Journal: Cancer research

Article Title: Biomarker based PET Imaging of Diffuse Intrinsic Pontine Glioma in Mouse Models

doi: 10.1158/0008-5472.CAN-16-2850

Figure Lengend Snippet: (a) Immunohistochemical staining of DIPG biopsy tissue for PARP1 protein and H&E. From left to right: low magnification overview, viable tumor tissue, tumor area with microvascular proliferation (MVP), and necrosis (N). (b) PARP1 staining of a DIPG autopsy specimen shows strong infiltrative growth of PARP1-positive tumor cells into the dentate nucleus (first row), while PARP1 expression and cellular density in the frontal cortex of the same brain (second row) is low (H&E in Supplementary Fig. 1a). (c) Quantification of PARP1 in biopsy and (d) autopsy specimens based on histological staining (brown stained area (=PARP1) vs. whole tissue area). N=4 histopathologically confirmed cases of DIPG; n=1 DIPG autopsy brain.

Article Snippet: Staining was carried out using primary antibodies against PARP1 (sc-7150, Santa Cruz Biotechnology), Ki67 (proliferation; AB16667, Abcam), and CD31 (endothelial cells; DIA-310, Dianova) using formalin-fixed, paraffin-embedded sections (FFPE) or frozen sections (indicated in the respective results section).

Techniques: Immunohistochemical staining, Staining, Expressing

Journal: Cancer research

Article Title: Biomarker based PET Imaging of Diffuse Intrinsic Pontine Glioma in Mouse Models

doi: 10.1158/0008-5472.CAN-16-2850

Figure Lengend Snippet: (a) Immunohistochemical staining of formalin-fixed, paraffin-embedded tumor-bearing brains following tumor generation in ntv-a/p53fl/fl mice injected with DF1 cells (transfected with RCAS-PDGFB, RCAS-Cre) in the brainstem at 2–4 days of age or right hemisphere at 4–6 weeks of age (Supplementary Fig. 1c). Anti-PARP1, anti-Ki67 (proliferation), and H&E staining for morphological evaluation were carried out on adjacent sections. (b) Quantification of PARP1 staining in juvenile and adult tumor-bearing mice in order to calculate the relative PARP1-positive area in relation to the entire tissue area. ROIs were placed on tumor (Tu) regions and anatomically defined brain regions (Co=cortex, Po=pons, Ce=cerebellum, Th=thalamus; n≥3 animals/4–7 ROIs per region; data represented as mean ± standard error). Statistical significance was determined using an unpaired Student’s t-test, corrected for multiple comparisons by the Holm-Sidak method with an alpha of 0.01. Automated analysis based on color thresholding was carried out using Metamorph Software. (c) Tumor-to-brain-area ratios are displayed as mean values ± standard error. N=4 animals for the juvenile brain; n=3 for the adult brain.

Article Snippet: Staining was carried out using primary antibodies against PARP1 (sc-7150, Santa Cruz Biotechnology), Ki67 (proliferation; AB16667, Abcam), and CD31 (endothelial cells; DIA-310, Dianova) using formalin-fixed, paraffin-embedded sections (FFPE) or frozen sections (indicated in the respective results section).

Techniques: Immunohistochemical staining, Staining, Formalin-fixed Paraffin-Embedded, Injection, Transfection, Software

Journal: Cancer research

Article Title: Biomarker based PET Imaging of Diffuse Intrinsic Pontine Glioma in Mouse Models

doi: 10.1158/0008-5472.CAN-16-2850

Figure Lengend Snippet: (a) Juvenile brainstem tumor-bearing ntv-a/p53fl/fl mice were intravenously injected with 22.4 nmol PARPi-FL upon occurrence of symptoms of tumor growth (gait instability, weight loss, crouching, head swelling). Brains were processed for cryoconservation 2 h p.i. of PARPi-FL. Cryosections were co-stained with Hoechst DNA stain and evaluated for presence of PARPi-FL (green fluorescence) using confocal microscopy. Adjacent sections were stained for PARP1 expression and H&E. Representative staining from n=5. (b) High magnification images from (a) showing nuclear localization of PARPi-FL, Hoechst, and PARP1. (c) [18F]PARPi accumulation in DIPG and healthy control mice after intravenous injection. 150–170 μCi [18F]PARPi were injected in juvenile brainstem tumor-bearing ntv-a/p53fl/fl mice (n=4) or healthy ntv-a/p53fl/fl control mice (n=2). For autoradiography, animals were sacrificed 2 h p.i., brains were extracted and flash-frozen, and 20 μm coronal cryosections were cut. Sections were exposed to a storage phosphor autoradiography plate overnight at −20 °C and read the following day. Adjacent sections were submitted for H&E staining for morphological confirmation that activity hotspots represent tumor tissue. (d) For signal quantification, ROIs were placed on activity hotspots, tumor-adjacent brain, and corresponding sections in healthy brains (n=3–8 ROIs per specimen) and results were pooled. (e) To evaluate the difference between tumor-bearing and non-tumor-bearing brains, ROIs were placed over entire tumor-bearing cross-sections, independent of size and number of activity hotspots and intensities were compared to non-tumor-bearing brains. (f) Calculation of signal ratios using mean values of ROI categories; t=tumor, n=normal brain, ta=tumor adjacent, h=hotspot, s=section. Statistical significance was determined using an unpaired student’s t-test, assuming equal SD of populations.

Article Snippet: Staining was carried out using primary antibodies against PARP1 (sc-7150, Santa Cruz Biotechnology), Ki67 (proliferation; AB16667, Abcam), and CD31 (endothelial cells; DIA-310, Dianova) using formalin-fixed, paraffin-embedded sections (FFPE) or frozen sections (indicated in the respective results section).

Techniques: Injection, Staining, Fluorescence, Confocal Microscopy, Expressing, Control, Autoradiography, Activity Assay

Journal: Cancer research

Article Title: Biomarker based PET Imaging of Diffuse Intrinsic Pontine Glioma in Mouse Models

doi: 10.1158/0008-5472.CAN-16-2850

Figure Lengend Snippet: In vivo PET/CT imaging and quantification of [18F]PARPi in juvenile brainstem tumor-bearing mice (ntv-a/p53fl/fl mice injected with transfected DF1 cells RCAS-PDGFB and RCAS-Cre in the brainstem at 2–4 days of age). [18F]PARPi was intravenously injected in tumor-bearing (DIPG) or healthy mice (control); to control for specificity, 1 mg olaparib was injected 30 min prior to [18F]PARPi (Block) to occupy specific binding sites (n=3/group). After imaging, intracardiac perfusion with 4% PFA was carried out and brains were conserved for histology. (a) Representative PET/CT images of the brainstem region compared to H&E and PARP1 staining of the same animals. (b) Quantification of %ID/g of the entire brain was derived from the PET/CT data set using the CT as reference for creating VOIs. (c) Similarly, the %ID/g was analyzed for the brainstem region using the CT as reference for creating VOIs. Statistical significance was determined using an unpaired student’s t-test assuming equal SD. White arrow points at tumor location.

Article Snippet: Staining was carried out using primary antibodies against PARP1 (sc-7150, Santa Cruz Biotechnology), Ki67 (proliferation; AB16667, Abcam), and CD31 (endothelial cells; DIA-310, Dianova) using formalin-fixed, paraffin-embedded sections (FFPE) or frozen sections (indicated in the respective results section).

Techniques: In Vivo, Positron Emission Tomography-Computed Tomography, Imaging, Injection, Transfection, Control, Blocking Assay, Binding Assay, Staining, Derivative Assay

Journal: Cancer research

Article Title: Biomarker based PET Imaging of Diffuse Intrinsic Pontine Glioma in Mouse Models

doi: 10.1158/0008-5472.CAN-16-2850

Figure Lengend Snippet: To evaluate the ability and quality of [18F]PARPi to delineate brain tumors in vivo, we compared [18F]PARPi PET/CT imaging to MRI and histology. First row (left to right): CT, PET, and PET/CT 1 h p.i. of [18F]PARPi. Second row (left to right): T2-weighted 1.05T MRI image, PARP1 IHC (brown staining) and H&E. All images are from the same animal. PET/CT and MRI were conducted on the same day and the animal was sacrificed immediately after MRI to preserve the brain for histology. White arrow indicates tumor location. Orange arrow points at an accumulation of cerebrospinal fluid (CSF), which causes a strong MRI signal, but is not seen in [18F]PARPi imaging.

Article Snippet: Staining was carried out using primary antibodies against PARP1 (sc-7150, Santa Cruz Biotechnology), Ki67 (proliferation; AB16667, Abcam), and CD31 (endothelial cells; DIA-310, Dianova) using formalin-fixed, paraffin-embedded sections (FFPE) or frozen sections (indicated in the respective results section).

Techniques: In Vivo, Positron Emission Tomography-Computed Tomography, Imaging, Staining

Journal: Cancer research

Article Title: Biomarker based PET Imaging of Diffuse Intrinsic Pontine Glioma in Mouse Models

doi: 10.1158/0008-5472.CAN-16-2850

Figure Lengend Snippet: (a) Representative PET/CT images of the same tumor-bearing animal (adult model, right hemisphere) using [18F]PARPi (2 h p.i.), [11C]Choline (5 min p.i.), [18F]FLT (2 h p.i.), and MRI (T2 weighted) compared to PARP1 IHC and H&E histology. [18F]FLT and MRI were conducted 48 h after the [18F]PARPi and [11C]Choline imaging. (b) Quantification of the mean %ID/g of a VOI in the tumor area compared to a control area in the back region of the brain. Statistical significance was determined using a paired t-test.

Article Snippet: Staining was carried out using primary antibodies against PARP1 (sc-7150, Santa Cruz Biotechnology), Ki67 (proliferation; AB16667, Abcam), and CD31 (endothelial cells; DIA-310, Dianova) using formalin-fixed, paraffin-embedded sections (FFPE) or frozen sections (indicated in the respective results section).

Techniques: Positron Emission Tomography-Computed Tomography, Imaging, Control

Journal: Cancer research

Article Title: Biomarker based PET Imaging of Diffuse Intrinsic Pontine Glioma in Mouse Models

doi: 10.1158/0008-5472.CAN-16-2850

Figure Lengend Snippet: (a) Tumor development was followed over the course of 6 weeks using ntv-a;p53fl/fl mice injected with DF1 cells in the right hemisphere at 4–6 weeks old (n=4 total, n=3 that showed tumor growth displayed in figure). In the displayed example the white arrow indicates tumor location. For weekly PET/CT imaging animals were injected with 100–200 μCi [18F]PARPi 2 h prior to PET/CT imaging. H&E and PARP1 histology were conducted after the last imaging time point. (b) To quantify uptake, VOIs were created in the tumor region and control region, using the PET/CT and histologically confirmed tumor location. These were then applied to earlier imaging time points. Mean (c) and max (d) %ID/g were quantified between week 3 and 6 post-tumor inoculation. One animal showed no tumor development and was histologically confirmed to have no tumor (Supplementary Fig. 7b).

Article Snippet: Staining was carried out using primary antibodies against PARP1 (sc-7150, Santa Cruz Biotechnology), Ki67 (proliferation; AB16667, Abcam), and CD31 (endothelial cells; DIA-310, Dianova) using formalin-fixed, paraffin-embedded sections (FFPE) or frozen sections (indicated in the respective results section).

Techniques: Injection, Positron Emission Tomography-Computed Tomography, Imaging, Control

Journal: Advanced Science

Article Title: Targeting the Notch1‐YY1‐ICAM1 Signaling Axis Enhances the Efficacy of Immunotherapy in HCC by Activating CD8 + T‐Cell‐Driven Cancer Cell Pyroptosis

doi: 10.1002/advs.202512845

Figure Lengend Snippet: High Notch1 expression indicates poor therapeutic efficacy of immune checkpoint inhibitors and poor outcomes in HCC patients. A) Therapeutic response to anti‐PD‐1/PD‐L1 monoclonal antibodies in two representative HCC patients with high or low N1ICD expression. Representative CT images, immunohistochemical staining of N1ICD and PD‐L1, serum AFP levels, and PFS data are shown. The tumor border is marked by red lines in the MR images. The red arrow indicates the timing of anti‐PD‐1/PD‐L1 treatment in HCC patients. B) High N1ICD expression correlated with poor progression‐free survival in HCC patients after receiving adjuvant anti‐PD‐L1/PD‐1 treatment ( n = 34 HCC patients; cohort 1). C) Therapeutic response to immunotherapy in HCC patients with low or high N1ICD expression according to the mRECIST guidelines according to the CT/MRI results. CR, complete response; PR, partial response; PD, progressive disease; SD, stable disease. D) Immunotherapeutic response in HCC patients with high or low N1ICD ( n = 34 HCC patients; cohort 1). Each sample on the violin plots represents individual patient data (NR = nontonder, R = responder). E) Western blot analysis confirmed the knockdown of N1ICD in Hepa‐1‐6 cells. F) C57BL/6 mice were orthotopically injected with Hepa‐1‐6 shN1ICD or Hepa‐1‐6 scr . The liver tumor‐bearing mice were intraperitoneally injected with 5 mg kg −1 PD‐L1 antibody or IgG control antibody on day 7 and treated twice a week for up to 2 weeks ( n = 5 mice per group). A representative gross tumor image from each group is shown. The bar chart shows the final tumor volume of each group. The means ± SEMs are given. ** p < 0.01, *** p < 0.001, **** p < 0.0001. B) Log‐rank test. D) Student's t ‐test. The scale bars in (A) represent 2 cm (white), A) 100 µm (black), and F) 1 cm.

Article Snippet: Once the tumors reached 50 mm 3 , the mice were randomly divided into two groups, which were given DC‐pulsed CD8 + T cells (i.e., adoptive cell transfer, ACT) in the presence of an anti‐PD‐L1 monoclonal antibody (aPD‐L1) (BioXCell, Cat. no. BP0101‐25MG) or an anti‐IgG control antibody (IgG) (DIA‐AN, Cat. no. Q6007‐10 mg).

Techniques: Expressing, Drug discovery, Clinical Proteomics, Bioprocessing, Immunohistochemical staining, Staining, Adjuvant, Western Blot, Knockdown, Injection, Control

Journal: Advanced Science

Article Title: Targeting the Notch1‐YY1‐ICAM1 Signaling Axis Enhances the Efficacy of Immunotherapy in HCC by Activating CD8 + T‐Cell‐Driven Cancer Cell Pyroptosis

doi: 10.1002/advs.202512845

Figure Lengend Snippet: N1ICD expression in cancer cells regulates human cytotoxic T lymphocyte‐mediated killing in vitro and in vivo. A) Both Western blot and RT‒PCR confirmed the knockdown of N1ICD in Huh7 cells. B) Preparation process of cancer cell lysate‐pulsed dendritic cells primed with CD8 + T cells (created with BioRender.com). C–E) LDH release assay of HepG2 N1ICD /HepG2 ctrl cells, Huh7 shN1ICD /Huh7 scr cells or MHCC‐97H shN1ICD /MHCC‐97H scr cells after co‐culture with tumor‐specific CD8 + T cells at different E/T ratios as indicated ( n = 3 independent experiments). F) Flow cytometry analysis of CD107a expression on tumor‐specific CD8 + T cells after co‐culture with HepG2 N1ICD /HepG2 ctrl cells, Huh7 shN1ICD /Huh7 scr cells or MHCC‐97H shN1ICD /MHCC‐97H scr cells (E/T ratio: 10:1) as indicated. G) Bar chart showing the ratio of CD8 + CD107a + T cells in each group. H) LDH release assays of Huh7 shN1ICD /MHCC‐97H shN1ICD cells after co‐culture with tumor‐specific CD8 + T cells (E/T ratio: 10:1) in the presence of the DMSO solvent control or BMS‐1 (10 µ m ). I) NOD/SCID mice were subcutaneously injected with 3 × 10 6 Huh7 shN1ICD cells, which were treated with either an anti‐PD‐L1 (aPD‐L1) or anti‐IgG (IgG) antibody together with adoptive cell transfer (ACT: tumor‐specific CD8 + T cells). A representative gross tumor image from each group is shown. J) Representative images of H&E‐stained sections from each group are shown. K) Tumor growth curves of Huh7 shN1ICD cells after treatment with tumor‐specific CD8 + T cells in the presence of aPD‐L1 or IgG ( n = 5 mice per group). L) Bar chart showing the final tumor volume in each treatment group ( n = 3 mice per group). The means ± SEMs are given. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. A,C–E,G,H,K,L) Student's t ‐test. The scale bars in (I) represent 1 cm, and those in (J) represent 50 µm.

Article Snippet: Once the tumors reached 50 mm 3 , the mice were randomly divided into two groups, which were given DC‐pulsed CD8 + T cells (i.e., adoptive cell transfer, ACT) in the presence of an anti‐PD‐L1 monoclonal antibody (aPD‐L1) (BioXCell, Cat. no. BP0101‐25MG) or an anti‐IgG control antibody (IgG) (DIA‐AN, Cat. no. Q6007‐10 mg).

Techniques: Expressing, In Vitro, In Vivo, Western Blot, Knockdown, Lactate Dehydrogenase Assay, Co-Culture Assay, Flow Cytometry, Solvent, Control, Injection, Staining

Journal: Advanced Science

Article Title: Targeting the Notch1‐YY1‐ICAM1 Signaling Axis Enhances the Efficacy of Immunotherapy in HCC by Activating CD8 + T‐Cell‐Driven Cancer Cell Pyroptosis

doi: 10.1002/advs.202512845

Figure Lengend Snippet: N1ICD regulates ICAM expression in cancer cells to determine the immunotherapeutic response in HCC. A) Heatmap showing the RNA sequencing results of N1ICD‐depleted Huh7 cells compared with scramble‐transfected cells. B) GO enrichment analysis revealed a significant difference in several biological processes between Huh7 shN1ICD cells and Huh7 scr cells. C) Venn diagram analysis of the GO biological processes revealed that the expression of IL18R1, CD47, LGALS3, ANXA1, TNFSF4, ZP3, ICAM1, IL7R, CD81, FUT7, MYB, IL18, PRKCZ, FCER1G, HLA‐DMB, and F2RL1 was altered in Huh7 shN1ICD cells compared with Huh7 scr cells . D) RT‒qPCR analysis of altered gene expression in HepG2 N1ICD /HepG2 ctrl cells, Huh7 shN1ICD /Huh7 scr cells, and MHCC‐97H shN1ICD /MHCC‐97H scr cells ( n = 3 independent experiments). F) Western blot analysis of ICAM1 expression in HepG2 N1ICD /HepG2 ctrl cells or Huh7 shN1ICD /Huh7 scr cells. G) Low ICAM1 expression correlated with poor progression‐free survival in HCC patients who received anti‐PD‐1/PD‐L1 antibody treatment ( n = 34 HCC patients; cohort 1). H) Therapeutic response to immunotherapy in HCC patients with low or high ICAM1 expression according to the mRECIST guidelines. I) Immunotherapeutic response in HCC patients with high or low ICAM1 ( n = 34 HCC patients, cohort 1). Each sample on the violin plots represents individual patient data. J) Representative high‐throughput automated confocal images and LDH release assay of ICAM1‐overexpressing Huh7 (Huh7 ICAM1 )/control empty vector‐transfected (Huh7 ctrl ) cells after co‐culture with tumor‐specific CD8 + T cells. K) At 7 days after orthotopic Hepa‐1‐6 N1ICD cell injection, the tumor‐bearing mice were treated with the PEI‐ICAM1 complex (2 mg kg −1 , i.v.) every three days for up to 7 days together with IgG or aPD‐L1 (5 mg kg −1 , i.p.) every 3 days for a total of 3 times. A representative gross tumor image from each treatment group is shown. The bar chart shows the final tumor volume in each group ( n = 5 mice per group). The means ± SEMs are given. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. C–E,I–K) Student's t test. (G) Log‐rank test. Scale bars in (L) represent 50 µm, (K) 1 cm.

Article Snippet: Once the tumors reached 50 mm 3 , the mice were randomly divided into two groups, which were given DC‐pulsed CD8 + T cells (i.e., adoptive cell transfer, ACT) in the presence of an anti‐PD‐L1 monoclonal antibody (aPD‐L1) (BioXCell, Cat. no. BP0101‐25MG) or an anti‐IgG control antibody (IgG) (DIA‐AN, Cat. no. Q6007‐10 mg).

Techniques: Expressing, RNA Sequencing, Transfection, Gene Expression, Western Blot, Clinical Proteomics, High Throughput Screening Assay, Lactate Dehydrogenase Assay, Control, Plasmid Preparation, Co-Culture Assay, Injection

Journal: Advanced Science

Article Title: Targeting the Notch1‐YY1‐ICAM1 Signaling Axis Enhances the Efficacy of Immunotherapy in HCC by Activating CD8 + T‐Cell‐Driven Cancer Cell Pyroptosis

doi: 10.1002/advs.202512845

Figure Lengend Snippet: Combined treatment with the PEI‐siYY1 complex and PD‐L1 antibody significantly repressed orthotopic HCC tumor growth without causing any adverse side effects. A) Schematic diagram of the combined treatment of PD‐L1 monoclonal antibody and DAPT or PEI‐siYY1 complex in the HCC mouse orthotopic model (created with BioRender.com). Seven days after orthotopic Hepa‐1‐6 cell injection, the tumor‐bearing mice were treated with either DAPT (10 mg kg −1 , s.c.) for 7 consecutive days or the PEI‐siYY1 complex (2 mg kg −1 , i.v.) every 3 days for up to 7 days together with the IgG control or PD‐L1 antibody (aPD‐L1) (5 mg kg −1 , i.p.) every 3 days for up to 3 times. Tumor growth was monitored via in vivo ultrasound imaging every 3 days for a total of 3 days ( n = 5 mice per group). B,C) Representative gross Hepa1‐6 N1ICD (B)‐ or Hepa1‐6 shN1ICD (C)‐derived tumor images from each treatment group are shown (left), and the final tumor volumes are shown in a bar chart (right). D) Representative images of immunohistochemical staining for YY1 in the heart, lung, spleen, and kidney. E) Representative ultrasound scanning images (left), gross tumor images (middle), and final tumor volume quantification (right) of Hepa1‐6 orthotopic tumor models treated with DAPT combined with an anti‐PD‐L1 antibody (or solvent control) are shown ( n = 5 mice per group). F) Representative ultrasound scanning images (left), gross tumor images (middle), and final tumor volume quantification (right) of Hepa1‐6 orthotopic tumor models treated with PEI‐siYY1 combined with an anti‐PD‐L1 antibody (or solvent control) are shown ( n = 5 mice per group). The means ± SEMs are given. ** p < 0.01, *** p < 0.001, **** p < 0.0001. B,C,E,F) Student's t ‐test. The scale bars in (E) represent 1 mm, (B,C,E,F) 1 cm, and (D) 50 µm.

Article Snippet: Once the tumors reached 50 mm 3 , the mice were randomly divided into two groups, which were given DC‐pulsed CD8 + T cells (i.e., adoptive cell transfer, ACT) in the presence of an anti‐PD‐L1 monoclonal antibody (aPD‐L1) (BioXCell, Cat. no. BP0101‐25MG) or an anti‐IgG control antibody (IgG) (DIA‐AN, Cat. no. Q6007‐10 mg).

Techniques: Injection, Control, In Vivo, Imaging, Derivative Assay, Immunohistochemical staining, Staining, Solvent

Journal: Translational Cancer Research

Article Title: Mitochondrial gene APOO reprograms lipid metabolism to influence the prognosis of breast cancer

doi: 10.21037/tcr-2025-aw-2554

Figure Lengend Snippet: Expression pattern, diagnostic value, and prognostic significance of APOO in breast cancer. (A) Paired t -test analysis of APOO mRNA expression between BC and adjacent normal tissues from the TCGA database (n=98). (B) ROC curve analysis evaluating the diagnostic performance of APOO expression in discriminating tumor from normal tissues in the TCGA-BRCA cohort. (C) Immunohistochemical comparison of APOO protein levels between BC ( https://www.proteinatlas.org/ENSG00000184831-APOO/cancer/breast+cancer#img ) and normal tissues ( https://www.proteinatlas.org/ENSG00000184831-APOO/tissue/breast#img ) from the HPA database. (D) APOO mRNA expression levels across various cell lines. (E,F) Kaplan-Meier curves depicting OS and DFS based on APOO expression stratification in TCGA-BRCA patients. *, P<0.05; ***, P<0.001. APOO, apolipoprotein O; AUC, area under the curve; BC, breast cancer; CI, confidence interval; DFS, disease-free survival; FPR, false positive rate; mRNA, messenger RNA; OS, overall survival; ROC, receiver operating characteristic; TCGA, The Cancer Genome Atlas; TCGA-BRCA, TCGA Breast Invasive Carcinoma cohort; TPM, transcripts per million; TPR, true positive rate.

Article Snippet: Immunohistochemical images of APOO protein expression were obtained from the Human Protein Atlas (HPA) database to evaluate differential protein expression between normal breast and breast cancer tissues.

Techniques: Expressing, Diagnostic Assay, Immunohistochemical staining, Comparison