polyclonal anti eltd1  (Bioss)

Journal: BMC cancer

Article Title: Tumor endothelial ELTD1 as a predictive marker for treatment of renal cancer patients with sunitinib.

doi: 10.1186/s12885-020-06770-z

Figure Lengend Snippet: Fig. 2 Representative immunohistochemical images of ELTD1, CD34 and VEGFR2. Images demonstrating low ELTD1 (a), CD34 (b), VEGFR2 (c) and high ELTD1 (d), CD34 (e) and VEGFR2 (f) staining in the primary renal tumor vasculature in patients later treated for metastatic disease with sunitinib in the first or second line setting

Article Snippet: In this study we used the primary rabbit polyclonal antibody towards ELTD1 (HPA025229, Atlas Antibodies, Stockholm, Sweden), CD34 (CAB000018, Dako Cat#7165, Agilent (Formerly DakoCytomation) and VEGFR2 (CAB004028, Cell Signaling Technology Cat#2479, Cell Singaling Technology, Inc).

Techniques: Immunohistochemical staining, Staining

Journal: BMC cancer

Article Title: Tumor endothelial ELTD1 as a predictive marker for treatment of renal cancer patients with sunitinib.

doi: 10.1186/s12885-020-06770-z

Figure Lengend Snippet: Fig. 3 a and b: Progression free survival (3A) and overall survival (3B) and expression of ELTD1 in sunitinib treated patients. Patients treated for metastatic renal cell cancer with sunitinib in the first or second line setting (n = 77) comparing ELTD1 low versus ELTD1 high. c and d: Progression free survival (3C) and overall survival (3D) in sorafenib treated and expression of ELTD1. Patients treated for metastatic renal cell cancer with sorafenib in the first or second line setting (n = 53) comparing ELTD1 low versus ELTD1 high

Article Snippet: In this study we used the primary rabbit polyclonal antibody towards ELTD1 (HPA025229, Atlas Antibodies, Stockholm, Sweden), CD34 (CAB000018, Dako Cat#7165, Agilent (Formerly DakoCytomation) and VEGFR2 (CAB004028, Cell Signaling Technology Cat#2479, Cell Singaling Technology, Inc).

Techniques: Expressing

Journal: International Journal of Biological Sciences

Article Title: ELTD1 promotes invasion and metastasis by activating MMP2 in colorectal cancer

doi: 10.7150/ijbs.62293

Figure Lengend Snippet: Upregulation of ELTD1 expression in colon tumors from AOM/DSS-treated mice. (A) Establishment of the AOM/DSS-induced CAC model. (B, C) Representative photographs of macroscopic and histological observations (H&E) in colon tissue. (D) qRT-PCR measurement of ALDH1A3, ELTD1, EYA4, MYOD, and TERT expression in tumor tissues from AOM/DSS-treated mice or colon tissues from negative control mice. The results are shown as the mean ± SD (n = 10 for each group), **p<0.01 and *p<0.05. Scale bar=100 μm.

Article Snippet: Tissue slides were sequentially incubated with polyclonal rabbit anti-ELTD1 antibodies (Genetex, USA) at a 1:1000 dilution at 4°C overnight.

Techniques: Expressing, Quantitative RT-PCR, Negative Control

Journal: International Journal of Biological Sciences

Article Title: ELTD1 promotes invasion and metastasis by activating MMP2 in colorectal cancer

doi: 10.7150/ijbs.62293

Figure Lengend Snippet: ELTD1 was highly expressed in CRC and predicted poor prognosis. (A) Relative ELTD1 expression levels in CRC tissues and adjacent normal CRC tissues as detected by qRT-PCR (n=86). (B) Representative images of IHC staining of ELTD1 in CRC tissues and adjacent normal tissues. (C) Survival probability curves based on the expression of ELTD1 in CRC patients (n=279). *p<0.05. Scale bar=100 μm.

Article Snippet: Tissue slides were sequentially incubated with polyclonal rabbit anti-ELTD1 antibodies (Genetex, USA) at a 1:1000 dilution at 4°C overnight.

Techniques: Expressing, Quantitative RT-PCR, Immunohistochemistry

Journal: International Journal of Biological Sciences

Article Title: ELTD1 promotes invasion and metastasis by activating MMP2 in colorectal cancer

doi: 10.7150/ijbs.62293

Figure Lengend Snippet: Relationship between ELTD1 expression and clinicopathologic features of CRC patients (n = 86)

Article Snippet: Tissue slides were sequentially incubated with polyclonal rabbit anti-ELTD1 antibodies (Genetex, USA) at a 1:1000 dilution at 4°C overnight.

Techniques: Expressing

Journal: International Journal of Biological Sciences

Article Title: ELTD1 promotes invasion and metastasis by activating MMP2 in colorectal cancer

doi: 10.7150/ijbs.62293

Figure Lengend Snippet: Knockdown of ELTD1 inhibited CRC cell migration and invasion. (A, B) The efficiency of ELTD1 siRNA in HT29, RKO and HCT116 cells was verified by qRT-PCR (A) and Western blotting (B) . (C) Representative DAPI staining and statistical results of the migration of ELTD1-silenced CRC cells in the Transwell assay. (D) Invasion abilities of the two CRC cell lines were assessed by Transwell assay, followed by crystal violet staining and statistical analysis. The results are shown as the mean ± standard deviation (SD) of three independent experiments. **p <0.01 and *p<0.05. Scale bar=100 μm.

Article Snippet: Tissue slides were sequentially incubated with polyclonal rabbit anti-ELTD1 antibodies (Genetex, USA) at a 1:1000 dilution at 4°C overnight.

Techniques: Knockdown, Migration, Quantitative RT-PCR, Western Blot, Staining, Transwell Assay, Standard Deviation

Journal: International Journal of Biological Sciences

Article Title: ELTD1 promotes invasion and metastasis by activating MMP2 in colorectal cancer

doi: 10.7150/ijbs.62293

Figure Lengend Snippet: Overexpression of ELTD1 promoted CRC cell migration and invasion. (A, B) The mRNA and protein expression levels of ELTD1 were measured by qRT-PCR and Western blotting, respectively after transfection with the pEnCMV-ELTD1-3xFLAG plasmid. β-actin was used as the internal control. (C) Representative DAPI staining and statistical results of CRC cells in the Transwell assay. (D) Representative crystal violet staining and statistical results of CRC cells in the invasion assay. The results are shown as the mean ± standard deviation (SD) of three independent experiments. **p<0.01 and *p<0.05. Scale bar=100 μm.

Article Snippet: Tissue slides were sequentially incubated with polyclonal rabbit anti-ELTD1 antibodies (Genetex, USA) at a 1:1000 dilution at 4°C overnight.

Techniques: Over Expression, Migration, Expressing, Quantitative RT-PCR, Western Blot, Transfection, Plasmid Preparation, Control, Staining, Transwell Assay, Invasion Assay, Standard Deviation

Journal: International Journal of Biological Sciences

Article Title: ELTD1 promotes invasion and metastasis by activating MMP2 in colorectal cancer

doi: 10.7150/ijbs.62293

Figure Lengend Snippet: ELTD1 promoted CRC cell metastasis in vivo. (A) Representative gross photographs and in vivo fluorescence images of lung metastasis of mice treated with ELTD1 or vector as indicated. (n=5 for each group) (B) Representative HE-stained lung tissue samples. (C) Statistical results of metastasis nodule weight from the ELTD1 overexpression and control groups. Scale bar=100 μm.

Article Snippet: Tissue slides were sequentially incubated with polyclonal rabbit anti-ELTD1 antibodies (Genetex, USA) at a 1:1000 dilution at 4°C overnight.

Techniques: In Vivo, Fluorescence, Plasmid Preparation, Staining, Over Expression, Control

Journal: International Journal of Biological Sciences

Article Title: ELTD1 promotes invasion and metastasis by activating MMP2 in colorectal cancer

doi: 10.7150/ijbs.62293

Figure Lengend Snippet: ELTD1 regulated the expression of MMP2 at the transcriptional level. (A) mRNA expression levels of invasiveness-related genes in CRC cells were measured after ELTD1 knockdown. (B) Transcriptional activity of the MMP2 promoter was assessed after silencing ELTD1 expression in HT29, RKO and HCT116 cells. The results are shown as the mean ± standard deviation (SD) of three independent experiments. **p<0.01, *p<0.05

Article Snippet: Tissue slides were sequentially incubated with polyclonal rabbit anti-ELTD1 antibodies (Genetex, USA) at a 1:1000 dilution at 4°C overnight.

Techniques: Expressing, Knockdown, Activity Assay, Standard Deviation

Journal: International Journal of Biological Sciences

Article Title: ELTD1 promotes invasion and metastasis by activating MMP2 in colorectal cancer

doi: 10.7150/ijbs.62293

Figure Lengend Snippet: ELTD1 actively regulated the migration and invasion of CRC cells through MMP2. (A, B) The efficiency of the cotransfection of ELTD1 siRNA and MMP2-expressing plasmids into HT29, RKO and HCT116 cells was verified by qRT-PCR and Western blotting. (C, D) Transwell migration and invasion results of HT29 and RKO cells cotransfected with the MMP2 expression vector and si-ELTD1. The results are shown as the mean ± standard deviation (SD) of three independent experiments. **p<0.01, *p<0.05, ## p<0.01 and # p<0.05. Scale bar=100 μm.

Article Snippet: Tissue slides were sequentially incubated with polyclonal rabbit anti-ELTD1 antibodies (Genetex, USA) at a 1:1000 dilution at 4°C overnight.

Techniques: Migration, Cotransfection, Expressing, Quantitative RT-PCR, Western Blot, Plasmid Preparation, Standard Deviation

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: Monoclonal anti‐ELTD1 treatment is more effective in increasing animal survival and decreasing tumour volumes (TV). A, Per cent survival curve for all treatment groups; untreated control. pAb and mAb treatments were able to significantly increase the overall survival post‐tumour detection. B, Tumour volumes of each treatment group 9 days post‐tumour detection. pAb and mAb treatment significantly decreased TV compared with UT (* P = .0384, ** P = .0067). Representative morphological MR images for untreated (C), pAb treatment (D) and mAb treatment (E) 9 d post‐tumour detection with the tumour outlined in yellow

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: Monoclonal anti‐ELTD1 treatment normalizes vasculature within the tumour. Representative morphological images with respective MR perfusion maps for each treatment group at tumour maximum volume (TV:120‐160 mm 2 ): untreated control (A,B), pAb‐treated animals (C,D) and mAb‐treated animals (E,F). G, Quantitative analysis of tumour rCBF differences. The rCBF perfusion levels were significantly increased with both anti‐ELTD1 treatments. The mAb treatment was also able to normalize the perfusion levels (*** P = .0001 UT vs pAb, **** P < .0001 UT vs mAb)

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: Anti‐ELTD1 antibody therapy is effective in decreasing the microvessel density (MVD). Representative IHC images (20×) for CD34 from untreated (A), polyclonal anti‐ELTD1 (pAb)‐treated (B) and monoclonal anti‐ETLD1 (mAb)‐treated animals (C) at tumour maximum volume (TV 120‐160 mm 2 ). Dark red/brown staining in the slides represents vessels in the tumour region highlighted by the arrows. D, MVD analysis for all of the treatment groups. The pAb and mAb treatments were able to significantly decrease MVD (**** P < .0001 for both). There was also a significant decrease in MVD for the mAb vs the pAb (** P < .01)

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques: Staining

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: mAb ELTD1 probe has significantly higher binding specificity against the tumour. A, Molecular probe construct. Gd‐DTPA signal was used to detect the probe via MR imaging while the biotin tag allowed for localization in the tumour tissue post‐termination. B, Per cent relative expression of our molecular probes indicates a change in either T1 Relaxation or SI due to the presence of the Gd‐DTPA component. The mAb‐attached probe had significantly higher signal intensity and T1 relaxation time than the IgG control (T1: * P = .0307 (IgG vs pAb ELTD1 probe), *** P = .0002 (IgG vs mAb ELTD1 probe); SI: ** P = .008 (IgG vs mAb ELTD1 probe)), (C, D) localization and clustering of our monoclonal‐attached molecular probes (C) and non‐specific IgG‐attached molecular probe (D). E, Kinetics of the antibody‐attached probes, non‐specific IgG control, pAb and mAb against ELTD1. F‐H, Representative images (20×) stained with SA‐HRP to localize the non‐specific IgG‐attached probes (F), pAb‐attached probe (G) and mAb‐attached probe (H) at tumour maximum (TV: 120‐160 mm 2 ). The brown staining seen in the pAb‐ and mAb‐attached probes is the localized probes

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques: Binding Assay, Construct, Imaging, Expressing, Staining

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: mAb treatment against ELTD1 decrease Notch1 levels. A‐D, Representative images (20×) of IHC stained tumours with Notch1 of untreated (A), pAb treatment (B), mAb treated (C) and contralateral control (D). E, Quantitative positivity Notch staining of the samples. mAb against ELTD1‐treated mice significantly lowered Notch levels when compared to both untreated and pAb‐treated animals. There was no significant difference between untreated vs pAb treatment, and mAb treatment and contralateral (healthy control). Contralateral (Cont) tissue Notch levels were significantly lower than untreated mice and pAb‐treated animals (* P = .0357 (mAb vs pAb), ** P = .0015 (Cont vs pAb), *** P = .0006 (UT vs mAb), **** P < .0001 (UT vs Cont))

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques: Staining

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: A, Gene‐fold changes when comparing ELTD1 mAb‐treated mice to UT from up‐regulated (red) to down‐regulated (blue), obtained from RNA‐seq analysis. B, Gene‐gene correlations for the genes repressed after anti‐ELT1 mAb treatment. Red = positively correlated, green = negatively correlated. Using literature analysis software to categorize the groups of genes in terms of their published commonalities, they roughly fall into four categories (developmental genes, nestin‐related, cell proliferation/angiogenesis, astrocyte microglia inflammation)

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques: RNA Sequencing Assay, Software

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: Monoclonal anti‐ELTD1 treatment is more effective in increasing animal survival and decreasing tumour volumes (TV). A, Per cent survival curve for all treatment groups; untreated control. pAb and mAb treatments were able to significantly increase the overall survival post‐tumour detection. B, Tumour volumes of each treatment group 9 days post‐tumour detection. pAb and mAb treatment significantly decreased TV compared with UT (* P = .0384, ** P = .0067). Representative morphological MR images for untreated (C), pAb treatment (D) and mAb treatment (E) 9 d post‐tumour detection with the tumour outlined in yellow

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: Monoclonal anti‐ELTD1 treatment normalizes vasculature within the tumour. Representative morphological images with respective MR perfusion maps for each treatment group at tumour maximum volume (TV:120‐160 mm 2 ): untreated control (A,B), pAb‐treated animals (C,D) and mAb‐treated animals (E,F). G, Quantitative analysis of tumour rCBF differences. The rCBF perfusion levels were significantly increased with both anti‐ELTD1 treatments. The mAb treatment was also able to normalize the perfusion levels (*** P = .0001 UT vs pAb, **** P < .0001 UT vs mAb)

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: Anti‐ELTD1 antibody therapy is effective in decreasing the microvessel density (MVD). Representative IHC images (20×) for CD34 from untreated (A), polyclonal anti‐ELTD1 (pAb)‐treated (B) and monoclonal anti‐ETLD1 (mAb)‐treated animals (C) at tumour maximum volume (TV 120‐160 mm 2 ). Dark red/brown staining in the slides represents vessels in the tumour region highlighted by the arrows. D, MVD analysis for all of the treatment groups. The pAb and mAb treatments were able to significantly decrease MVD (**** P < .0001 for both). There was also a significant decrease in MVD for the mAb vs the pAb (** P < .01)

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques: Staining

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: mAb ELTD1 probe has significantly higher binding specificity against the tumour. A, Molecular probe construct. Gd‐DTPA signal was used to detect the probe via MR imaging while the biotin tag allowed for localization in the tumour tissue post‐termination. B, Per cent relative expression of our molecular probes indicates a change in either T1 Relaxation or SI due to the presence of the Gd‐DTPA component. The mAb‐attached probe had significantly higher signal intensity and T1 relaxation time than the IgG control (T1: * P = .0307 (IgG vs pAb ELTD1 probe), *** P = .0002 (IgG vs mAb ELTD1 probe); SI: ** P = .008 (IgG vs mAb ELTD1 probe)), (C, D) localization and clustering of our monoclonal‐attached molecular probes (C) and non‐specific IgG‐attached molecular probe (D). E, Kinetics of the antibody‐attached probes, non‐specific IgG control, pAb and mAb against ELTD1. F‐H, Representative images (20×) stained with SA‐HRP to localize the non‐specific IgG‐attached probes (F), pAb‐attached probe (G) and mAb‐attached probe (H) at tumour maximum (TV: 120‐160 mm 2 ). The brown staining seen in the pAb‐ and mAb‐attached probes is the localized probes

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques: Binding Assay, Construct, Imaging, Expressing, Staining

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: mAb treatment against ELTD1 decrease Notch1 levels. A‐D, Representative images (20×) of IHC stained tumours with Notch1 of untreated (A), pAb treatment (B), mAb treated (C) and contralateral control (D). E, Quantitative positivity Notch staining of the samples. mAb against ELTD1‐treated mice significantly lowered Notch levels when compared to both untreated and pAb‐treated animals. There was no significant difference between untreated vs pAb treatment, and mAb treatment and contralateral (healthy control). Contralateral (Cont) tissue Notch levels were significantly lower than untreated mice and pAb‐treated animals (* P = .0357 (mAb vs pAb), ** P = .0015 (Cont vs pAb), *** P = .0006 (UT vs mAb), **** P < .0001 (UT vs Cont))

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques: Staining

Journal: Journal of Cellular and Molecular Medicine

Article Title: Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model

doi: 10.1111/jcmm.14867

Figure Lengend Snippet: A, Gene‐fold changes when comparing ELTD1 mAb‐treated mice to UT from up‐regulated (red) to down‐regulated (blue), obtained from RNA‐seq analysis. B, Gene‐gene correlations for the genes repressed after anti‐ELT1 mAb treatment. Red = positively correlated, green = negatively correlated. Using literature analysis software to categorize the groups of genes in terms of their published commonalities, they roughly fall into four categories (developmental genes, nestin‐related, cell proliferation/angiogenesis, astrocyte microglia inflammation)

Article Snippet: Once tumours reached 6‐7 mm 3 (determined via MRI), mice were either left UT or were treated with 2 mg/kg of either polyclonal anti‐ELTD1 (Bioss, ETL/ELTD1 Polyclonal Antibody, bs‐13111R) or an optimized mAb against ELTD1 every 3‐4 days (treated M/Th, T/F, W/Sat).

Techniques: RNA Sequencing Assay, Software