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RNA-seq of tissue biopsies obtained from metastatic lesions of patients with treatment-naïve pancreatic carcinoma at pre- and post-treatment with gemcitabine/nab-paclitaxel/indoximod.

ABSTRACT: RNA-seq of tissue biopsies obtained from metastatic lesions of patients with treatment-naïve pancreatic carcinoma at pre- and post-treatment with gemcitabine/nab-paclitaxel/indoximod.

PROVIDER: PRJNA926359 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23190100_1.fastq.gz	Fastqsanger.gz
	SRR23190100_2.fastq.gz	Fastqsanger.gz
	SRR23190075_1.fastq.gz	Fastqsanger.gz
	SRR23190075_2.fastq.gz	Fastqsanger.gz
	SRR23190076_1.fastq.gz	Fastqsanger.gz

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RNA-seq of tissue biopsies obtained from metastatic lesions of patients with treatment-naïve pancreatic carcinoma at pre- and post-treatment with gemcitabine/nab-paclitaxel/indoximod.

Project description:To investigate the impact of first-line treatment with gemcitabine/nab-paclitaxel/indoximod on the transcriptional profile of metastatic lesions in patients with pancreatic carcinoma, we collected tissue biopsies at pre- and post- (8wks) treatment and performed RNAseq.

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Project description:Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with limited and very often, ineffective medical and surgical therapeutic options. The treatment of patients with advanced unresectable PDAC is restricted to systemic chemotherapy, a therapeutic intervention to which most eventually develop resistance. Recently, nab-paclitaxel has been added to the arsenal of first line therapies, and the combination of gemcitabine and nab-paclitaxel has modestly prolonged median overall survival. However, patients almost invariably succumb to the disease, and little is known about the mechanisms underlying nab-paclitaxel (n-PTX) resistance. Using the conditionally reprogrammed (CR) cell approach, we established and verified continuously growing cell cultures from treatment-naive PDAC patients. To study the mechanisms of primary drug resistance, nab-paclitaxel-resistant (n-PTX-R) cells were generated from primary cultures and drug resistance was verified in vivo, both in zebrafish and in athymic nude mouse xenograft models. Molecular analyses identified the sustained induction of c-MYC in the nab-paclitaxel-resistant cells. Depletion of c-Myc restored nab-paclitaxel sensitivity, as did treatment with either the MEK inhibitor, trametinib, or a small molecule activator of protein phosphatase 2a (SMAP). Implications: The strategies we have devised, including the patient-derived primary cells and the unique drug resistant isogenic cells, are rapid and easily applied in vitro and in vivo platforms to better understand the mechanisms of drug resistance and for defining effective therapeutic options on a patient by patient basis

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Label-free proteomics quantification of pancreatic ductal adenocarcinoma patient-derived xenografts with treatment combining Gemcitabine and nab-Paclitaxel

Project description:Tumor-stroma interactions are critical in pancreatic ductal adenocarcinoma (PDAC) progression and therapeutics. Patient-derived xenograft (PDX) models faithfully recapitulate tumor-stroma interactions in PDAC, but conventional antibody-based immunoassay is largely inadequate to resolve or quantify tumor and stromal proteins. A species-deconvolved proteomics approach embedded in the ultra-high-resolution (UHR)-IonStar workflow can unambiguously quantify the proteins from tumor (human-derived) and stroma (mouse-derived) in PDX samples, enabling unbiased investigation of their proteomes with excellent quantitative reproducibility. With this strategy, 3 PDAC PDXs were analyzed. They were showed differential responses to treatment with Gemcitabine combined with nab-Paclitaxel (GEM+PTX), which is a first-line treatment regimen for PDAC. For each PDAC PDX, samples were collected after 24 hour and 192 hour with/without treatment, and each condition contained four biological replicates.

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Neoadjuvant BMS-813160, nivolumab, gemcitabine and nab-paclitaxel for pancreatic cancer

Project description:Background: Targeting tumor-associated macrophages through C-C chemokine receptor type 2 (CCRs) in pancreatic ductal adenocarcinoma (PDAC) improves the efficacy of chemotherapy and restores T cell immunity. Methods: We conducted a phase I/II single institution study (NCT03496662) combining chemotherapy gemcitabine and nab-paclitaxel (GnP), an oral CCR2/5 inhibitor BMS-813160 and nivolumab for four 28-day cycles as a neoadjuvant therapy for patients with borderline resectable (BR) or locally advanced (LA) PDAC. The recommended phase 2 dose (RP2D) of BMS-813160 was established in the standard 3+3 design. Primary end points were safety and objective response rate (ORR). Secondary end points included resection rate, progression-free survival (PFS) and overall survival (OS). Results: 8 patients were treated with GnP alone (control arm) and 31 patients (29 response evaluable) were treated at RP2D. No grade 3 or 4 toxicities attributed to nivolumab or BMS-813160 were identified. After all 4 cycles of study treatment (N=26), ORR was 35.7%, 16.7% among BR- and LA-PDAC patients, compared to 0% of control arm patients. 78.6% BR- and 16.7% of LA-PDAC patients who completed study treatment underwent surgical resection. For intent-to-treat analyses, BR-PDAC patients had a mPFS and mOS of 14.6 and 20.4 months respectively; and LA-PDAC patients had a mPFS and mOS of 14.7 and 17 months respectively. Single cell RNAseq analysis showed enhanced proliferating CD4 and CD8 T cells and gene signatures indicative of effector function. Conclusions: Neoadjuvant BMS-813160/nivolumab/GnP was well tolerated and appears to achieve higher ORR and resectability than historical data, warranting a larger randomized phase II study.

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(Phospho-)proteomic analysis of gemcitabine resistant pancreatic cancer cells reveals that microtubule-associated protein 2 upregulation associates with taxane treatment response

Project description:Chemoresistance hampers the treatment of patients suffering from pancreatic ductal adenocarcinoma (PDAC). The present study aimed to evaluate the proteome and phosphoproteome of gemcitabine-sensitive and -resistant PDAC cells to identify novel targets and predictive biomarkers.The oncogenic capabilities of sensitive and resistant PDAC cells were evaluated in vitro and in vivo. Cultured cells were subsequently analysed by label-free mass spectrometry. Differential proteins and phosphopeptides were evaluated for Gene Ontology and predictive and / or prognostic biomarker potential by immunohistochemistry of tissue microarrays (TMAs). Differential analyses showed that resistant proteins are associated with membrane organization and microtubule regulation. Importantly, resistant cells displayed an increased sensitivity for paclitaxel treatment in vitro (p < 0.001) and nab-paclitaxel had a strong anti-tumour efficacy in vivo. Microtubule-associated protein 2 (MAP2) was found to be highly upregulated and phosphorylated in resistant cells. The identified resistance marker MAP2 emerged as a novel prognostic marker in PDAC patients treated with gemcitabine.

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