Journal: Cancer Science

Article Title: Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/ Akt /mammalian target of rapamycin

doi: 10.1111/cas.13479

Figure Lengend Snippet: Mesenchymal stem cells conditioned media ( MSC ‐ CM ) promoted proliferation and inhibited apoptosis of head and neck cancer ( HNC ) cells. (A) Cell proliferation was assessed using CCK ‐8 assay. (B) Cell apoptosis assay was assessed by flow cytometric analysis of Annexin V and propidium iodide. (C) Flow cytometric analysis of cell cycle distribution. (D) Real‐time PCR analysis of P21 and P16 mRNA expression. (** P < .01)

Article Snippet: Human HNC cell lines CAL 27 were obtained from ATCC and HN4 were obtained from NIH.

Techniques: CCK-8 Assay, Apoptosis Assay, Real-time Polymerase Chain Reaction, Expressing

Journal: Cancer Science

Article Title: Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/ Akt /mammalian target of rapamycin

doi: 10.1111/cas.13479

Figure Lengend Snippet: Mesenchymal stem cells conditioned media ( MSC ‐ CM ) promoted migration of head and neck cancer ( HNC ) cells. (A,B) Transwell assay shows that MSC ‐ CM promoted the migration of CAL 27 and HN 4 cells. (C,D) Wound‐healing assay shows that MSC ‐ CM promoted the migration of CAL 27 and HN 4 cells. (** P < .01)

Article Snippet: Human HNC cell lines CAL 27 were obtained from ATCC and HN4 were obtained from NIH.

Techniques: Migration, Transwell Assay, Wound Healing Assay

Journal: Cancer Science

Article Title: Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/ Akt /mammalian target of rapamycin

doi: 10.1111/cas.13479

Figure Lengend Snippet: Mesenchymal stem cells conditioned media ( MSC ‐ CM ) promoted epithelial‐mesenchymal transformation ( EMT ) of head and neck cancer ( HNC ) cells. CAL 27 or HN 4 cells were treated with MSC ‐ CM or control media for 72 h, then gene and protein expression levels of EMT ‐related molecules were detected. (A) Real‐time PCR assay of Snail, Twist, E‐cadherin, N‐cadherin and Vimentin. (B) Western blot and quantification analysis of E‐cadherin, N‐cadherin and Vimentin. (* P < .05 and ** P < .01)

Article Snippet: Human HNC cell lines CAL 27 were obtained from ATCC and HN4 were obtained from NIH.

Techniques: Transformation Assay, Control, Expressing, Real-time Polymerase Chain Reaction, Western Blot

Journal: Cancer Science

Article Title: Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/ Akt /mammalian target of rapamycin

doi: 10.1111/cas.13479

Figure Lengend Snippet: Mesenchymal stem cells conditioned media ( MSC ‐ CM ) activated the phosphoinositide 3‐kinase ( PI 3K)/ Akt /mammalian target of rapamycin ( mTOR ) pathway and promoted Periostin ( POSTN ) in head and neck cancer ( HNC ) cells. CAL 27 and HN 4 cells were cultured in MSC ‐ CM or control media for 72 h. (A) Western blot assay of p‐ PI 3K, p‐ Akt and p‐ mTOR . (B) Real‐time PCR analysis of POSTN mRNA expression. (C) Western blot analysis of POSTN . (* P < .05 and ** P < .01)

Article Snippet: Human HNC cell lines CAL 27 were obtained from ATCC and HN4 were obtained from NIH.

Techniques: Cell Culture, Control, Western Blot, Real-time Polymerase Chain Reaction, Expressing

Journal: Cancer Science

Article Title: Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/ Akt /mammalian target of rapamycin

doi: 10.1111/cas.13479

Figure Lengend Snippet: Periostin ( POSTN )‐activated phosphoinositide 3‐kinase ( PI 3K)/ Akt /mammalian target of rapamycin ( mTOR ) signaling pathway promoted head and neck cancer ( HNC ) cells. (A) POSTN was silenced effectively by si RNA . (B) PI 3K/ Akt / mTOR pathway was inhibited when POSTN was silent. (C) Cell proliferation ability tested by CCK ‐8 assay. (D) mRNA expression of P16 and P21. (E) Cell migration ability tested by Transwell assay. (F) Western blot analysis of E‐cadherin, N‐cadherin and Vimentin. (G) Western blot assay of p‐ PI 3K and p‐ mTOR . (H) Cell proliferation ability. (I) mRNA expression of P16 and P21. (J) Cell migration ability. (** P < .01)

Article Snippet: Human HNC cell lines CAL 27 were obtained from ATCC and HN4 were obtained from NIH.

Techniques: CCK-8 Assay, Expressing, Migration, Transwell Assay, Western Blot

Journal: Cancer Science

Article Title: Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/ Akt /mammalian target of rapamycin

doi: 10.1111/cas.13479

Figure Lengend Snippet: Bone marrow mesenchymal stem cells ( BMMSC ) promoted tumorigenesis in murine models of head and neck cancer ( HNC ). CAL 27 in control medium, mesenchymal stem cells conditioned media ( MSC ‐ CM ), and mixed cells of CAL 27 and MSC were injected into the middle of the tongue of BALB /C mice. (A,B) Tumor invasion was assessed using H&E staining and immunohistochemistry ( IHC ) staining of Ki67. (C) Numbers of neck lymph node metastases were assessed. (D) Western blot analysis of Periostin ( POSTN ) in tumor tissues. (E) Western blot analysis of E‐cadherin and N‐cadherin in tumor tissues. (* P < .05 and ** P < .01)

Article Snippet: Human HNC cell lines CAL 27 were obtained from ATCC and HN4 were obtained from NIH.

Techniques: Control, Injection, Staining, Immunohistochemistry, Western Blot

Journal: Cancer Science

Article Title: Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/ Akt /mammalian target of rapamycin

doi: 10.1111/cas.13479

Figure Lengend Snippet: Periostin ( POSTN ) and N‐cadherin were highly expressed in head and neck cancer ( HNC ) cancer samples. Positive staining of POSTN and N‐cadherin was mainly located in the cell cytoplasm which showed brown granules. (A) Immunohistochemistry ( IHC ) staining of POSTN in well, moderate and poorly differentiated HNC tissues. (B) IHC staining of N‐cadherin in well, moderate and poorly differentiated HNC tissues

Article Snippet: Human HNC cell lines CAL 27 were obtained from ATCC and HN4 were obtained from NIH.

Techniques: Staining, Immunohistochemistry

Journal: Respiratory Research

Article Title: Integrative bioinformatics and machine learning reveal an association of LTF and MMP8 with systemic inflammation and lung injury

doi: 10.1186/s12931-026-03704-4

Figure Lengend Snippet: Correlation analysis of LTF and MMP8 expression levels with immune cell infiltration. ( A ) Expression levels of LTF and MMP8 in control and systemic inflammation groups from the human dataset ( GSE32707 ). ( B ) Expression levels of the mouse orthologs Ltf and Mmp8 in normal control and LPS-induced lung injury groups from the murine model ( GSE216943 ). Data are presented as box plots. ( C ) ROC curve of LTF for systemic inflammation diagnosis (AUC = 0.788, 95% CI: 0.694–0.871). ( D ) ROC curve of MMP8 for systemic inflammation diagnosis (AUC = 0.774, 95% CI: 0.681–0.855). ( E ) Immune cell infiltration profiles in control and systemic inflammation groups. ( F ) Correlation of LTF and MMP8 with immune cell types and inter-cell correlations. ( G ) Correlation dot plot of LTF expression with immune infiltration (color and dot size indicate correlation coefficient and strength). ( H ) Correlation dot plot of MMP8 expression with immune infiltration. ( I – J ) GSEA showing association between LTF expression and GO terms ( I ) and KEGG pathways ( J )

Article Snippet: Antibodies against LTF (Proteintech, 10933-1-AP) and MMP8 (ABclonal, A1963) were used.

Techniques: Expressing, Control, Biomarker Discovery

Journal: Respiratory Research

Article Title: Integrative bioinformatics and machine learning reveal an association of LTF and MMP8 with systemic inflammation and lung injury

doi: 10.1186/s12931-026-03704-4

Figure Lengend Snippet: Verification of LTF and MMP8 expression levels in lung injury using human specimens and cell models. ( A ) Serum levels of LTF and MMP8 in controls and ALI patients. ( B ) Western blot of LTF and MMP8 in lung tissues. ( C ) Semi-quantitative analysis of protein expression. ( D ) qPCR of LTF and MMP8 mRNA in lung tissues. ( E ) Cell treatment flowchart: BEAS-2B and RAW264.7 cells treated with MP and LPS. ( F–G ) Western blot ( F ) and semi-quantification ( G ) of LTF and MMP8 in BEAS-2B cells. ( H–I ) Western blot ( H ) and semi-quantification ( I ) in RAW264.7 cells. ( J ) qPCR of LTF and MMP8 in BEAS-2B cells. ( K ) qPCR of Ltf and Mmp8 in RAW264.7 cells. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: Antibodies against LTF (Proteintech, 10933-1-AP) and MMP8 (ABclonal, A1963) were used.

Techniques: Expressing, Western Blot

Journal: Respiratory Research

Article Title: Integrative bioinformatics and machine learning reveal an association of LTF and MMP8 with systemic inflammation and lung injury

doi: 10.1186/s12931-026-03704-4

Figure Lengend Snippet: Validation of LTF and MMP8 expression levels in lung injury using animal models. ( A ) Flowchart of the mouse lung injury model experiment. Mice were intraperitoneally injected with MP and LPS, and 6 hours later, intratracheally instilled with LPS or saline. Mice were sacrificed 6 hours later, and lung tissue samples were collected. ( B ) HE staining results demonstrate successful model establishment. ( C ) Serum levels of LTF and MMP8 measured by ELISA in mice. ( D ) qPCR quantification analysis of animal tissue samples. qPCR analysis of Ltf and Mmp8 mRNA expression in lung tissues. ( E-F ) Western blot analysis of the protein expression of LTF and MMP8 in lung tissues. ( G-H ) Immunohistochemical staining results showing the expression of LTF and MMP8 in lung tissues ( G ) and a corresponding semi-quantitative bar graph ( H ). Data are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: Antibodies against LTF (Proteintech, 10933-1-AP) and MMP8 (ABclonal, A1963) were used.

Techniques: Biomarker Discovery, Expressing, Injection, Saline, Staining, Enzyme-linked Immunosorbent Assay, Western Blot, Immunohistochemical staining

Journal: Respiratory Research

Article Title: Integrative bioinformatics and machine learning reveal an association of LTF and MMP8 with systemic inflammation and lung injury

doi: 10.1186/s12931-026-03704-4

Figure Lengend Snippet: Interaction and regulatory networks of LTF and MMP8. ( A - B ) Three-dimensional protein structures of LTF (A) and MMP8 ( B ). ( C ) PPI network. Nodes represent proteins, and lines represent interactions between proteins. ( D ) Co-IP of HA-LTF and Flag-MMP8 in HEK293T cells using anti-Flag and anti-HA antibodies. ( E ) Endogenous Co-IP analysis of LTF and MMP8 in BEAS-2B cells. ( F ) Gene regulatory network centered on the LTF gene. Blue nodes represent the LTF gene, green nodes represent miRNAs, and pink nodes represent other genes. ( G - H ) Predicted molecular docking structures showing the binding affinity of LTF ( G ) and MMP8 ( H ) with MP. The red dashed areas indicated by red arrows represent the simulated binding sites of MP

Article Snippet: Antibodies against LTF (Proteintech, 10933-1-AP) and MMP8 (ABclonal, A1963) were used.

Techniques: Co-Immunoprecipitation Assay, Binding Assay

Journal: International Journal of Molecular Sciences

Article Title: Macrophage Profiling in Head and Neck Cancer to Improve Patient Prognosis and Assessment of Cancer Cell–Macrophage Interactions Using Three-Dimensional Coculture Models

doi: 10.3390/ijms241612813

Figure Lengend Snippet: Coculture of FaDu cells and macrophages in spheroids. ( A ) Photographs of spheroids containing cancer cells with or without macrophages. ( B ) Quantification of spheroid volumes for the different coculture conditions (scale = 250 μm). ( C ) Comparison of Ki-67 proliferation marker expression by immunofluorescence in the different coculture conditions on day 7. ( D ) Quantitative data of Ki-67 expression performed with QuPath. Mean + SD, ANOVA one-way, and Tukey’s post hoc test (* p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001), n = 8.

Article Snippet: The FaDu human HNC cell line (ATCC ® HTB-43, Manassas, VA, USA) was cultured in RPMI (Roswell Park Memorial Institute Medium 1640, Lonza, Basel, Switzerland) containing 10% heat-inactivated fetal bovine serum (FBS Premium South America, PAN BIOTECH, Aidenbach, Germany); 5% L–glutamine (200 mM, Gibco, Thermo Fisher Scientific, Waltham, MA, USA); and 1% penicillin/streptomycin (10,000 U/mL/10,000 μg/mL, Gibco, Thermo Fisher Scientific) and maintained at 37 °C under 5% CO 2 .

Techniques: Comparison, Marker, Expressing, Immunofluorescence

Journal: International Journal of Molecular Sciences

Article Title: Macrophage Profiling in Head and Neck Cancer to Improve Patient Prognosis and Assessment of Cancer Cell–Macrophage Interactions Using Three-Dimensional Coculture Models

doi: 10.3390/ijms241612813

Figure Lengend Snippet: Effect of cancer cells on monocyte polarization. ( A ) Evaluation of the expression of macrophage phenotypic markers: CD68, CD86, and CD206 on day 7 in the different coculture conditions (scale = 50 μm); M1–FaDu and M2–FaDu were used as positive control. ( B , C ) FACS analyses to quantify the percentage of M1 and M2 markers in FaDu–monocyte dissociated spheroids. Dot plots of CD206 expressed on FaDu spheroids, used as a negative control (no macrophage), and in monocytes–FaDu spheroids.

Article Snippet: The FaDu human HNC cell line (ATCC ® HTB-43, Manassas, VA, USA) was cultured in RPMI (Roswell Park Memorial Institute Medium 1640, Lonza, Basel, Switzerland) containing 10% heat-inactivated fetal bovine serum (FBS Premium South America, PAN BIOTECH, Aidenbach, Germany); 5% L–glutamine (200 mM, Gibco, Thermo Fisher Scientific, Waltham, MA, USA); and 1% penicillin/streptomycin (10,000 U/mL/10,000 μg/mL, Gibco, Thermo Fisher Scientific) and maintained at 37 °C under 5% CO 2 .

Techniques: Expressing, Positive Control, Negative Control

Journal: International Journal of Molecular Sciences

Article Title: Macrophage Profiling in Head and Neck Cancer to Improve Patient Prognosis and Assessment of Cancer Cell–Macrophage Interactions Using Three-Dimensional Coculture Models

doi: 10.3390/ijms241612813

Figure Lengend Snippet: mRNA relative expression (2 −ΔCt ) to characterize macrophage phenotype using ( A ) M1 markers (CD80, CD86) and ( B ) M2 markers (IL10, CD206). The analyses by RT-qPCR and the normalization with 18S expression were conducted on dissociated FaDu and monocytes–FaDu, M1–FaDu, and M2–FaDu spheroids. Mean + SD, t -test, * = p ≤ 0.05, *** p ≤ 0.001.

Article Snippet: The FaDu human HNC cell line (ATCC ® HTB-43, Manassas, VA, USA) was cultured in RPMI (Roswell Park Memorial Institute Medium 1640, Lonza, Basel, Switzerland) containing 10% heat-inactivated fetal bovine serum (FBS Premium South America, PAN BIOTECH, Aidenbach, Germany); 5% L–glutamine (200 mM, Gibco, Thermo Fisher Scientific, Waltham, MA, USA); and 1% penicillin/streptomycin (10,000 U/mL/10,000 μg/mL, Gibco, Thermo Fisher Scientific) and maintained at 37 °C under 5% CO 2 .

Techniques: Expressing, Quantitative RT-PCR

Journal: International Journal of Molecular Sciences

Article Title: Macrophage Profiling in Head and Neck Cancer to Improve Patient Prognosis and Assessment of Cancer Cell–Macrophage Interactions Using Three-Dimensional Coculture Models

doi: 10.3390/ijms241612813

Figure Lengend Snippet: mRNA relative expression (2 −ΔCt ) to characterize EMT markers (E-cadherin and Vimentin). The analyses by RT-qPCR and the normalization with 18S expression were performed on dissociated FaDu and monocytes–FaDu spheroids. Mean + SD, t -test, * = p ≤ 0.05.

Article Snippet: The FaDu human HNC cell line (ATCC ® HTB-43, Manassas, VA, USA) was cultured in RPMI (Roswell Park Memorial Institute Medium 1640, Lonza, Basel, Switzerland) containing 10% heat-inactivated fetal bovine serum (FBS Premium South America, PAN BIOTECH, Aidenbach, Germany); 5% L–glutamine (200 mM, Gibco, Thermo Fisher Scientific, Waltham, MA, USA); and 1% penicillin/streptomycin (10,000 U/mL/10,000 μg/mL, Gibco, Thermo Fisher Scientific) and maintained at 37 °C under 5% CO 2 .

Techniques: Expressing, Quantitative RT-PCR

Journal: International Journal of Molecular Sciences

Article Title: Macrophage Profiling in Head and Neck Cancer to Improve Patient Prognosis and Assessment of Cancer Cell–Macrophage Interactions Using Three-Dimensional Coculture Models

doi: 10.3390/ijms241612813

Figure Lengend Snippet: Human Cytokine Array Membrane ( A , B ) of supernatant of FaDu cancer cell spheroids and monocytes–FaDu spheroids on day 7. ( A ) Membranes. ( B ) Quantification showing the mean signal intensity ( n = 3) normalized to positive control (Ctrl+). mRNA relative expression (2 −ΔCt ) of CCL2 and IL8 cytokines ( C , D ). Analyses by RT-qPCR and normalization with 18S expression on dissociated FaDu and monocytes–FaDu spheroids. Mean + SD, t -test, * = p ≤ 0.05, *** p ≤ 0.001.

Article Snippet: The FaDu human HNC cell line (ATCC ® HTB-43, Manassas, VA, USA) was cultured in RPMI (Roswell Park Memorial Institute Medium 1640, Lonza, Basel, Switzerland) containing 10% heat-inactivated fetal bovine serum (FBS Premium South America, PAN BIOTECH, Aidenbach, Germany); 5% L–glutamine (200 mM, Gibco, Thermo Fisher Scientific, Waltham, MA, USA); and 1% penicillin/streptomycin (10,000 U/mL/10,000 μg/mL, Gibco, Thermo Fisher Scientific) and maintained at 37 °C under 5% CO 2 .

Techniques: Membrane, Positive Control, Expressing, Quantitative RT-PCR

Journal: The Journal of Biological Chemistry

Article Title: Plasma membrane proteoglycans syndecan-2 and syndecan-4 engage with EGFR and RON kinase to sustain carcinoma cell cycle progression

doi: 10.1016/j.jbc.2022.102029

Figure Lengend Snippet: SSTN-induced cell cycle arrest depends on activated p38MAPK. A , quantification of p38MAPK activation by antibody array (pT180/pY182) in nontransformed keratinocytes (HTE, NOK, and HaCaT) and HNSCC cells (UM-SCC47, SCC25) treated with 30 mM SSTN EGFR ( left ) or in-cell western of UM-SCC47 cells following treatment with SSTNEGFR, RON kinase inhibitors (BMS-777607 or CAS-913376-84-8), or ABL1 inhibitors (GNF-5 or PPY-A)( right ); B , detection of pT180/pY182 p38MAPK following treatment with vehicle alone or 30 μM SSTN EGFR in nontransformed NOKs or transformed HNSCC cells; C , in nontransformed (MCF10A) or transformed (MDA-MB-231, MDA-MB-468, SKBr3) mammary epithelial cells; D , EdU-Click-IT–labeled UM-SCC47 cells treated for 3 h with either vehicle (control), 30 μM SSTN EGFR , 3 μM BMS-777607 (RON inhibitor), 0.2 μM PPY-A (ABL1 inhibitor), or 5 mM hydroxyurea (HU) in the presence or absence of 0.1 μM p38MAPK inhibitor BIRB-796 (Bar = 50 μm); E , quantification of EdU incorporation into cells treated with 30 μM SSTN EGFR with or without p38MAPK inhibitors BIRB-796 or Losmapimod for 3 h; ∗∗∗ p ≤ 0.001. EdU, 5-ethynyl-2′-deoxyuridine; HNSCC, head and neck squamous cell carcinoma; HTE, human tonsillar epithelial cell; NOK, normal oral keratinocyte; P38MAPK, p38 mitogen-activated protein kinase.

Article Snippet: Human mammary MCF10A (CVCL 0598), MDA-MB-231 (CVCL 0062), MDA-MB-468 (CVCL 0419) cells, and human SCC25 HNC (CVCL 1682) cells were from ATCC.

Techniques: Activation Assay, Ab Array, In-Cell ELISA, Transformation Assay, Labeling, Control

Journal: International Journal of Molecular Medicine

Article Title: Tribbles pseudokinase 3 drives cancer stemness in oral squamous cell carcinoma cells by supporting the expression levels of SOX2 and EGFR

doi: 10.3892/ijmm.2025.5485

Figure Lengend Snippet: TRIB3 expression is positively correlated with the poorer overall survival in the TCGA HNC dataset. (A) The differential expression levels of TRIB3 mRNA in normal (green) and HNC (red) tissues were analyzed using the Gene Expression Profiling Interactive Analysis 2 website, a tool for analyzing TCGA RNA sequencing data . The expression data were first log2(TPM+1) transformed for differential analysis and presented as log2FC, which is defined as the median level of tumor samples-the median level of normal samples. Data were presented as mean ± SD. Tumor samples, n=519; normal samples, n=44, according to the information of TCGA database. (B) TRIB3 mRNA expression levels in 19 paired HNSC and normal tissues from the TCGA database were compared using the paired Student's t-test. (C) Overall survival curves for patients with HNSC with the highest 25% (n=124) and the lowest 25% (n=124) TRIB3 mRNA expression levels were analyzed using Kaplan Meier curves and the log-rank test. * P<0.05; *** P<0.001. TRIB3, tribbles pseudokinase 3; TCGA, The Cancer Genome Atlas; HNC, head and neck cancer; HNSC, head-neck squamous cell carcinoma.

Article Snippet: A human HNC tissue microarray paraffin sections containing 70 samples were purchased from TissueArray.Com (cat. no. HN802d).

Techniques: Expressing, Quantitative Proteomics, Gene Expression, RNA Sequencing, Transformation Assay

Journal: International Journal of Molecular Medicine

Article Title: Tribbles pseudokinase 3 drives cancer stemness in oral squamous cell carcinoma cells by supporting the expression levels of SOX2 and EGFR

doi: 10.3892/ijmm.2025.5485

Figure Lengend Snippet: TRIB3 expression is positively correlated with E2F1, SOX2 and EGFR expression in HNC tissues. (A) Representative immunohistochemistry images of TRIB3, E2F1, SOX2 and EGFR expression in human HNC tissue microarray samples. Scale bar, 50 μ m. Correlation analyses of protein expression levels in 70 HNC tissue samples: (B) TRIB3 vs. E2F1 (C) TRIB3 vs. SOX2 (D) E2F1 vs. SOX2 and (E) TRIB3 vs. EGFR. Staining intensities were quantified using TissueFAXS software (version 7.0; TissueGnostics GmbH) and expressed as pixel density. Correlations were analyzed using Pearson's correlation coefficient (r). n=70. TRIB3, tribbles pseudokinase 3; IHC, immunohistochemistry; E2F1, E2F transcription factor 1; HNC, head and neck cancer.

Article Snippet: A human HNC tissue microarray paraffin sections containing 70 samples were purchased from TissueArray.Com (cat. no. HN802d).

Techniques: Expressing, Immunohistochemistry, Microarray, Staining, Software