Biogenesis (9E11), Caltag Laboratories (polyclonal), Chemicon, Fitzgerald (polyclonal), Novocastra (polyclonal), Oncogene (9E10, 8, 33), Pharmingen (9E10) and Serotec (CT14, polyclonal).

Several clones, including 9E10, are immunoreactive in acetone- or formalin-fixed, paraffin-embedded tissue sections.

Myc is the product of the early-response genemyc. The myc family of oncogenes, c-myc and N-myc, on chromosome 8, encodes three highly related regulatory cycle-specific nuclear phosphoproteins. Myc protein contains a transcriptional activation domain and a basic helix-loop-helix-leucine zipper DNA-binding and dimerization domain. As a heterodimer with a structurally related protein, Max, Myc can bind DNA in a sequence-specific manner, suggesting that the Myc/Max heterodimer functions as a transcriptional activator of genes critical for the regulation of cell growth (Prins et al, 1993; Vastrik et al, 1994). When overexpressed or hyperactivated as a result of mutation in certain types of cells,myc can cause uncontrolled proliferation. There is evidence thatmyc may have a critical role in the normal control of cell proliferation and cells in whichmyc expression is specifically prevented in vitro will not divide even in the presence of growth factors. Conversely, cells in whichmyc expression is specifically switched on independently of growth factors cannot enter G. If the cells are in G when Myc protein is provided, they will leave G0 and begin to divide even in the absence of growth factors, a behavior that ultimately causes them to undergo programed cell death or apoptosis.
The presence of a single oncogene is not usually sufficient to turn a normal cell into a cancer cell. In transgenic mice that are endowed withmyc oncogene, some of the tissues that express the oncogene grow to an exaggerated size and with the passage of time, some cells undergo further changes and give rise to cancers. However, the vast majority of cells in the transgenic mouse that express themyc oncogene do not give rise to cancers, showing that the presence of a single oncogene is not enough to cause neoplastic transformation. Nonetheless,myc expression produces an increased risk as the presence of another oncogene such as ras results in a synergistic effect known as oncogene collaboration. The synergism increases the incidence of cancers in the transgenic mouse to a much higher rate, although the cancers originate as scattered isolated tumors among noncancerous cells. Even with the presence of two expressed oncogenes, the cells must undergo further, randomly generated changes to become cancerous.
In follicular B-cell lymphomas, collaboration between myc and thebcl-2 gene occurs. If myc alone is overexpressed, cells are driven round the cell cycle inappropriately but this does not result in lymphoma because the progeny of such forced divisions die by apoptosis. Ifbcl-2 is overexpressed at the same time, the excess progeny survive and proliferate asbcl-2 acts as an oncogene by inhibiting apoptosis.

The ability to stain for c-Myc in tissue sections has understandably been received with great interest and several attempts have been made to use the oncoprotein as a prognostic marker. For example, in squamous cell carcinoma of the head and neck significant negative correlation has been shown between c-Myc levels and the number of metastatic nodes and clinical stage of disease but no correlation was found with tumor size or degree of differentiation (Gapany et al, 1994). Other recent applications have included c-Myc protein expression, in prostatic carcinoma (Fox et al, 1993), pituitary adenomas (Lloyd & Osamura, 1997, ovary (King et al, 1996), lung (Prins et al, 1993) and colon (Agnantis et al, 1991), among other tumors.
The examination of c-Myc as a marker for persons at risk of various types of cancer including breast carcinoma is another potential useful application (Hehir et al, 1993).

Clone 9E10 is immunoreactive in formalin-fixed, paraffin-embedded tissue sections.

•Agnantis NJ, Aapostolikas N, Sficas C et al 1991 Immunohistochemical detection of ras p21 and c-myc p62 in colonic adenomas and carcinomas. Hepatogastroenterology 38: 239-242.

•Fox SB, Persad RA, Royds J et al 1993. P53 and c-myc expression in stage A1 prostatic adenocarcinoma: useful prognostic determinants? Journal of Urology 150:490-494.

•Gapany M, Pavelic ZP, Kelley DJ et al 1994 Immunohistochemical detection of c-myc protein in head and neck tumors. Archives of Otolaryngology and Head and Neck Surgery 120:255-259.

•Hehir DJ, McGreal G, Kirwan WO et al 1993 C-myc oncogene expression: a marker for females at risk of breast carcinoma. Journal of Surgical Oncology 54:207-209.

•King LA, Okagaki T, Gallup DG et al 1996 Mitotic count, nuclear atypia, and immunohistochemical determination of Ki-67, c-myc, p21-ras, c-erbB2, and p53 expression in granulosa cell tumors of the ovary: mitotic count and Ki-67 are indicators of poor prognosis. Gynecological Oncology 61:227-232.

•Lloyd RV, Osamura RY 1997 Transcription factors in normal and neoplastic pituitary tissues. Miscroscopic Research and Technology 39:168-181.

•Prins J, De Vries EG, Mulder NH 1993 The myc family of oncogenes and their presence and importance in small cell carcinoma and other tumor types. Anticancer Research 13: 1373-1385.

•Vastrik I, Makela TP, Koskinen PJ et al 1994. Myc protein: partners and antagonists. Critical Reviews in Oncology 5:59-68.

Manual of diagnostic antibodies for immunohistology / Anthony S.-Y. Leong, Kumarasen Cooper, F. Joel W.-M. Leong.