OE33

Cat.No.: CSC-C9231W

Species: Homo sapiens (Human)

Source: Esophagus

Morphology: epithelial

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Cat.No.
CSC-C9231W
Description
Established from the primary tumor of a 73-year-old white woman with Barrett-esophageal adenocarcinoma in 1993
Species
Homo sapiens (Human)
Source
Esophagus
Recommended Medium
Morphology
epithelial
Disease
Barrett Adenocarcinoma
Storage and Shipping
frozen with 70% medium, 20% FBS, 10% DMSO
Synonyms
OE-33; JROECL 33; JROECL33; OEC33
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

OE33 is a human esophageal adenocarcinoma cell line, originally isolated from a poorly differentiated adenocarcinoma located in the lower portion of the esophagus. The cell line has been used extensively as an in vitro tumor model system for studying the biology of esophageal adenocarcinoma (EAC), including tumor progression and Barrett's esophagus-associated carcinogenesis. OE33 cells exhibit epithelial morphology and form an adherent monolayer when maintained under typical cell culture conditions.

On a molecular level, OE33 cells share many of the genetic alterations found in esophageal adenocarcinoma, including TP53 mutations and genomic copy number alterations that regulate cell proliferation, apoptosis, and signal transduction. Therefore, OE33 can be used as a representative model cell line to study dysregulated pathways involved in EGFR- and HER2-dependent signaling and chemotherapy/radiotherapy resistance mechanisms. These cells have been used to study tumor cell proliferation, migration and invasion, epithelial-mesenchymal transition, and drug response. The cells can also be used to generate xenografts in immunodeficient mice.

Authentication of human esophageal adenocarcinoma cell line OE33.

Fig. 1. Authentication of human esophageal adenocarcinoma cell line OE33. A and B ) Hematoxylin- and eosin-stained sections of the original tissue and xenograft of OE33 showing a poorly differentiated adenocarcinoma. C ) In vitro growth pattern of cell line OE33. D ) Short tandem repeat profile of the primary normal tissue (P) and cell line OE33 (C) indicating correct derivation of the cell line (Boonstra J J, van Marion R, et al., 2010).

Mn Frequencies and CBPI Score in TK6 and OE33 Cells Upon Plasma Treatment

In this paper, Naser et al. studied the potential genotoxic effects of human plasma from healthy volunteers, as well as patients with gastro-oesophageal reflux disease, Barrett's oesophagus (BO) and oesophageal adenocarcinoma (OAC) using the oesophageal adenocarcinoma cell line (OE33) and the lymphoblastoid cell line (TK6).

Micronucleus (Mn) frequencies were assessed in TK6 and OE33 cells after treatment with patient plasma samples. In TK6 cells (77 samples), plasma from Barrett's esophagus (BO) patients significantly increased Mn frequency versus healthy volunteers (Fig. 1B), though with considerable inter-individual variability (0.43-fold decrease to 5-fold increase). Neither donor age (p=0.4631) nor gender (p=0.3514) affected Mn production. In OE33 cells (26 samples), plasma from BO and esophageal adenocarcinoma (OAC) patients showed non-significant Mn increases (p=0.4302 and p=0.4939; Fig. 2B), with similar variability (0.62-fold decrease to 1.79-fold increase). Age (p=0.2854) and gender (p=0.3956) had no effect. Cytokinesis-block proliferation index (CBPI) was unaffected by plasma treatment in both cell lines (TK6: 37 samples; OE33: 28 samples), though individual variation existed (TK6: 1.7-2.1; OE33: 1.2-1.56; Fig. 3).

Mn score in TK6 cells treated with plasma.

Fig. 1. Mn score in TK6 cells treated with plasma (Naser H, Munn K, et al., 2024).

Mn frequency in OE33 cells treated with plasma.

Fig. 2. Mn frequency in OE33 cells treated with plasma (Naser H, Munn K, et al., 2024)

CBPI score in TK6 and OE33 cells treated with plasma.

Fig. 3. CBPI score in TK6 and OE33 cells treated with plasma (Naser H, Munn K, et al., 2024).

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