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human dlbcl cell lines su dhl 4 (ATCC)

Name: human dlbcl cell lines su dhl 4
Brand: ATCC
Rating: 96 (431 reviews)

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ATCC human dlbcl cell lines su dhl 4
$(A) Genomic alterations of OSTM1 across human cancers were derived from TCGA. Shown are the top 5 cancer types with the most frequent alterations. (B) Frequency of OSTM1 genomic deletions across BCL subtypes from published datasets, including <t>DLBCL,</t> multiple myeloma (MM), follicular lymphoma (FL), B-CLL, and Burkitt lymphoma (BL). (C) OSTM1 log2 copy number variations (CNVs) and percent loss across BCL subtypes in the TCGA Mature B-cell Malignancies dataset (MD Anderson Cancer Center, MDACC). (D) Spearman correlations between fraction genome altered (FGA; genomic instability) and OSTM1 copy number (left) and the Kaplan–Meier survival of patients with or without OSTM1 deletion in the same dataset in mature B-cell malignancies (dataset from C). (E) Correlations between FGA and OSTM1 deletions (left) or mRNA expression levels (right) in DLBCL patients (TCGA Firehose Legacy). (F) OSTM1 mRNA expression in normal lymphoid tissues vs. BCL subtypes using published datasets. (G) qRT-PCR analysis of OSTM1 expression in cell lines from DLBCL, MCL, MM, and BL compared to PBMCs from healthy donors. (H) Kaplan–Meier survival analyses across multiple BCL datasets, stratified by median OSTM1 expression (upper median: high expression; lower median: low expression).$
Human Dlbcl Cell Lines Su Dhl 4, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 431 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway"

Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

Journal: bioRxiv

doi: 10.64898/2026.01.23.701155

$(A) Genomic alterations of OSTM1 across human cancers were derived from TCGA. Shown are the top 5 cancer types with the most frequent alterations. (B) Frequency of OSTM1 genomic deletions across BCL subtypes from published datasets, including DLBCL, multiple myeloma (MM), follicular lymphoma (FL), B-CLL, and Burkitt lymphoma (BL). (C) OSTM1 log2 copy number variations (CNVs) and percent loss across BCL subtypes in the TCGA Mature B-cell Malignancies dataset (MD Anderson Cancer Center, MDACC). (D) Spearman correlations between fraction genome altered (FGA; genomic instability) and OSTM1 copy number (left) and the Kaplan–Meier survival of patients with or without OSTM1 deletion in the same dataset in mature B-cell malignancies (dataset from C). (E) Correlations between FGA and OSTM1 deletions (left) or mRNA expression levels (right) in DLBCL patients (TCGA Firehose Legacy). (F) OSTM1 mRNA expression in normal lymphoid tissues vs. BCL subtypes using published datasets. (G) qRT-PCR analysis of OSTM1 expression in cell lines from DLBCL, MCL, MM, and BL compared to PBMCs from healthy donors. (H) Kaplan–Meier survival analyses across multiple BCL datasets, stratified by median OSTM1 expression (upper median: high expression; lower median: low expression).$
Figure Legend Snippet: (A) Genomic alterations of OSTM1 across human cancers were derived from TCGA. Shown are the top 5 cancer types with the most frequent alterations. (B) Frequency of OSTM1 genomic deletions across BCL subtypes from published datasets, including DLBCL, multiple myeloma (MM), follicular lymphoma (FL), B-CLL, and Burkitt lymphoma (BL). (C) OSTM1 log2 copy number variations (CNVs) and percent loss across BCL subtypes in the TCGA Mature B-cell Malignancies dataset (MD Anderson Cancer Center, MDACC). (D) Spearman correlations between fraction genome altered (FGA; genomic instability) and OSTM1 copy number (left) and the Kaplan–Meier survival of patients with or without OSTM1 deletion in the same dataset in mature B-cell malignancies (dataset from C). (E) Correlations between FGA and OSTM1 deletions (left) or mRNA expression levels (right) in DLBCL patients (TCGA Firehose Legacy). (F) OSTM1 mRNA expression in normal lymphoid tissues vs. BCL subtypes using published datasets. (G) qRT-PCR analysis of OSTM1 expression in cell lines from DLBCL, MCL, MM, and BL compared to PBMCs from healthy donors. (H) Kaplan–Meier survival analyses across multiple BCL datasets, stratified by median OSTM1 expression (upper median: high expression; lower median: low expression).

Techniques Used: Derivative Assay, Expressing, Quantitative RT-PCR

(A) OSTM1 copy number variations (CNVs) were available in DLBCL patients in TCGA Firehose Legacy. While 25% patients had shallow deletion, 12.5% had deep deletion. (B) OSTM1 deletions correlated with decreased mRNA expression in the same patients. (C) RPMI-8226 cell line stably expressing OSTM1-Flag, PBMC isolated from three healthy donors, and indicated BCL cell lines were probed for ectopically expressed or endogenous OSTM1. (D) ImageJ quantification of the ratio between non-glycosylated (∼37 kDa) and glycosylated (∼60 kDa) OSTM1.

Figure Legend Snippet: (A) OSTM1 copy number variations (CNVs) were available in DLBCL patients in TCGA Firehose Legacy. While 25% patients had shallow deletion, 12.5% had deep deletion. (B) OSTM1 deletions correlated with decreased mRNA expression in the same patients. (C) RPMI-8226 cell line stably expressing OSTM1-Flag, PBMC isolated from three healthy donors, and indicated BCL cell lines were probed for ectopically expressed or endogenous OSTM1. (D) ImageJ quantification of the ratio between non-glycosylated (∼37 kDa) and glycosylated (∼60 kDa) OSTM1.

Techniques Used: Expressing, Stable Transfection, Isolation

(A) Oncoprint visualization of OSTM1 and CDKN2A co-deletions across different BCLs as reported in the indicated studies. (B) Frequencies of CDKN2A deletions among patients with OSTM1 deletions across BCLs (left), and the frequencies of OSTM1 deletion among patients with CDKN2A deletions (right), in the indicated studies. (C) Progression-free survival of DLBCL patients stratified by the presence of chr. 6q deletion ( OSTM1 DEL), 9p21.3 deletion ( CDKN2A DEL), both ( Co-DEL ), or neither (WT). Patients with co-deletions had worse survival. ( D ) Frequencies of individual clonotypes obtained from Igh V(D)J sequencing of mouse spleen samples. Each clonotype is color-coded according to its rank of prevalence within the corresponding sample. ( E ) Comparison of the frequency of the most expanded clonotype across samples, grouped by genotype. ( F ) Percent identity between BCL Igh V(D)J sequences and their corresponding germline sequences, grouped by genotype.

Figure Legend Snippet: (A) Oncoprint visualization of OSTM1 and CDKN2A co-deletions across different BCLs as reported in the indicated studies. (B) Frequencies of CDKN2A deletions among patients with OSTM1 deletions across BCLs (left), and the frequencies of OSTM1 deletion among patients with CDKN2A deletions (right), in the indicated studies. (C) Progression-free survival of DLBCL patients stratified by the presence of chr. 6q deletion ( OSTM1 DEL), 9p21.3 deletion ( CDKN2A DEL), both ( Co-DEL ), or neither (WT). Patients with co-deletions had worse survival. ( D ) Frequencies of individual clonotypes obtained from Igh V(D)J sequencing of mouse spleen samples. Each clonotype is color-coded according to its rank of prevalence within the corresponding sample. ( E ) Comparison of the frequency of the most expanded clonotype across samples, grouped by genotype. ( F ) Percent identity between BCL Igh V(D)J sequences and their corresponding germline sequences, grouped by genotype.

Techniques Used: Sequencing, Comparison

$(A) Left: Pie chart showing the percentage of DLBCL patients with chr. 11p amplification (17.4%). Right: Pie chart showing the fraction of DLBCL patients (n = 48, TCGA Firehose Legacy) with PDE3B amplification (16.7%). (B) Percentage of patients with PDE3B gains across B-cell malignancies (TCGA, MDACC dataset), with individual log2 copy-number values overlaid. (C) Spearman correlation between PDE3B log2 copy-number value and fraction genome altered (FGA) in mature B-cell malignancies. (D) PDE3B expression across indicated BCL cohorts, comparing normal B cells with BCLs; P values were calculated by grouping all normal samples and cancer samples separately and comparing the two groups using Student’s t-test. (E) DLBCL patient samples were obtained from the Rutgers Cancer Institute. The tumor tissue lysates and PBMC from a healthy donor were probed for PDE3B expression. (F) Kaplan-Meier survival curves in DLBCL (GSE4475) and multiple myeloma (GSE2658) patients showing reduced survival in patients with high PDE3B expression, stratified by median expression. (G) PDE3B-His was stably expressed in Ba/F3 cells. Cells were cultured in the presence or absence of IL3, and cell growth was determined by counting cell numbers. ****p<0.0001. (H) PDE3B was detected by IB across cell lines from different BCL subtypes. (I) PDE3B-His was stably expressed in indicated BCL cell lines, and cell proliferation was measured. ***p<0.001. (J and K) PDE3B was silenced with 2 sgRNAs in RPMI-8226 and OPM2 cell lines. Cell proliferation was measured. P-value calculation was done using multiple t-test comparisons, one per row ***p<0.001; ****p<0.0001. (L and M) Spleens from two-month-old C -/- and DKO mice were harvested for scRNA-seq. (L) Pan-cell-type UMAP embeddings with cells from both C -/- and DKO mice combined (n=10,000 cells per mouse). (M) Dot-plot of B-cell markers stratified by sub-population. Color represents average log fold expression.$
Figure Legend Snippet: (A) Left: Pie chart showing the percentage of DLBCL patients with chr. 11p amplification (17.4%). Right: Pie chart showing the fraction of DLBCL patients (n = 48, TCGA Firehose Legacy) with PDE3B amplification (16.7%). (B) Percentage of patients with PDE3B gains across B-cell malignancies (TCGA, MDACC dataset), with individual log2 copy-number values overlaid. (C) Spearman correlation between PDE3B log2 copy-number value and fraction genome altered (FGA) in mature B-cell malignancies. (D) PDE3B expression across indicated BCL cohorts, comparing normal B cells with BCLs; P values were calculated by grouping all normal samples and cancer samples separately and comparing the two groups using Student’s t-test. (E) DLBCL patient samples were obtained from the Rutgers Cancer Institute. The tumor tissue lysates and PBMC from a healthy donor were probed for PDE3B expression. (F) Kaplan-Meier survival curves in DLBCL (GSE4475) and multiple myeloma (GSE2658) patients showing reduced survival in patients with high PDE3B expression, stratified by median expression. (G) PDE3B-His was stably expressed in Ba/F3 cells. Cells were cultured in the presence or absence of IL3, and cell growth was determined by counting cell numbers. ****p<0.0001. (H) PDE3B was detected by IB across cell lines from different BCL subtypes. (I) PDE3B-His was stably expressed in indicated BCL cell lines, and cell proliferation was measured. ***p<0.001. (J and K) PDE3B was silenced with 2 sgRNAs in RPMI-8226 and OPM2 cell lines. Cell proliferation was measured. P-value calculation was done using multiple t-test comparisons, one per row ***p<0.001; ****p<0.0001. (L and M) Spleens from two-month-old C -/- and DKO mice were harvested for scRNA-seq. (L) Pan-cell-type UMAP embeddings with cells from both C -/- and DKO mice combined (n=10,000 cells per mouse). (M) Dot-plot of B-cell markers stratified by sub-population. Color represents average log fold expression.

Techniques Used: Amplification, Expressing, Stable Transfection, Cell Culture

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Journal: bioRxiv

Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

doi: 10.64898/2026.01.23.701155

Figure Lengend Snippet: (A) Genomic alterations of OSTM1 across human cancers were derived from TCGA. Shown are the top 5 cancer types with the most frequent alterations. (B) Frequency of OSTM1 genomic deletions across BCL subtypes from published datasets, including DLBCL, multiple myeloma (MM), follicular lymphoma (FL), B-CLL, and Burkitt lymphoma (BL). (C) OSTM1 log2 copy number variations (CNVs) and percent loss across BCL subtypes in the TCGA Mature B-cell Malignancies dataset (MD Anderson Cancer Center, MDACC). (D) Spearman correlations between fraction genome altered (FGA; genomic instability) and OSTM1 copy number (left) and the Kaplan–Meier survival of patients with or without OSTM1 deletion in the same dataset in mature B-cell malignancies (dataset from C). (E) Correlations between FGA and OSTM1 deletions (left) or mRNA expression levels (right) in DLBCL patients (TCGA Firehose Legacy). (F) OSTM1 mRNA expression in normal lymphoid tissues vs. BCL subtypes using published datasets. (G) qRT-PCR analysis of OSTM1 expression in cell lines from DLBCL, MCL, MM, and BL compared to PBMCs from healthy donors. (H) Kaplan–Meier survival analyses across multiple BCL datasets, stratified by median OSTM1 expression (upper median: high expression; lower median: low expression).

Article Snippet: Human DLBCL cell lines SU-DHL-4 (CRL-2957), SU-DHL-5 (CRL-2958), and SU-DHL-10 (CRL-2963), Burkitt’s lymphoma cell lines Daudi and Ramos, as well as mantle cell lymphoma cell lines Z-138 and JeKo-1 were obtained from American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Derivative Assay, Expressing, Quantitative RT-PCR

Journal: bioRxiv

Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

doi: 10.64898/2026.01.23.701155

Figure Lengend Snippet: (A) OSTM1 copy number variations (CNVs) were available in DLBCL patients in TCGA Firehose Legacy. While 25% patients had shallow deletion, 12.5% had deep deletion. (B) OSTM1 deletions correlated with decreased mRNA expression in the same patients. (C) RPMI-8226 cell line stably expressing OSTM1-Flag, PBMC isolated from three healthy donors, and indicated BCL cell lines were probed for ectopically expressed or endogenous OSTM1. (D) ImageJ quantification of the ratio between non-glycosylated (∼37 kDa) and glycosylated (∼60 kDa) OSTM1.

Techniques: Expressing, Stable Transfection, Isolation

Journal: bioRxiv

Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

doi: 10.64898/2026.01.23.701155

Figure Lengend Snippet: (A) Oncoprint visualization of OSTM1 and CDKN2A co-deletions across different BCLs as reported in the indicated studies. (B) Frequencies of CDKN2A deletions among patients with OSTM1 deletions across BCLs (left), and the frequencies of OSTM1 deletion among patients with CDKN2A deletions (right), in the indicated studies. (C) Progression-free survival of DLBCL patients stratified by the presence of chr. 6q deletion ( OSTM1 DEL), 9p21.3 deletion ( CDKN2A DEL), both ( Co-DEL ), or neither (WT). Patients with co-deletions had worse survival. ( D ) Frequencies of individual clonotypes obtained from Igh V(D)J sequencing of mouse spleen samples. Each clonotype is color-coded according to its rank of prevalence within the corresponding sample. ( E ) Comparison of the frequency of the most expanded clonotype across samples, grouped by genotype. ( F ) Percent identity between BCL Igh V(D)J sequences and their corresponding germline sequences, grouped by genotype.

Techniques: Sequencing, Comparison

Journal: bioRxiv

Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

doi: 10.64898/2026.01.23.701155

Figure Lengend Snippet: (A) Left: Pie chart showing the percentage of DLBCL patients with chr. 11p amplification (17.4%). Right: Pie chart showing the fraction of DLBCL patients (n = 48, TCGA Firehose Legacy) with PDE3B amplification (16.7%). (B) Percentage of patients with PDE3B gains across B-cell malignancies (TCGA, MDACC dataset), with individual log2 copy-number values overlaid. (C) Spearman correlation between PDE3B log2 copy-number value and fraction genome altered (FGA) in mature B-cell malignancies. (D) PDE3B expression across indicated BCL cohorts, comparing normal B cells with BCLs; P values were calculated by grouping all normal samples and cancer samples separately and comparing the two groups using Student’s t-test. (E) DLBCL patient samples were obtained from the Rutgers Cancer Institute. The tumor tissue lysates and PBMC from a healthy donor were probed for PDE3B expression. (F) Kaplan-Meier survival curves in DLBCL (GSE4475) and multiple myeloma (GSE2658) patients showing reduced survival in patients with high PDE3B expression, stratified by median expression. (G) PDE3B-His was stably expressed in Ba/F3 cells. Cells were cultured in the presence or absence of IL3, and cell growth was determined by counting cell numbers. ****p<0.0001. (H) PDE3B was detected by IB across cell lines from different BCL subtypes. (I) PDE3B-His was stably expressed in indicated BCL cell lines, and cell proliferation was measured. ***p<0.001. (J and K) PDE3B was silenced with 2 sgRNAs in RPMI-8226 and OPM2 cell lines. Cell proliferation was measured. P-value calculation was done using multiple t-test comparisons, one per row ***p<0.001; ****p<0.0001. (L and M) Spleens from two-month-old C -/- and DKO mice were harvested for scRNA-seq. (L) Pan-cell-type UMAP embeddings with cells from both C -/- and DKO mice combined (n=10,000 cells per mouse). (M) Dot-plot of B-cell markers stratified by sub-population. Color represents average log fold expression.

Techniques: Amplification, Expressing, Stable Transfection, Cell Culture