myc family oncogene amplification in tumor cell lines established from small cell lung cancer patients and its relationship to clinical status and course.

MYC oncogenes and human neoplastic disease

“…In addition to the infrequent L-MYC ampli®cation in SCLC discussed above, both C-MYC and N-MYC ampli®cation and overexpression have also been observed (Little et al, 1983;Saksela et al, 1984;Nau et al, 1986;Funa et al, 1987;Johnson et al, 1987Johnson et al, , 1992Gu et al, 1988;Takahashi et al, 1989;Noguchi et al, 1990;Makela et al, 1992;Rygaard et al, 1993). The frequency of ampli®cation/overexpression for either gene has generally ranged from 2 ± 30% of all tumors, xenografts or cell lines and the extent of ampli®cation has ranged from 5 ± 4100-fold.…”

“…Nau et al (1985) were the ®rst to report the cloning of L-MYC and its ampli®cation in SCLC. Subsequently, numerous con®rmatory reports of L-MYC ampli®cation and overexpression in SCLC cell lines, primary tumors, and tumor xenografts have appeared (Johnson et al, 1987(Johnson et al, , 1992Gu et al, 1988;Takahashi et al, 1989;Noguchi et al, 1990;Gazzeri et al, 1990;Makela et al, 1992;Rygaard et al, 1993). In general, the incidence of L-MYC ampli®cation and/or overexpression in primary SCLC tumors have been reported to be in the range of 5 ± 10% (Johnson et al, 1987(Johnson et al, , 1992Takahashi et al, 1989;Noguchi et al, 1990).…”

“…Subsequently, numerous con®rmatory reports of L-MYC ampli®cation and overexpression in SCLC cell lines, primary tumors, and tumor xenografts have appeared (Johnson et al, 1987(Johnson et al, , 1992Gu et al, 1988;Takahashi et al, 1989;Noguchi et al, 1990;Gazzeri et al, 1990;Makela et al, 1992;Rygaard et al, 1993). In general, the incidence of L-MYC ampli®cation and/or overexpression in primary SCLC tumors have been reported to be in the range of 5 ± 10% (Johnson et al, 1987(Johnson et al, , 1992Takahashi et al, 1989;Noguchi et al, 1990). This range is higher (perhaps up to 50%) in SCLC cell lines, xenografts, and in cell lines derived from treated versus untreated patients (Johnson et al, 1987;Gu et al, 1988;Gazzeri et al, 1990;Rygaard et al, 1993), although this has not invariably been the case (Johnson et al, 1992).…”

“…In general, the incidence of L-MYC ampli®cation and/or overexpression in primary SCLC tumors have been reported to be in the range of 5 ± 10% (Johnson et al, 1987(Johnson et al, , 1992Takahashi et al, 1989;Noguchi et al, 1990). This range is higher (perhaps up to 50%) in SCLC cell lines, xenografts, and in cell lines derived from treated versus untreated patients (Johnson et al, 1987;Gu et al, 1988;Gazzeri et al, 1990;Rygaard et al, 1993), although this has not invariably been the case (Johnson et al, 1992). In most of the above studies in which it was investigated, up to 40-fold ampli®cation and overexpression relative to control tissues or cell lines were observed.…”

Modeling human lung cancer in mice: similarities and shortcomings

“…NSCLC specimens contain activating K-ras mutations in 20 ± 50% of the tumors (Rodenhuis and Slebos et al, 1990;Mills et al, 1995); 50% have deletions or mutations of p53 (Kondo et al, 1992;Mitsudomi et al, 1992); 60% show deletion or reduced expression of p16 INK4a (Kamb et al, 1994;Okamoto et al, 1994Okamoto et al, , 1995Merlo et al, 1995;Shapiro et al, 1995;Xiao et al, 1995); and up to 30% show deletion or reduced expression of Rb (Xu et al, 1991;Reissmann et al, 1993). SCLC specimens demonstrate overexpression of the myc family of protooncogenes due to gene ampli®cation in 10 ± 40% of the tumors (Little et al, 1983;Johnson et al, 1987;Takahashi et al, 1989;Noguchi et al, 1990); 80% have p53 mutations or deletions Hensel et al, 1991;Takahashi et al, 1991;Sameshima et al, 1992); and 90% have deletions of Rb (Yokota et al, 1988;Hensel et al, 1990). Chromosome 3p deletions, which occur at a chromosomal fragile site and often include the FHIT gene, are found in 50% of NSCLC and 90% of SCLC primary tumors (Brauch et al, 1987;Sozzi et al, 1996).…”