IGR-37

Cat.No.: CSC-C0343

Species: Homo sapiens (Human)

Source: Lymph Node Metastasis

Morphology: epithelial-like cells growing as monolayers

Culture Properties: monolayer

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Cat.No.

CSC-C0343

Description

Established from the lymph node metastasis (groin) of a 26-year-old man with malignant melanoma (primary tumor histology: SSM level IV); same patient as cell line IGR-39; described as very tumorigenic in nude mice

Species

Homo sapiens (Human)

Source

Lymph Node Metastasis

Recommended Medium

85% DMEM + 15% h.i.FBS

Culture Properties

monolayer

Morphology

epithelial-like cells growing as monolayers

Karyotype

Human flat-moded hypertriploid karyotype with 11% polyploidy - 78(67-78)<3n>XXY, +1, +3, +5, +7, +7, +8, +9, -10, -12, -13, -14, -15, -17, +18, +20, +20, +2mar, der(1)t(1;?21)(p13;q11)x2, del(9)(p13p21), der(10)t(9;10)(q11/21;q23/25), i(13q)x1-2, der(16)t

Disease

Melanoma

Quality Control

Mycoplasma: contamination was eliminated with Baytril (enrofloxacin), then negative in DAPI, microbiological culture, RNA hybridization assays
Immunology: cytokeratin -, cytokeratin-7 -, cytokeratin-8 -, cytokeratin-17 -, cytokeratin-18 -, cytokeratin-19

Storage and Shipping

Frozen with 70% medium, 20% FBS, 10% DMSO at about 5 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen

Synonyms

IgR-37; IGR 37; IGR37; MM1; Institut Gustave Roussy-37

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.

IGR-37 is a human melanoma cell line established from a lymph node metastasis (groin) of a 26‑year‑old male patient with malignant melanoma, primary tumor histology superficial spreading melanoma (SSM) level IV. The same patient also gave rise to the primary melanoma cell line IGR‑39 (CSC-C0344), making IGR‑37 a syngeneic, patient‑matched metastatic counterpart.

The primary IGR‑39 and metastatic IGR‑37 represent a unique, genetically correlated pair of human melanoma cells from the same donor. This allows direct molecular, phenotypic, and functional comparisons without confounding inter‑individual genetic variation. IGR‑37 consistently exhibits greater tumorigenicity in nude mice, forms larger tumors, and may harbor metastatic‑specific modifications such as altered ganglioside signatures (e.g., O‑acetylation of GM2, GD3 and GD2). This paired system is therefore an invaluable resource for identifying biomarkers of metastasis and for modeling the melanoma progression cascade.

IGR‑37 cells display an epithelial‑like morphology, a doubling time of approximately 48-72 hours, and a hypertriploid karyotype. They carry the BRAF V600E mutation but are wildtype for NRAS Q61, reflecting a common driver mutation in cutaneous melanoma. The line is inherently resistant to TRAIL‑induced apoptosis, an established model for studying apoptosis evasion and for testing sensitizing strategies.

Comparison of The Oncolytic Activity of A Replication-Competent and A Replication-Deficient Herpes Simplex Virus 1

In 2015, the oncolytic herpes simplex virus 1 (HSV-1) T-VEC (talimogene laherparepvec) was approved for intratumoral injection in non-resectable malignant melanoma. To determine whether viral replication is required for oncolytic activity, we compared replication-deficient HSV-1 d106S with replication-competent T-VEC.

High infectious doses of HSV-1 d106S killed melanoma (n = 10), head-and-neck squamous cell carcinoma (n = 11), and chondrosarcoma cell lines (n = 2) significantly faster than T-VEC as measured by MTT metabolic activity, while low doses of T-VEC were more effective over time. HSV-1 d106S and, to a lesser extent T-VEC, triggered caspase-dependent early apoptosis as shown by pan-caspase inhibition and specific induction of caspases 3/7, 8, and 9. HSV-1 d106S induced a higher ratio of apoptosis-inducing infected cell protein (ICP) 0 to apoptosis-blocking ICP6 than T-VEC. T-VEC was oncolytic for an extended period of time as viral replication continued, which could be partially blocked by the antiviral drug aciclovir. High doses of T-VEC, but not HSV-1 d106S, increased interferon-β mRNA as part of the intrinsic immune response. When markers of immunogenic cell death were assessed, ATP was released more efficiently in the context of T-VEC than HSV-1 d106S infection, whereas HMGB1 was induced comparatively well.

Overall, the early oncolytic effect on three different tumor entities was stronger with the non-replicative strain, while the replication-competent virus elicited a stronger innate immune response and more pronounced immunogenic cell death.