programed death-ligand 1; ROR1, receptor tyrosine kinase–like orphan receptor-1.

    Article Snippet: A, three brain tissue microarrays with patient core tissue samples of GBM and normal tissues (#T174T from Biomax.us.) were stained for GBM markers.

    Techniques: Staining, Microarray

    Cell surface GRP78 colocalizes with ROR1, Cripto, and PD-L1 on late-stage patient GBM tissues but not on normal brain cerebrum tissues. A, three brain tissue microarrays with patient core tissue samples of GBM and normal tissues (#T174T from Biomax.us.) were stained for GBM markers. B, one microarray was stained with 4′,6-diamidino-2-phenylindole (DAPI) ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), ROR1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B2 (stage 4 GBM) and C7 (normal cerebrum) are pictured. C, a second microarray was stained with DAPI ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), PD-L1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B6 (stage 4 GBM) and C5 (normal cerebrum) are pictured. D, a third microarray was stained with DAPI ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), PD-L1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B6 (stage 4 GBM) and C5 (normal cerebrum) are pictured. Scale bars represent 400 μm (10×). All images are from the same magnification of (10×) 400 μm. GBM, glioblastoma multiforme; GRP78, glucose-regulated protein 78; PD-L1, programed death-ligand 1; ROR1, receptor tyrosine kinase–like orphan receptor-1.

    Journal: The Journal of Biological Chemistry

    Article Title: Inhibition of cell surface GRP78 on brain tumors reverses drug resistance and stops cancer stem cell expansion

    doi: 10.1016/j.jbc.2026.111146

    Figure Lengend Snippet: Cell surface GRP78 colocalizes with ROR1, Cripto, and PD-L1 on late-stage patient GBM tissues but not on normal brain cerebrum tissues. A, three brain tissue microarrays with patient core tissue samples of GBM and normal tissues (#T174T from Biomax.us.) were stained for GBM markers. B, one microarray was stained with 4′,6-diamidino-2-phenylindole (DAPI) ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), ROR1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B2 (stage 4 GBM) and C7 (normal cerebrum) are pictured. C, a second microarray was stained with DAPI ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), PD-L1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B6 (stage 4 GBM) and C5 (normal cerebrum) are pictured. D, a third microarray was stained with DAPI ( blue -DNA), and antibodies to cell surface GRP78 ( green -FITC), PD-L1 ( red -PE). The last column is an overlay of all three stains to show colocalization. Cores B6 (stage 4 GBM) and C5 (normal cerebrum) are pictured. Scale bars represent 400 μm (10×). All images are from the same magnification of (10×) 400 μm. GBM, glioblastoma multiforme; GRP78, glucose-regulated protein 78; PD-L1, programed death-ligand 1; ROR1, receptor tyrosine kinase–like orphan receptor-1.

    Article Snippet: Briefly, three human brain tumors and normal brain tissue microarrays (T174c; Biomax. us) were deparaffinized with xylene and washed with PBS.

    Techniques: Staining, Microarray