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Phase II Clinical Trial of Nab-Paclitaxel (NAB)Plus Cisplatin (PLA) Plus Gemcitabine (GEM) (NABPLAGEM) in Patients with Untreated Advanced Pancreatic Cancer.

ABSTRACT: Phase II Clinical Trial of Nab-Paclitaxel (NAB)Plus Cisplatin (PLA) Plus Gemcitabine (GEM) (NABPLAGEM) in Patients with Untreated Advanced Pancreatic Cancer.

PROVIDER: PRJNA977689 | ENA |

REPOSITORIES: ENA

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A Phase II Study of Neoadjuvant Gemcitabine Plus Doxorubicin Followed by Gemcitabine Plus Cisplatin in Breast Cancer

Project description:This phase II study examined the pathological complete response (pCR) rate and safety of two gemcitabine-based combinations administered sequentially in breast cancer. We also examined gene expression profiles from tumor biopsies to identify biomarkers predictive of response. Methods: Indian women with large or locally advanced breast cancer received 4 cycles of gemcitabine 1200 mg/m2 plus doxorubicin 60 mg/m2 (Gem+Dox), then 4 cycles of gemcitabine 1000 mg/m2 plus cisplatin 70 mg/m2 (Gem+Cis), and surgery. To examine dynamic changes in molecular profiles after one dose of therapy, we used three alternate sequences during cycle 1 (Gem d1, 8; Dox d2; Gem d1, 8; Dox d1; or Gem d2, 8; Dox d1). Results: Of 65 women (median age 46) treated, 13 (24.5% of 53 patients with surgery) had a pCR and 22 (33.8%) had a complete clinical response. Patients who received Gem d1, 8 and Dox d2 in cycle 1 (20/65) reported more toxicities, with G3/4 neutropenic infection/febrile neutropenia (7/20) and vomiting (5/20) as the most common cycle 1 events. Four drug-related deaths occurred. 46/65 patients yielded successful pretreatment gene expression profiles. Ten-fold cross-validated supervised analyses identified gene expression patterns that predicted with >73% accuracy (1) clinical complete response after eight cycles, (2) overall clinical complete response, and (3) pCR. Conclusions: This neoadjuvant regimen showed strong activity. A subset of patients receiving Gem d1, 8 and Dox d2 experienced unacceptable toxicity, whereas patients on other sequences had more manageable safety profiles. The predictive gene expression patterns may provide a method for selecting patients most likely to benefit from gemcitabine-containing neoadjuvant therapy. Key words: breast cancer, chemotherapy, gemcitabine, , gene expression, microarrays, neoadjuvant therapy Keywords: Dose response

2008-01-12 | GSE8465 | GEO

Effect of Gemcitabine and nab-paclitaxel in pancreatic cancer cachexia

Project description:The aim of the study is to test if Gemcitabine in combination with nab-paclitaxel can prevent muscle wasting and cardiac dysfunction in a mouse model of pancreatic cancer cachexia.

2025-04-04 | GSE234545 | GEO

Phase II Clinical Trial of Nab-Paclitaxel (NAB)Plus Cisplatin (PLA) Plus Gemcitabine (GEM) (NABPLAGEM) in Patients with Untreated Advanced Pancreatic Cancer.

Project description:We applied DNA content flow cytometry to pancreatic ductal adenocarcinoma (PDAC) biopsies. We interrogated purified sorted tumor fractions with whole genome copy number variant (CNV) and next generation sequencing (NGS) analyses. These identified a variety of somatic genomic lesions targeting genes and cellular pathways in PDAC. Of significant interest are lesions that may affect responses to therapies.

2023-06-30 | GSE233746 | GEO

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.

2023-07-05 | PXD042267 | Pride

Gene expression of VPA and GEM

Project description:Background: Histone deacetylase (HDAC) is strongly associated with epigenetic regulation and carcinogenesis, and its inhibitors induce the differentiation or apoptosis of cancer cells. Valproic acid (VPA) is one of the clinically available HDAC inhibitors. We investigated the anticancer effects of VPA in combination with gemcitabine (GEM) in cholangiocarcinoma cell line, and explored the mechanisms of the anticancer effects using microarray analysis. Methods: A human cholangiocarcinoma cell line (HuCCT1) was used. The anticancer effects of VPA, or gemcitabine (GEM), and the effects of VPA combined with GEM, were studied by cell proliferation assay. The microarray analysis was performed, the genes were picked up using Gene Spring GX11.5, Ingenuity Pathways Analysis (IPA) was performed, and then the gene-expression was determined by RT-PCR. Results: GEM (5nM) and VPA (0.5mM) reduced by 23%, which significantly augmented the anticancer effect of GEM alone or VPA alone (P<0.01). Using the microarray analysis, forty-three genes were identified with the comparison between GEM group and GEM plus VPA combination group. The interactions were shown between genes of the “Cellular Development” relevant to the differentiation of cancer cell using IPA.

2011-02-09 | GSE27036 | GEO

Targeting cancer-associated fibroblast-mediated LIF/LIFR axis improves the therapeutic efficacy of gemcitabine and nab-paclitaxel in pancreatic cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) responds poorly to chemotherapeutics due to inherent drug resistance orchestrated by crosstalk between cancer cells and cancer-associated fibroblasts (CAFs). The LIF/LIFR axis activated by this crosstalk contributes significantly to cancer cell stemness and is a potential therapeutic target. Combined targeting of LIFR with small molecular inhibitors along with standard of care remains unexplored.The efficacy of LIFR small molecule inhibitor, EC359 was evaluated in combination with standard-of-care using human and mouse cell lines, tumoroids, KPC (KrasG12D; TP53R172H; Pdx1-Cre), and orthotopically co-implanted murine models. The impact of LIFR targeting on PDAC was analyzed by RNA-sequencing, immunohistochemistry, western blot, and immune profiles by flow cytometry.In co-implantation murine models, EC359 (5mg/kg body weight), in combination with gemcitabine (Gem, 25mg/kg body weight), reduced the tumor burdens up to 90% compared to the untreated controls (p<0.001) and by 55% compared to Gem alone. The RNA-seq analysis of treated tumors showed significant alterations in stemness markers, extracellular matrix modulation, microtubule structure assembly, and adaptive immune response, suggesting the simultaneous targeting of cell-intrinsic and TME-mediated mechanisms by EC359. The EC359 in autochthonous KPC tumors improved the efficacy of Gem and nab-paclitaxel targeting, increased the dendritic cells, but reduced regulatory T-cells, systemically. Mechanistically, EC359 reduces the PDAC cell stemness, stabilizes the microtubule assembly, and reduces the immunosuppressive microenvironment, contributing to improved efficacy of standard of care in PDAC.

2025-08-27 | GSE300401 | GEO

Effect of Gemcitabine and nab-paclitaxel in pancreatic cancer cachexia

Project description:Effect of Gemcitabine and nab-paclitaxel in pancreatic cancer cachexia

| PRJNA982000 | ENA

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.

2023-06-22 | GSE223463 | GEO

mRNA Expression profiles of parental Panc cell lines and Gemcitabine resistance Panc1cell lines

Project description:Gemcitabine (GEM) is a key drug for treating PDAC, and it is commonly used for adjuvant chemotherapy. Although the majority of PDAC is sensitive to GEM at first, GEM cannot control PDAC for very long, suggesting that PDAC develops resistance to GEM after prolonged exposure. No reliable predictors of susceptibility to gemcitabine chemotherapy exist in pancreatic ductal adenocarcinoma. This study assesses gemcitabine resistant PDAC for its specific mRNA expression pattern. Gemcitabine resistant variants of Panc1, a human pancreatic adenocarcinoma cell line, were established. mRNA screening was investigated by microarray.

2016-04-26 | GSE80617 | GEO

microRNA Expression profiles of parental Panc1 cell lines and Gemcitabine resistance Panc1 cell lines

Project description:Gemcitabine (GEM) is a key drug for treating PDAC, and it is commonly used for adjuvant chemotherapy. Although the majority of PDAC is sensitive to GEM at first, GEM cannot control PDAC for very long, suggesting that PDAC develops resistance to GEM after prolonged exposure. No reliable predictors of susceptibility to gemcitabine chemotherapy exist in pancreatic ductal adenocarcinoma. MicroRNAs (miR) are epigenetic gene regulators with tumorsuppressive or oncogenic roles in various carcinomas. This study assesses gemcitabine resistant PDAC for its specific miR expression pattern. Gemcitabine resistant variants of Panc1, a human pancreatic adenocarcinoma cell line, were established. MicroRNA screening was investigated by microarray.

2016-04-26 | GSE80616 | GEO

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