already hypothesized [2] that expression of Bcl-2 is particularly attractive for stabilizing syncytia and should ultimately be important in facilitating inva- sion and metastasis of cancer [2]. I was, thus, pleased to read the pre-publication abstract of experimental work by Trisciuoglio, Desideri, Ciuff- reda, et al. [3]. Although they do not refer to cell fusion as a causative mechanism for advancement of melanoma, they do note that over-expression of Bcl-2 facilitates aggressive behavior specifically invasion and metastasis. It is also noteworthy that they observed a correlation of expression of metal- loprotease-2 (MMP-2) with aggressive behavior. Xuan, Tuck, Wilson, et al. [4] have also noted that MMP-2 is associated with aggressive behavior, but that other factors associated with cell fusion are essential for metastasis. Busund, Killie, Bartnes, et al. [5] also noted that heterotypic cell fusion was a mechanism through which aggressive pheno- types could be achieved. Mutations certainly con- tribute to development of neoplasia, but neither mutations nor aneuploidy alone can account for the variety of stable multinuclear cells, syncytia, karyoplasts and other products of cell fusion typi- cally observed in clinically significant cancers. References [1] Parris GE. Clinically significant cancer evolves from transient mutated and/or aneuploid neoplasia by cell fusion to form unstable syncytia that give rise to ecologically viable parasite species. Med Hypotheses 2005 [in press]. [2] Parris GE. The role of viruses in cell fusion and its importance to evolution, invasion and metastasis of cancer clones. Med Hypotheses 2005;64:1011–4. [3] Trisciuoglio D, Desideri M, Ciuffreda L, et al. Bcl-2 overex- pression in melanoma cells increases tumor progression- associated properties and in vivo tumor growth. J Cell Physiol 2005 [Epub ahead of print]. [4] Xuan JW, Tuck AB, Wilson SM, Chin JL, Chambers AF. MMP-2 expression associated with, but not sufficient for, malignant conversion of murine LTA cells. Anticancer Res 1998;18: 743–9. [5] Busund LT, Killie MK, Bartnes K, Seljelid R. Spontaneously formed tumorigenic hybrids of Meth A sarcoma cells and macrophages in vivo. Int J Cancer 2003;106:153–9. George Parris 9601 Warfield Road Gaithersburg, Maryland 20882 United States Tel.: +1 301 963 7037 E-mail address: antimony_121@hotmail.com doi:10.1016/j.mehy.2005.06.004 Incidence of mandibular osteoradionecrosis may be low in head and neck cancer patients treated with concurrent radiation and weekly paclitaxel To the Editor, Osteoradionecrosis (ORN) is a condition of nonvi- tal bone in a site of radiation injury. The presen- tation of ORN after radiotherapy (RT) for head and neck cancer varies from small, asymptomatic bone exposures that may remain stable for months to years or heal with conservative man- agement, to severe necroses necessitating surgical intervention and reconstruction. The mandible is the most common site of radiation-induced tissue damages following treatment of head and neck cancer, with an incidence of 5–15% of cases, probably because it is often necessary to deliver a high RT dose to tumors near the mandible and possibly also because the blood supply may be less abundant than that of the maxilla [1]. Hyperbaric oxygen therapy (HBO) is one of the option for this complication. In practice, uncontrolled studies showed recovery rates from osteroradionecrosis of 15–45% with HBO alone, and 20–90% with HBO combined to surgery. Unfortunately, recent randomized study showed that patients with overt mandibular ORN did not benefit from HBO [2]. Chemotherapy as a radiosensitizer has been inte- grated into the initial treatment of patients with locally advanced squamous cell cancer of the head and neck to improve locoregional control and sur- vival. Because of its inherent activity against squamous cell cancer of the head and neck and its radiation-sensitizing properties, weekly paclit- axel is a valuable agent in the treatment of this 994 Correspondence