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. 2003 Oct 1;31(19):5635–5643. doi: 10.1093/nar/gkg786

Table 2. Independent validation of cancer-specific splicing.

Gene LOD Alt splice? Splice form cancer specific? Functional impact?
ACT1 (NFκB activator 1) 2.5 Confirmed (34) Confirmed to be dominant in 10 cancer cell lines (‘epithelial-like’ adherent cancer cells, non-adherent cancer cells, melanomas), but did not examine same normal samples (34) Cancer form shown to activate NFκB, but no specific change demonstrated
BIN1 (tumor suppressor) 1.6 Confirmed (18) Confirmed in eight melanoma cell lines, compared with fetal melanocytes (normal) (18) Eliminates tumor suppressor activity
CC3 (metastasis suppressor) 0.9 Confirmed (35) Cancer-specific splice form (TC3) confirmed to be present in all tumor cell lines expressing CC3, versus only very low levels in normal tissues (35) Switches CC3 activity from inducing apoptosis to inhibiting apoptosis
FGFR1 (fibroblast growth factor receptor 1) 0.9 Confirmed (36) Confirmed in a panel of matched glioblastomas versus normal brain white matter. The level of the cancer-specific form correlated strongly with tumor malignancy (36,37) Changes fibroblast growth factor receptor from low-affinity form (normal brain) to high affinity form (tumor)
LDHC (lactate dehydrogenase) 2.8 Confirmed (12) Confirmed in a large panel of lung cancer and melanoma samples, versus many normal tissues (12) Removes NAD binding
NABC1 (breast carcinoma amplified 1) 3.2 Confirmed (38) Observed at higher levels in breast tumors (and not in breast normal) (38) Unknown
NER (nuclear hormone receptor) 0.7 Confirmed (10) Confirmed in 116 of 128 primary cancers and in 31 of 39 cancer cell lines, and absent in the corresponding normal tissues (10) Removes DNA binding domain