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> Disorders > Neoplastic Process > Pancreatic Carcinoma

Pancreatic Carcinoma

Pancreatic Carcinoma is a malignant neoplasm originating from epithelial cells of the pancreas.
It is one of the most aggressive and deadly forms of cancer, often diagnosed at an advanced stage due to the lack of early symptoms.
Pancreatic Carcinoma can arise from various cell types within the pancreas, including exocrine glandular cells and endocrine cells.
Common subtypes include ductal adenocarcinoma, the most prevalent form, as well as less common types like acinar cell carinoma and neuroendocrine tumors.
Symptoms may include abdominal pain, weight loss, jaundice, and digestive issues.
Accurate diagnosis and effective treatment remain significant challenges, highlighting the need for continued research and development of new therapeutic approaches.

Most cited protocols related to «Pancreatic Carcinoma»

1
Streptozotocin-Induced Pancreatic Beta Cell Depletion
Cited 67 times
STZ is a broad-spectrum antibiotic that is toxic to the insulin producing β cells of pancreatic islets. It is currently used clinically for the treatment of metastatic islet cell carcinoma of the pancreas [12 ] and has been used investigationally in a wide variety of large and small animal species [2 (link)–5 , 13 (link)–17 (link)]. The method of STZ action in β cell depletion has been studied extensively over the years. It is generally assumed that STZ is taken up via the cell membrane GLUT2 glucose transporter and causes DNA alkylation and eventual β cell death [15 (link), 17 (link)], although streptozotocin’s actions as a protein alkylating agent [18 (link)] and nitric oxide donor may contribute to its cytotoxicity [19 (link)]. Because STZ enters the cell via GLUT2, the toxic action is not specific to β cells and can cause damage to other tissues including the liver and kidney [5 , 15 (link), 17 (link), 19 (link)].
Deeds M., Anderson J., Armstrong A., Gastineau D., Hiddinga H., Jahangir A., Eberhardt N, & Kudva Y. (2011). Single Dose Streptozotocin Induced Diabetes: Considerations for Study Design in Islet Transplantation Models. Laboratory animals, 45(3), 131-140.
Publication 2011
Alkylating Agents Alkylation Animals Antibiotics Cell Death Cells Cytotoxin Glucose Transporter Islets of Langerhans Kidney Liver Nitric Oxide Donors Pancreatic beta Cells Pancreatic Carcinoma Plasma Membrane SLC2A2 protein, human Staphylococcal Protein A Tissues Toxic Actions
2
Comparative Evaluation of Amino Acid Profiling Methods
Cited 36 times
Technical consistency (i.e. reproducibility and linearity) of the 3AA method was compared to two conventional chromatographic separations used for small molecule and amino acid analyses. Pancreatic cancer cell extracts (biological triplicates) either undiluted or diluted five-fold, were analyzed using (i) the 3AA method, as well as (ii) a 15 min gradient on a Kinetex HILIC column (150 × 2.1 mm i.d., 1.7 μm particle size – Phenomenex, Torrance, CA, USA) and (iii) a 23 min gradient on an Acquity UHPLC BEH Amide Column (2.1×100 mm, 1.7μm – Waters, Milford, MA, USA). In (ii), samples were analyzed on the Kinetex HILIC at 350 μl/min (mobile phases: A: ACN; B: 18 mΩ H2O, 20 mM (NH4)2CO3, 0.1% NH4OH; gradient: 1.5 min hold at 5% B; 5-60% B in 8.5 min; 60-95% B in 0.5 min at 0.5 ml/min; 95% hold for 2 min; 95-5% B in 0.5 min; 5 hold for 2 min; column temperature: 25°C). In (iii), samples were analyzed on the Acquity UHPLC BEH Amide Column (2.1×100 mm, 1.7μm – Waters, Milford, MA, USA) at 500 μl/min (mobile phases: A: 18 mΩ H2O, 20 mM (NH4)2CO3 pH 4.00; B: acetonitrile; gradient: 3 min hold 85% B; 85-30% B in 9 min; 30-2% B in 3 min; 2-85% of B in 1 min; 85% equilibration for 7 min; column temperature: 60°C).
The UHPLC system was coupled online with a QExactive mass spectrometer (Thermo, San Jose, CA, USA), scanning in Full MS mode (2 μscans) at 70,000 resolution from 60-900 m/z, with 4 kV spray voltage, 15 sheath gas and 5 auxiliary gas, operated in positive ion mode. Calibration was performed before each analysis using a positive calibration mix (Piercenet – Thermo Fisher, Rockford, IL, USA). Limits of detection (LOD) were characterized by determining the smallest injected amino acid amount required to provide a signal to noise (S/N) ratio greater than three using < 5 ppm error on the accurate intact mass. Based on a conservative definition for Limit of Quantitation (LOQ), these values were calculated to be three fold higher than determined LODs.
MS data acquired from the QExactive was converted from .raw file format to.mzXML format using MassMatrix (Cleveland, OH, USA). Amino acid assignments were performed using MAVEN (Princeton, NJ, USA). The MAVEN software platform provides tools for peak picking, feature detection and metabolite assignment against the KEGG pathway database. Assignments were further confirmed using a process for chemical formula determination using isotopic patterns and accurate intact mass (Clasquin et al. 2012 ). Analyte retention times were confirmed by comparison with external standard retention times, as indicated above.
Relative quantitation was performed by exporting integrated peak areas values into Excel (Microsoft, Redmond, CA, USA) for statistical analysis including T-Test and ANOVA (significance threshold for p-values < 0.05) and unsupervised Principal Component Analysis (PCA) (Pan et al. 2007 (link); Fonville et al. 2010 ), calculated through the MultiBase macro (freely available at www.NumericalDynamics.com).
Nemkov T., D'Alessandro A, & Hansen K.C. (2015). Three Minute Method for Amino Acid Analysis by UHPLC and high resolution quadrupole orbitrap mass spectrometry. Amino acids, 47(11), 2345-2357.
Publication 2015
acetonitrile Amides Amino Acids Biopharmaceuticals Cell Extracts Chemical Processes Chromatography Isotopes neuro-oncological ventral antigen 2, human Pancreatic Carcinoma Retention (Psychology)
3
Preclinical Mouse Models for Immunotherapy
Cited 20 times
Five to seven week old female C57BL/6 and BALB/c mice were obtained from NCI Production (Frederick, MD) and Jackson Laboratory (Bar Harbor, ME) and maintained under pathogen free conditions. All animal experiments were performed according to protocols approved by the Institute of Animal Care and Use Committee of the University of Pennsylvania. For B16-F10 melanoma, 5×104 B16-F10 cells were mixed with an equal volume of Matrigel (BD Biosciences) and subcutaneously injected on the right flank of C57BL/6 mice on day 0 and the left flank on day 2. The right flank tumor site was irradiated with 20 Gy on day 8. Blocking antibodies were given on days 5, 8 and 11. For the concurrent vs. sequential RT experiment, the right flank was irradiated on either day 8 (sequential) or 12 (concurrent), while blocking antibodies were given on days 9, 12, and 15. For TSA breast cancer, 1×105 TSA cells were mixed with an equal volume of Matrigel (BD Biosciences) and subcutaneously injected on the right flank of BALB/c on day 0 and the left flank on day 2. The right flank of the mice was irradiated with 8 Gy on three consecutive days starting on day 10 or 11 post tumor implantation. Blocking antibodies were started 3 days prior to RT and given every 3 days for a total of 3 doses. For the pancreatic cancer model, 4×105 PDA.4662 cells were subcutaneously injected on the right flank. The right flank was irradiated with 20 Gy on day 8. Blocking antibodies were given on days 5, 8, and 11. For melanoma and breast cancer models, we used the optimal dose and fraction of radiation as previously reported23 (link),24 (link). All irradiation was performed using the Small Animal Radiation Research Platform (SARRP). Antibodies used for in vivo immune checkpoint blockade experiments were given intraperitoneally at a dose of 200 μg/mouse and include: CTLA4 (9H10), PD-1 (RMP1-14), PDL-1 (10F.9G2), CD8 (2.43), and rat IgG2B isotype (LTF-2) (BioXCell). Anti-CD8 was given 2 days prior to tumor implantations (day −2), day 0, then every 4 days for the duration of the experiment. Perpendicular tumor diameters were measured using calipers. Volume was calculated using the formula L × W2 × 0.52, where L is the longest dimension and W is the perpendicular dimension.
Victor C.T., Rech A.J., Maity A., Rengan R., Pauken K.E., Stelekati E., Benci J.L., Xu B., Dada H., Odorizzi P.M., Herati R.S., Mansfield K.D., Patsch D., Amaravadi R.K., Schuchter L.M., Ishwaran H., Mick R., Pryma D.A., Xu X., Feldman M.D., Gangadhar T.C., Hahn S.M., Wherry E.J., Vonderheide R.H, & Minn A.J. (2015). Radiation and Dual Checkpoint Blockade Activates Non-Redundant Immune Mechanisms in Cancer. Nature, 520(7547), 373-377.
Publication 2015
Animals Antibodies Antibodies, Blocking Cells CTLA4 protein, human IgG2B Immune Checkpoint Blockade Immunoglobulin Isotypes Malignant Neoplasm of Breast matrigel Melanoma Melanoma, B16 Mice, Inbred BALB C Mice, Inbred C57BL Mus Neoplasms Ovum Implantation Pancreatic Carcinoma pathogenesis Radiation Radiotherapy Woman
4
Genomic Analysis of Metastatic Pancreatic Cancer
Cited 18 times
Thirteen patients with pancreatic cancer were studied, with written informed consent for sample collection and analysis. Ten patients had multiple metastases collected at autopsy performed within 6 hours of death, as described27 (link). We also studied primary tumours collected from three patients undergoing resection with curative intent. Representative samples of primary carcinoma or metastases were minced with sterile blades, and the tissues gently pressed through a 45-micron mesh to disaggregate epithelial and stromal cells. For low passage cell lines, filtered cells were resuspended into culture media and passaged up to five times to remove contaminating fibroblasts.
Protocols for massively parallel, paired-end sequencing have been described in detail elsewhere13 (link),14 (link). Genomic DNA from the tumour samples was randomly fragmented, and fragments 400–500bp in size selected by gel purification. Libraries were synthesised following our standard protocol, as described28 (link), and sequenced on a Genome Analyzer II (Illumina Inc) to give 37bp reads from both ends of 50–150 million DNA fragments. In our experience, this identifies ~50–60% of rearrangements in a sample13 (link),14 (link). This level of genome coverage is insufficient to allow accurate identification of point mutations11 (link), but allows patterns of genomic rearrangement to be studied across multiple cancer samples without bias in size or type of rearrangement.
Sequencing data were aligned to the human reference genome (NCBI build 36) using the MAQ algorithm29 . Clusters of anomalously mapping reads spanning putative rearrangements were identified informatically13 (link). PCR across the breakpoint was performed in tumour and normal DNA, allowing rearrangements to be classified as somatically acquired, germline or artefactual. PCR products underwent capillary sequencing to annotate breakpoints to base-pair resolution. In 10 patients, primers for somatic rearrangements were used to genotype by PCR all other metastases and, where available, the primary tumour from that patient. The sensitivity of PCR for detection of genomic rearrangements is at least 1/1000 cells30 (link), considerably better than can be achieved for point mutations.
Campbell P.J., Yachida S., Mudie L.J., Stephens P.J., Pleasance E.D., Stebbings L.A., Morsberger L.A., Latimer C., McLaren S., Lin M.L., McBride D.J., Varela I., Nik-Zainal S.A., Leroy C., Jia M., Menzies A., Butler A.P., Teague J.W., Griffin C.A., Burton J., Swerdlow H., Quail M.A., Stratton M.R., Iacobuzio-Donahue C, & Futreal P.A. (2010). The patterns and dynamics of genomic instability in metastatic pancreatic cancer. Nature, 467(7319), 1109-1113.
Publication 2010
Autopsy Base Pairing Capillaries Carcinoma Cell Lines Cells Culture Media Diploid Cell DNA, Neoplasm Fibroblasts Gene Rearrangement Genome Genome, Human Genotype Germ Line Hypersensitivity Malignant Neoplasms Neoplasm Metastasis Neoplasms Oligonucleotide Primers Pancreatic Carcinoma Patients Point Mutation Specimen Collection Sterility, Reproductive Stromal Cells Tissues
5
Differential Expression Analysis of Tumor Stroma
Cited 11 times
The RMA (Robust Multichip Average) algorithm was first applied to the microarray raw data to obtain gene expression data. All statistical analyses were performed using R and the Bioconductor suite (http://www.r-project.org/).
PCA was performed using the prcomp R function with default parameters.
Hierarchical cluster analysis was based on Pearson correlation between the samples. Differentially expressed genes between tumor and normal samples were identified with the limma package of Bioconductor, which applies empirical-based methods to a moderated t-statistic and takes multiple testing into account by providing an estimate of the false discovery rate (FDR). This analysis was performed in a paired way, .i.e. comparing tumor and normal samples from the same patient.
For the pairwise correlation analysis, the Pearson correlation was calculated in the ExpO breast and prostate subsets. Gene expression and annotation data from the ExpO consortium (http://www.intgen.org/expo/) were downloaded from GEO (GSE2109) in December 2008, including batches 1–16. The breast and prostate cancer subsets (354, respectively 83 samples) were extracted and processed separately with the RMA procedure (quantile normalization at probe-level data).
For comparison with published stromal signatures, multiple testing correction was done with the Bonferroni procedure. We re-analyzed the expression data of Ma et al.[13] (link) to obtain a list of differentially expressed genes comparing invasive breast ductal carcinoma stroma versus normal stroma. For that we used the expression data deposited in GEO (series GSE14548) and performed a paired analysis of differential expression using limma. The probesets with FDR<1% were then selected and used for the comparison. We compared our upregulated stromal genes with the ones found upregulated in breast carcinoma-associated fibroblasts compared to normal mammary fibroblasts in Bauer et al.[22] We compared our data with the pancreatic cancer stroma genes set identified in Binkley et al.[15] (link) For the comparison with the mouse study from Bacac et al.[16] (link) we considered the list containing the mouse genes found to be upregulated in invasive compared to pre-invasive prostate tumor stroma. These genes were converted into human genes using HomoloGene (build 62) and taking into account only the mouse genes with a unique homologene human ortholog.
Planche A., Bacac M., Provero P., Fusco C., Delorenzi M., Stehle J.C, & Stamenkovic I. (2011). Identification of Prognostic Molecular Features in the Reactive Stroma of Human Breast and Prostate Cancer. PLoS ONE, 6(5), e18640.
Publication 2011
Breast Cancer-Associated Fibroblasts Fibroblasts Gene, Cancer Gene Expression Genes Genes, Neoplasm Genes, vif Invasive Ductal Carcinoma, Breast Mice, Laboratory Microarray Analysis Neoplasms Oncogenes Pancreas Pancreatic Carcinoma Patients Prostate Prostate Cancer Prostatic Neoplasms

Most recents protocols related to «Pancreatic Carcinoma»

1
Clinicopathological and Hematological Characteristics of Pancreatic Diseases
Detailed baseline and clinicopathological information, including sex, age, tumor location, tumor size, pathological type, differentiation, lymph node metastasis, and TNM stage of the patients with pancreatic diseases and HC, were obtained from the medical records of the inpatients or outpatients. The preoperative hematological parameters and liver function tests included neutrophils (× 109/L), lymphocytes (× 109/L), monocytes (× 109/L), platelets (× 109/L), plasma fibrinogens (g/L), serum albumins (g/L), prealbumin (mg/L), and CA199 (U/L) within seven days before surgery (average 2—7 days) were gathered from the medical records. TNM staging was performed using the 8th edition of the AJCC Cancer Staging Manual for Pancreatic Cancer.
Gu Y., Hua Q., Li Z., Zhang X., Lou C., Zhang Y., Wang W., Cai P, & Zhao J. (2023). Diagnostic value of combining preoperative inflammatory markers ratios with CA199 for patients with early-stage pancreatic cancer. BMC Cancer, 23, 227.
Publication 2023
Blood Platelets Fibrinogen Inpatient Liver Function Tests Lymph Node Metastasis Lymphocyte Monocytes Neoplasms Neoplasms by Site Neutrophil Outpatients Pancreatic Carcinoma Pancreatic Diseases Patients Plasma Prealbumin Serum Albumin
2
Cultivation of NK92 and Pancreatic Cancer Cell Lines
Human natural killer cell line NK92 was purchased from the American Type Culture Collection and grown in α-MEM medium (Cat. No.12571089; Life Technologies, Carlsbad, CA, USA) supplemented with 12.5% fetal bovine serum (FBS; Cat. No.1614007; Gibco, Grand Island, NY, USA), 12.5% horse serum (Cat. No. 26050070; Gibco), 1.5 g/L sodium bicarbonate, 2 mM L-glutamine (Cat. No. 25030149; Gibco), 100 to 200 U/ml recombinant IL-2 (Cat. No. 200-02; PeproTech, Rocky Hill, NJ, USA,), 0.1 mM 2-mercaptoethanol, 0.2 mM inositol (Cat. No. I5125; Sigma-Aldrich, St. Louis, MO, USA), 0.02 mM folic acid, and 1% penicillin-streptomycin solution (Cat. No. SV30010; Solarbio, Beijing, China). Mouse pancreatic carcinoma cell line PAN02 and human pancreatic carcinoma cell line PANC28, PANC1, SW1990 were purchased from the American Type Culture Collection and cultured in DMEM medium contained 10% FBS (Gibco, Gaithersburg, MD, USA) at 37 °C in an atmosphere of 5% CO2.
Guo D., Jin C., Gao Y., Lin H., Zhang L., Zhou Y., Yao J., Duan Y., Ren Y., Hui X., Ge Y., Yang R, & Jiang W. (2023). GPR116 receptor regulates the antitumor function of NK cells via Gαq/HIF1α/NF-κB signaling pathway as a potential immune checkpoint. Cell & Bioscience, 13, 51.
Publication 2023
2-Mercaptoethanol Atmosphere Bicarbonate, Sodium Cell Lines Culture Media Equus caballus Folic Acid Glutamine Homo sapiens Inositol Mus Natural Killer Cells Pancreatic Carcinoma Penicillins Serum Streptomycin
3
Oxaliplatin Response in Locally Advanced PDAC
A total of 76 locally advanced PDAC specimens were collected from patients (median age, 61.2 years; age range, 32-79 years; 43 male patients, 33 female patients) who received a platinum-based chemotherapy program at Guangdong Provincial People's Hospital and Sun Yat-sen Memorial Hospital (both Guangzhou, China) between July 2015 and June 2021. Patients with locally advanced PDAC underwent laparoscopic biopsy or endoscopic ultrasound-guided sample acquisition from a solid pancreatic mass. The samples were confirmed as PDAC by two certified pathologists. Patients were included if they i) were 18-80 years of age; ii) had advanced PDAC stage III or IV, according to the pathology results; iii) had received oxaliplatin chemotherapy; and iv) had provided written informed consent. Patients were excluded if they i) had received other specific pancreatic cancer treatments (surgery, preoperative chemotherapy or chemoradiation); ii) had a pathologic diagnosis of a benign tumor; iii) had a history of other malignancies; or iv) had a mental illness. In accordance with the Guangdong Provincial People's Hospital's Protection of Human Subjects Committee (approval no. KY-H-2022-011-01), the protocol was approved, and all of the patients provided written informed consent before the biopsy sample collection. Progression-free survival (PFS) was measured from the date of chemotherapy to the occurrence of an event (progressive disease, death or diagnosis of a second malignant neoplasm). The response of oxaliplatin chemotherapy was assessed 4 months after the start of chemotherapy, complete response (CR) and partial response (PR) were classified as oxaliplatin-sensitive (35 cases), while stable disease (SD) and progressive disease (PD) were classified as oxaliplatin-resistant (41 cases).
Xia R., Hu C., Ye Y., Zhang X., Li T., He R., Zheng S., Wen X, & Chen R. (2023). HNF1A regulates oxaliplatin resistance in pancreatic cancer by targeting 53BP1. International Journal of Oncology, 62(4), 45.
Publication 2023
Anophthalmia with pulmonary hypoplasia Benign Neoplasm Biopsy Chemoradiotherapy Diagnosis Homo sapiens Laparoscopy Males Malignant Neoplasms Mental Disorders Neoplasms, Second Primary Operative Surgical Procedures Oxaliplatin Pancreas Pancreatic Carcinoma Pathologists Patients Pharmacotherapy Platinum Specimen Collection Ultrasonography, Endoscopic Woman
4
MRI-CT Image Fusion for MR-LINAC Radiotherapy

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Publication 2023
Abdomen Abdominal Cavity Cancer of Liver Diagnosis Ethics Committees Females Inhalation Inhalation Therapy Males Metals Pancreatic Carcinoma Patients Prosthesis Radiation Oncologists Stents Woman
5
Prognostic Impact of Duodenal Wall Invasion in Pancreatic Cancer
This study was approved by the Institutional Review Board at our institution (IRB #202,100,888). Pancreatic adenocarcinoma patients with different TNM stages who had undergone Whipple resection and/or distal pancreatectomy at a tertiary care hospital during the period between January 2008 and May 2021 were reviewed in the study, and patients who underwent Whipple resection with or without total pancreatectomy who survived more than 30 days following surgery were analyzed. The following information was obtained from the electronic medical record and tumor registry at our institution: age, gender, and clinical follow-up concerning progression, recurrence, and survival (as of July 1, 2021).
All gross descriptions and hematoxylin and eosin slides were reviewed by three board-certified anatomic pathologists with experience in gastrointestinal pathology (AA, BB, AG) for the following parameters: tumor size (maximum tumor dimension in the pathology report), histologic grade, margin status (R0: negative and R1: positive or less 1 mm for the retroperitoneal margin), the presence of intraductal papillary mucinous neoplasm (IPMN), perineural invasion (PNI), lymphovascular invasion (LVI), DWI (involvement of muscularis propria of the duodenal wall and/or ampullary involvement), extrapancreatic common bile duct invasion by tumor, the number of examined lymph nodes, and the number of involved lymph nodes. All cases were grossed according to our institution’s protocol which includes at least 1 routine section from ampulla (including duodenal wall and pancreas), and cases were staged according to the 8th edition of the AJCC.
The patients were divided into 2 groups: group 1 with DWI and group 2 without DWI, and the clinicopathologic features were compared between the two groups. Descriptive summaries included frequencies and percentages for categorical variables and means (and range) for continuous variables. Univariate analyses were done to compare group 1 and group 2. Means (and ranges) of continuous variables with normal distributions were compared using the two-tailed Student t-test. Pearson’s chi-squared test or Fisher’s exact test were used as applicable to compare the categorical variables. Multivariate logistic regression with unadjusted and adjusted models was run to identify variables significantly associated with DWI.
Overall survival (OS) was calculated from the date of surgical resection to the date of death or last follow-up. Progression-free survival (PFS) was calculated from the date of surgical resection to the date of first recurrence or death, whichever came first. The OS rate and PFS time were calculated using Kaplan–Meier curves, and the log-rank test was used to determine the statistical significance of differences. Multivariate Cox regression analysis was conducted to identify whether DWI or any other parameters in the model were significantly associated with OS and PFS post-pancreatic cancer surgery using unadjusted and adjusted models. STATA/BE 17 was used for data management and statistical analysis. A P-value ≤ 0.05 was considered statistically significant.
Alkhasawneh A., Rashid T., Mohammed I., Elhaddad B., Al-Balas H., Virarkar M., Awad Z., Baskovich B, & Gopinath A. (2023). The prognostic significance of duodenal wall invasion in pancreatic adenocarcinoma. World Journal of Surgical Oncology, 21, 79.
Publication 2023
Adenocarcinoma Bladder Detrusor Muscle Choledochus Duodenum Eosin Gender Hematoxylin Neoplasm Invasiveness Neoplasms Neoplasms, Mucinous Nodes, Lymph Operative Surgical Procedures Pancreas Pancreatectomy Pancreatic Carcinoma Pathologists Patients Recurrence Retroperitoneal Space Student

Top products related to «Pancreatic Carcinoma»

1
Fetal bovine serum (fbs) by Thermo Fisher Scientific
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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Panc 1 by American Type Culture Collection
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PANC-1 is a cell line derived from a human pancreatic ductal adenocarcinoma. It is a commonly used model for in vitro studies of pancreatic cancer.
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Mia paca 2 by American Type Culture Collection
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MIA PaCa-2 is a human pancreatic carcinoma cell line derived from a primary tumor. It is a well-established model used in cancer research.
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Bxpc 3 by American Type Culture Collection
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BxPC-3 is a cell line derived from a human pancreatic adenocarcinoma. It is commonly used in research related to pancreatic cancer.
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AsPC-1 is a cell line derived from a human pancreatic adenocarcinoma. It is a commonly used in vitro model for pancreatic cancer research.
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Penicillin is a type of antibiotic used in laboratory settings. It is a broad-spectrum antimicrobial agent effective against a variety of bacteria. Penicillin functions by disrupting the bacterial cell wall, leading to cell death.

More about "Pancreatic Carcinoma"

Pancreatic Adenocarcinoma, Pancreatic Cancer, Pancreatic Ductal Adenocarcinoma (PDAC), Pancreatic Neoplasm, Pancreatic Tumor, Pancreatic Carcinogenesis, Pancreatic Malignancy, Pancreatic Exocrine Carcinoma, Pancreatic Endocrine Carcinoma, Pancreatic Acinar Cell Carcinoma, Pancreatic Neuroendocrine Tumor (PNET), Pancreatic Cystic Neoplasm, Pancreatic Islet Cell Tumor, Pancreatic Intraepithelial Neoplasia (PanIN), Pancreatic Ductal Epithelium, Pancreatic Duct, Pancreatic Acinar Cells, Pancreatic Islet Cells, Pancreatic Stellate Cells, Pancreatic Enzyme, Pancreatic Duct Obstruction, Pancreatic Duct Dilation, Pancreatic Duct Stricture, Pancreatic Duct Stones, Pancreatic Duct Cyst, Pancreatic Inflammation, Pancreatitis, Pancreatic Fibrosis, Pancreatic Stroma, Pancreatic Microenvironment, Pancreatic Angiogenesis, Pancreatic Metabolism, Pancreatic Signaling Pathways, Pancreatic Stem Cells, Pancreatic Organoids, Pancreatic Cell Lines (FBS, PANC-1, MIA PaCa-2, DMEM, BxPC-3, AsPC-1, RPMI 1640 medium), Pancreatic Cancer Biomarkers, Pancreatic Cancer Genetics, Pancreatic Cancer Epigenetics, Pancreatic Cancer Immunology, Pancreatic Cancer Metastasis, Pancreatic Cancer Therapy, Pancreatic Cancer Prognosis, Pancreatic Cancer Survivial, Pancreatic Cancer Risk Factors, Pancreatic Cancer Prevention, Pancreatic Cancer Screening, Pancreatic Cancer Diagnosis, Pancreatic Cancer Staging, Pancreatic Cancer Treatment (Surgery, Chemotherapy, Radiation Therapy, Targeted Therapy, Immunotherapy), Pancreatic Cancer Clinical Trials, Pancreatic Cancer Research, Pancreatic Cancer Epidemiology, Pancreatic Cancer Palliative Care, Pancreatic Cancer Supportive Care, Pancreatic Cancer Patient Education, Pancreatic Cancer Caregiver Support, Pancreatic Cancer Advocacy, Pancreatic Cancer Awareness, Pancreatic Cancer Funding, Pancreatic Cancer Organizations, Pancreatic Cancer Resources, Pancreatic Cancer Penicillin/streptomycin, Pancreatic Cancer Streptomycin.