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Quantitative proteomic analysis of tumor tissues before and during Bacillus Calmette-Guérin instillation in bladder cancer

ABSTRACT: The alteration of protein expression profile mediated by Bacillus Calmette-Guérin (BCG) treatment remains unclear and is rarely studied. Three paired before BCG(pre-BCG) and during BCG(on-BCG) tissues were collected for proteomicsanalyses to describe the proteomic changes caused by BCG.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Bladder

SUBMITTER: Jiangli Lu

LAB HEAD: Jiangli Lu

PROVIDER: PXD055011 | Pride | 2024-11-04

REPOSITORIES: pride

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			Action	DRS
	20230329_DIA_onBCG_1.raw	Raw
	20230329_DIA_onBCG_2.raw	Raw
	20230329_DIA_onBCG_3.raw	Raw
	20230329_DIA_preBCG_1.raw	Raw
	20230329_DIA_preBCG_2.raw	Raw

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1 - 5 of 8

Publications

Temporal dynamics of immune cell patterns in bladder cancer patients receiving Bacillus Calmette-Guérin therapy.

Lu Jiang-Li JL Ye Yun-Lin YL Zheng Dan-Dan DD Shi Xin-Yu XY Hu Li-Ling LL Yuan Xiao-Yi XY Cai Tao-Nong TN Meng Kun K Wen Neng-Qiao NQ Li Yu-Ying YY Wang Ding-Kang DK Shi Fu-Jin FJ Liu Dan-Ya DY He Qing-Yu QY Qin Zi-Ke ZK Zhang Chris Zhiyi CZ Cao Yun Y

British journal of cancer 20241031 12

<h4>Background</h4>Bacillus Calmette-Guérin (BCG) is capable of enhancing the infiltration of immune cells into the tumour. However the temporal dynamics of immune cell patterns in patients receiving BCG instillation remains unclear.<h4>Methods</h4>Ninety-six patients who underwent intravesical BCG therapy, comprising 46 responders and 50 non-responders, were retrospectively enroled to explore the evolving immune landscape. This study involved a detailed examination of sequential samples collect ...[more]

PMID: 39482453

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Project description:Patients with high-risk non-muscle-invasive bladder cancer (NMIBC) frequently relapse after standard intravesical BCG therapy and may have a dismal outcome. Resistance mechanisms to such immunotherapy remain misunderstood. Here, using cancer cell lines, freshly resected human bladder tumors and cohorts of bladder cancer patients pre- and post-BCG therapy, we demonstrate two distinct patterns of immune subversion upon BCG relapse. In the first pattern, intracellular BCG infection of cancer cells induced a post-transcriptional downregulation of HLA-I membrane expression via an inhibition of the autophagy flux. Patients with HLA-I deficient cancer cells post-BCG therapy displayed a myeloid immunosuppressive tumor microenvironment with epithelial-to-mesenchymal transition (EMT) characteristics and dismal outcomes. Conversely, patients with HLA-I proficient cancer cells post-BCG therapy presented with CD8+ T cell tumor infiltrates, upregulation of inflammatory cytokines and inhibitory immune checkpoint molecules. Those patients had a very favorable outcome. We surmise that HLA-I expression in bladder cancers at relapse post-BCG does not result from immunoediting but rather from an immune subversion process directly induced by BCG on cancer cells, which predicts dismal prognosis. Cancer cells HLA-I scoring by immunohistochemistry (IHC) staining can be easily implemented by pathologists in routine practice to stratify future urothelial cancer patient treatment strategies.

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BCG therapy downregulates HLA-I on malignant cells to subvert antitumor immune responses in bladder cancer [NanoString IO360]

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Longitudinal Transcription Profiling of Bladder Cancers Dictate the Response to BCG Treatment and Disease Progression

Project description:Although the intravesical instillation of Bacillus Calmette-Guerin (BCG) is widely used as adjuvant treatment for nonmuscle-invasive bladder cancers, the clinical benefit is variable across patients, and the molecular mechanisms underlying the sensitivity to BCG administration and disease progression are poorly understood. To establish the molecular signatures that predict the responsiveness and disease progression of bladder cancers treated with BCG, we performed transcriptome sequencing (RNA-seq) for 13 treatment-naïve and 22 post-treatment specimens obtained from 14 bladder cancer patients. To overcome disease heterogeneity, we used non-negative matrix factorization to identify the latent molecular features associated with drug responsiveness and disease progression. At least 12 molecular features were present, among which the immune-related feature was associated with drug responsiveness, indicating that pre-treatment anti-cancer immunity might dictate BCG responsiveness. We also identified disease progression-associated molecular features indicative of elevated cellular proliferation in post-treatment specimens. The progression-associated molecular features were validated in an extended cohort of BCG-treated bladder cancers. Our study advances understanding of the molecular mechanisms of BCG activity in bladder cancers and provides clinically relevant gene markers for evaluating and monitoring patients.

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Intravesical BCG induces CD4+ T Cell Expansion in a Clinically Relevant Immune Competent Model of Bladder Cancer

Project description:Intravesical BCG Immunotherapy is the standard of care in treating non-muscle invasive bladder cancer, yet its mechanism of action remains elusive. Both innate and adaptive immune responses have been implicated in BCG activity. While prior research has indirectly demonstrated the importance of T cells and shown a rise in CD4+ T cells in bladder tissue after BCG, T cell subpopulations have not been fully characterized. We investigated the relationship between effector and regulatory T cells in an immune competent, clinically relevant rodent model of bladder cancer. Our data demonstrate that cancer progression in the MNU rat model of bladder cancer is characterized by a decline in the CD8/FoxP3 ratio, consistent with decreased adaptive immunity. By contrast, treatment with intravesical BCG leads to a large, transient rise in the CD4+ T cell population in the urothelium, and is both more effective and immunogenic compared to intravesical chemotherapy. Interestingly, whole transcriptome expression profiling of post-treatment intravesical CD4+ and CD8+ T cells revealed minimal differences in gene expression after BCG treatment. Together, our results suggest that while BCG induces T cell recruitment to the bladder, the T cell phenotype does not markedly change, implying that combining T cell activating agents with BCG might improve clinical activity.

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