About PC-3
The H660 cell line, derived from a 63-year-old white male with lung cancer, serves as a model to study small cell lung cancer (SCLC). SCLC is a highly aggressive form of lung cancer that often displays resistance to treatment, making it a challenging disease to manage effectively. H660 cells express several markers that are characteristic of SCLC. These include elevated levels of neural cell adhesion molecule (NCAM) and chromogranin A. NCAM is involved in cell-cell adhesion and plays a role in tumor cell migration and invasion. Chromogranin A is a marker commonly found in neuroendocrine tumors, including SCLC. The expression of these markers in H660 cells reflects the neuroendocrine characteristics of SCLC and provides insights into the molecular features of this aggressive cancer type.
H660 cells feature mutations in the TP53 and RB1 tumor suppressor genes. TP53 is a crucial gene involved in regulating cell growth and preventing the development of cancer. Mutations in TP53 are commonly observed in various cancer types and can lead to dysregulation of cell cycle control and increased tumor cell proliferation. RB1 is another tumor suppressor gene that plays a role in controlling cell division and preventing excessive cell growth. Mutations in RB1 are frequently found in SCLC and contribute to its aggressive nature. The presence of TP53 and RB1 mutations in H660 cells allows researchers to investigate the functional consequences of these genetic alterations and their impact on SCLC development and treatment resistance.
Pharmacologically, H660 cells have demonstrated resistance to dinaciclib, epirubicin, and staurosporine. Dinaciclib is a cyclin-dependent kinase (CDK) inhibitor that targets cell cycle progression, while epirubicin is a chemotherapy agent commonly used in the treatment of lung cancer. Staurosporine is a broad-spectrum protein kinase inhibitor. The resistance of H660 cells to these drugs highlights the challenges in effectively treating SCLC and the need for developing alternative therapeutic strategies to overcome drug resistance.
H660 cell cultures grow as adherent monolayers, forming a characteristic pattern of cell growth. The doubling time of H660 cells, approximately 40 hours, reflects their moderately proliferative nature.
NCIH660 Tumor Kinetics in the SRG™ Rat
In vivo tumor models generated from PC-3 cells tend to display necrotic regions and exhibit angiogenesis, indicating compromised blood supply and active formation of new blood vessels to sustain tumor growth. These characteristics mimic the tumor microenvironment observed in aggressive prostate cancer cases, providing researchers with a relevant in vivo system to investigate tumor behavior and responses to interventions.
Products & Services
Xenograft Efficacy Studies
Includes collection of blood, tissues & tumor for ADME, PK/PD and analysis.
(Bi)weekly Tumor Sampling
Via fine needle aspiration (FNA). For longitudinal evaluation of drug exposure, histology and gene expression.
OncoRats
Cutting edge models optimized for engraftment.
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References (MLA):
- Ditlevsen, Dorte Kornerup, et al. “NCAM-Induced Intracellular Signaling Revisited .” Wiley Online Library, Nov. 2007, onlinelibrary.wiley.com/doi/10.1002/jnr.21551.
- Gkolfinopoulos, Stavros, et al. “Chromogranin A as a Valid Marker in Oncology: Clinical Application or False Hopes?” World Journal of Methodology, 26 Mar. 2017, www.wjgnet.com/2222-0682/full/v7/i1/9.htm.
- Hamid, Anis, et al. “Compound Genomic Alterations of TP53, PTEN, and RB1 Tumor Suppressors in Localized and Metastatic Prostate Cancer.” Science Direct, 12 Dec. 2018, www.sciencedirect.com/science/article/abs/pii/S0302283818309497?via%3Dihub.