DNA & Clones

DNA was prepared from cell line WM1361A. WM1361A is a tumorigenic (VGP) primary melanoma cell line with competence for metastasis. These cells display mesenchymal morphology in culture. This cell line contains a Q61R mutation at position 61 in the N-RAS gene. The Q61R is the most common NRAS mutation found in melanoma that is thought to occur due to UV and radiation exposure. This mutation leads to production of a constitutively active N-RAS protein that directs cells to grow and divide constantly. This cell line also expresses PTEN loss of function including hemizygous PTEN deletion and is wild type for BRAF, c-KIT, and CDK4. WM1361A cells produce xenograft tumors when injected into immunocompromised mice.

DNA was prepared from cell line WM1361A. WM1361A is a tumorigenic (VGP) primary melanoma cell line with competence for metastasis. These cells display mesenchymal morphology in culture. This cell line contains a Q61R mutation at position 61 in the N-RAS gene. The Q61R is the most common NRAS mutation found in melanoma that is thought to occur due to UV and radiation exposure. This mutation leads to production of a constitutively active N-RAS protein that directs cells to grow and divide constantly. This cell line also expresses PTEN loss of function including hemizygous PTEN deletion and is wild type for BRAF, c-KIT, and CDK4. WM1361A cells produce xenograft tumors when injected into immunocompromised mice.

DNA was prepared from cell line WM1366. WM1366 is a tumorigenic (VGP) primary melanoma cell line with competence for metastasis. This cell line was established from a right forearm in a 79-year-old male with stage IV superficial spreading melanoma. WM1366 cells produce xenograft tumors when injected into immunocompromised mice. This cell line features a Q61L mutation at position 61 in the N-RAS gene. The Q61L mutation results in an amino acid substitution at position 61 in NRAS, from a glutamine (Q) to a leucine (L). The role of N-RAS mutations for selecting/prioritizing anticancer treatment, including cytotoxic chemotherapy and targeted agents, is unknown at this time. This cell line is wild type for BRAF, PTEN c-KIT, and CDK4.

DNA was prepared from cell line WM1366. WM1366 is a tumorigenic (VGP) primary melanoma cell line with competence for metastasis. This cell line was established from a right forearm in a 79-year-old male with stage IV superficial spreading melanoma. WM1366 cells produce xenograft tumors when injected into immunocompromised mice. This cell line features a Q61L mutation at position 61 in the N-RAS gene. The Q61L mutation results in an amino acid substitution at position 61 in NRAS, from a glutamine (Q) to a leucine (L). The role of N-RAS mutations for selecting/prioritizing anticancer treatment, including cytotoxic chemotherapy and targeted agents, is unknown at this time. This cell line is wild type for BRAF, PTEN c-KIT, and CDK4.

DNA was prepared from cell line WM1366. WM1366 is a tumorigenic (VGP) primary melanoma cell line with competence for metastasis. This cell line was established from a right forearm in a 79-year-old male with stage IV superficial spreading melanoma. WM1366 cells produce xenograft tumors when injected into immunocompromised mice. This cell line features a Q61L mutation at position 61 in the N-RAS gene. The Q61L mutation results in an amino acid substitution at position 61 in NRAS, from a glutamine (Q) to a leucine (L). The role of N-RAS mutations for selecting/prioritizing anticancer treatment, including cytotoxic chemotherapy and targeted agents, is unknown at this time. This cell line is wild type for BRAF, PTEN c-KIT, and CDK4.

DNA was prepared from cell line WM1552C. WM1552C is a non-tumorigenic (RGP) primary human melanoma cell line without metastatic capability. This cell line was established from a subcutaneous tissue in a 72-year-old male with stage III superficial spreading melanoma. This cell line features the specific V600E (Val600Glu) mutation at codon 600 in the BRAF gene. This mutation causes constitutively active kinase activity and activation of MEK and ERK signaling pathway. This cell line also expresses PTEN loss of function including mutated and hemizygous PTEN deletion and is wild type for N-RAS, c-KIT, and CDK4. WM1552C cells produce xenograft tumors when injected into immunocompromised mice.

DNA was prepared from cell line WM1552C. WM1552C is a non-tumorigenic (RGP) primary human melanoma cell line without metastatic capability. This cell line was established from a subcutaneous tissue in a 72-year-old male with stage III superficial spreading melanoma. This cell line features the specific V600E (Val600Glu) mutation at codon 600 in the BRAF gene. This mutation causes constitutively active kinase activity and activation of MEK and ERK signaling pathway. This cell line also expresses PTEN loss of function including mutated and hemizygous PTEN deletion and is wild type for N-RAS, c-KIT, and CDK4. WM1552C cells produce xenograft tumors when injected into immunocompromised mice.

DNA was prepared from cell line WM1552C. WM1552C is a non-tumorigenic (RGP) primary human melanoma cell line without metastatic capability. This cell line was established from a subcutaneous tissue in a 72-year-old male with stage III superficial spreading melanoma. This cell line features the specific V600E (Val600Glu) mutation at codon 600 in the BRAF gene. This mutation causes constitutively active kinase activity and activation of MEK and ERK signaling pathway. This cell line also expresses PTEN loss of function including mutated and hemizygous PTEN deletion and is wild type for N-RAS, c-KIT, and CDK4. WM1552C cells produce xenograft tumors when injected into immunocompromised mice.

DNA was prepared from cell line WM164. WM164 is a metastatic human melanoma cell line established from a metastatic site (right upper arm) in a 22-year-old male with stage IV superficial spreading melanoma. WM164 cells produce xenograft tumors when injected into immunocompromised mice. This cell line features the specific V600E (Val600Glu) mutation at codon 600 in the BRAF gene. This mutation causes constitutively active kinase activity and activation of MEK and ERK signaling pathway.