A recent study conducted in Japan found that the tumor tissues of 5 of 5 analyzed adult patients with PF/PM lesions expressed a high level of an abnormal c-Fos protein. This protein was a fusion protein formed by a chromosomal translocation between two disparate genes: the c-Fos gene (also termed FOS), a potential cancer-causing oncogene, normally located at chromosome band 24.3 on the long arm (i.e. q arm) of chromosome 14 and the VIM gene, normally located at band 13 on the short arm (i.e. p arm) of chromosome 10. The FOS:VIM fusion gene along with its c-Fos-VIM protein (which possesses uncontrolled c-Fos activity) are associated with the development and/or progression of some other fibroblastic and myofibroblastic tumors as well as malignant sarcomas. The FOS:VIM fusion gene and c-Fos-VIM fusion protein were found primarily in the epithelioid ganglion-like cell cells but mostly absent in the spindle-shaped cells of these lesion. The tumor of the single young person (1 year/old male) analyzed showed no evidence of this fusion gene or fusion protein. While these findings must be confirmed in a larger number of individuals, they do suggest that: 1) the FOS:VIM fusion gene and c-Fos-VIM fusion protein may contribute to the development of PF/PM in adults; 2) this fusion gene and its protein product may not be involved in childhood PF/PM tumors which also differ from adult PF/PM tumors in their histopathology (see the above Pathology section); and 3) the epithelioid ganglion-like cells but not spindle-shaped cells or any other cell types in adult PF/PM tumors may be neoplastic. It is further suggested that spontaneously reversing and self-limiting PF/PM tumors in adults are "transient neoplasms" similar to other theorized transient neoplasms such as nodular<unk><unk>  ossificans, aneurysmal bone cyst, and giant cell lesion of small bones. Two other genetic abnormalities have been reported in PF/PM tumors: trisomy 2 (i.e. the presence of an extra chromosome 2) in the tumor cells of two cases and a translocation of genetic material between band 23 on the long arm of chromosome 6 and band 32 on the long arm of chromosome 14 in the tumor cells of one case. Neither of these abnormalities have been validated, further characterized, or confirmed in other studies. Finally, 2 of 20<unk><unk>  tumors tested positive for the abnormal expression of FOSB protein, a product of the FOSB oncogene.
Proliferative fasciitis and proliferative myositis
Interstitial granulomatous dermatitis with arthritis
Blistering distal dactylitis
Remitting seronegative symmetrical synovitis with pitting edema
Photosensitivity with HIV infection
Nodular fasciitis
Milia-like calcinosis
Villonodular synovitis