Target intelligence / Profile preview

Human pancreatic carcinoma cells

01

Overview

Human pancreatic carcinoma cells, predominantly representing Pancreatic Ductal Adenocarcinoma (PDAC), are the malignant cellular units characterized by high genomic instability and aggressive growth. These cells typically harbor signature mutations in the KRAS oncogene (>90%), along with the loss of tumor suppressor genes such as TP53, CDKN2A, and SMAD4 [Nature Reviews Disease Primers: 16022]. They are notable for their ability to survive in a hypoxic, nutrient-poor environment and for inducing a dense fibrotic reaction known as desmoplasia, which creates a physical barrier to therapeutic penetration [PMC: 7146316]. In a drug discovery context, 'Human pancreatic carcinoma cells' refers to the disease state or the cellular model used in assays rather than a specific molecular target. While drugs like Gemcitabine and nab-paclitaxel are used to treat these cells, they interact with specific intracellular enzymes or structural proteins rather than the cell as a singular receptor. Modern research focuses on identifying specific surface antigens on these cells, such as Mesothelin or Glypican-1, to develop more precise targeted therapies and immunotherapies [PubMed: 32679264].

Other names
Pancreatic cancer cellsPancreatic ductal adenocarcinoma cellsPDAC cellsPancreatic adenocarcinoma cellsMalignant pancreatic cells
02

Mechanism of action

Pharmacological agents do not target the cell as a whole but rather specific molecular components within the cell, such as inhibiting DNA polymerase (Gemcitabine), stabilizing microtubules (Paclitaxel), or inhibiting topoisomerase I (Irinotecan) [PubMed: 25170170]. Targeted therapies like Erlotinib inhibit the Epidermal Growth Factor Receptor (EGFR) signaling pathway often active in these cells [NIH: PDQ Pancreatic Cancer Treatment].

03

Biological functions

Cell proliferationMetastasisApoptosis evasionMetabolic reprogrammingEpithelial-mesenchymal transition (EMT)
04

Disease associations

Pancreatic cancerPancreatic ductal adenocarcinoma
05

Safety considerations

High rate of intrinsic and acquired chemoresistanceSevere systemic toxicity of combination regimens (e.g., FOLFIRINOX)Poor drug delivery due to dense desmoplastic stroma surrounding the cellsRapid clinical deterioration of patients
06

Interacting drugs

Gemcitabine

6 more in the full profile.

07

Biomarkers

Carbohydrate antigen 19-9 (CA 19-9)Carcinoembryonic antigen (CEA)KRAS mutation statusSMAD4/DPC4 expressionBRCA1/2 mutations

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