LETTERS TO THE EDITOR Squamous Cell Carcinomas of the Head, Neck, and Skin Monoclonal or Polyclonal Origin?
Recent cytogenetic studies on one- to two-week cultures of squamous cell carcinomas (SCCs) of the tongue [1], skin [2], and larynx [3] have shown the presence of multiple clones. The clones were pseudodiploid or had 45 or 47 chromosomes. Many of the chromosome changes were reciprocal translocations. Little or no consistency was seen with regard to the chromosomes that were involved in structural changes, apart from chromosome 1 aberrations, which were present in most of the clones from a carcinoma of the tongue [1]. The clones were considered to have been present in vivo rather than to have arisen in vitro, because metaphases belonging to the same clone were situated on different coverslips or at some distance from each other on the same coverslip. Thus, the findings were considered to indicate polyclonal, as opposed to monoclonal, tumorigenesis and to support the concept of "field cancerization" [1, 2, 4]. That an apparently polyclonal origin was a particular feature of SCCs of the head, neck, and skin remained a possibility, but could not be verified by reference to studies on direct chromosome preparations owing to the extreme paucity of such studies on these types of tumor. Cytogenetic studies on series of malignant tumors using direct techniques generally show: i) evidence of monoclonality; ii) modal chromosome numbers that in the majority of tumors are below 45 or above 47; and iii) a lack of reciprocal translocations [5]. This is true of SCCs of the cervix uteri [6]; our studies to date suggest that it is also true of extragenital SCCs. We have previously published a direct chromosome study of an SCC of the forehead [7]. The modal chromosomal number was 42 and there were several unbalanced clonal structural chromosome changes. Clonal changes (unpublished data) have also been found in another SCC of the skin (mode, about 88 chromosomes), in one of the larynx (mode, 42), and in two of probable nasopharyngeal origin (modes, 44 and 70). Moreover, our earlier cytophotometric studies of 14 extragenital SCCs (unpublished data), including three of the tongue, five of the larynx, and three of the esophagus, showed a discrete DNA mode in all, which was compatible with 4 5 - 4 7 chromosomes in only one (esophagus); of the others, one was equivalent to 40 chromosomes (larynx), while the remainder were in the hypotriploidohypertetraploid range. How can the data on cultures of SCCs be reconciled with those obtained on uncultured tumor material? The chromosomal findings on cultures are certainly intriguing and merit further investigation. Are the dividing cells neoplastic but at an earlier, preinvasive, stage? Or, are they normal epithelial or stromal cells? We have recently commented [8] on a report [9] in which it was claimed that a basal cell carcinoma was of polyclonal origin, on the basis of cytogenetic findings on cultures of the tumor. Unless the nature of the cells that are dividing in cultures of malignant tumors is known, it does not seem justified to conclude that their karyotypes are those of the tumor. 135 © 1991 Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010
Cancer Genet Cytogenet 54:135-136 (1991) 0165-4608/91/$03.50
136
N . B . Atkin and M. C. Baker
This work was supported by a grant from the Association for International Cancer Research. We thank Margaret F. Fox for assistance with the chromosome studies. NIELS B. ATKIN MARION C. BAKER
Department of Cancer Research Mount Vernon Hospital Northwood, Mi d d l esex HA6 2RN, United Kingdom
REFERENCES 1. Jin Y, Heim S, Mandahl N, Bi6rklund A, Wennerberg J, Mitelman F (1988): Multiple apparently unrelated clonal chromosome abnormalities in a squamous cell carcinoma of the tongue. Cancer Genet Cytogenet 32:93-101. 2. Heim S, Mertens F, Jin Y, Mandahl N, Johansson B, Bi6rklund A, Wennerberg J, Jonsson N, Mitelman F (1988): Diverse chromosome abnormalities in squamous cell carcinomas of the skin. Cancer Genet Cytogenet 39:69-76. 3. Jin Y, Helm S, Mandahl N, Bi6rklund A, Wennerberg J, Mitelman F (1990): Multiple clonal chromosome aberrations in squamous cell carcinomas of the larynx. Cancer Genet Cytogenet 44:209-216. 4. Heim S, Mandahl N, Mitelman F (1988): Genetic convergence and divergence in tumor progression. Cancer Res 48:5911-5916. 5. Atkin NB (19861: Lack of reciprocal translocations in carcinomas. Cancer Genet Cytogenet 21:275-278. 6. Atkin NB, Baker MC, Fox MF (1990): Chromosome changes in 43 carcinomas of the cervix uteri. Cancer Genet Cytogenet 44:229-241. 7. Atkin NB, Baker MC, Petkovic I (1988): Squamous cell carcinoma of the skin with an unusual marker chromosome. Cytobios 54:161-166. 8. Atkin NB, Baker MC (1990): Cytogenetic studies of basal cell carcinomas. Cancer Genet Cytogenet 49:281-282. 9. Scappaticci S, Fraccaro M, Orecchia G (1989): Multiple clonal chromosome abnormalities in a superficial basal cell epithelioma. Cancer Genet Cytogenet 42:309-311.
Recent cytogenetic studies on one- to two-week cultures of squamous cell carcinomas (SCCs) of the tongue [1], skin [2], and larynx [3] have shown the presence of multiple clones. The clones were pseudodiploid or had 45 or 47 chromosomes. Many of the chromosome changes were reciprocal translocations. Little or no consistency was seen with regard to the chromosomes that were involved in structural changes, apart from chromosome 1 aberrations, which were present in most of the clones from a carcinoma of the tongue [1]. The clones were considered to have been present in vivo rather than to have arisen in vitro, because metaphases belonging to the same clone were situated on different coverslips or at some distance from each other on the same coverslip. Thus, the findings were considered to indicate polyclonal, as opposed to monoclonal, tumorigenesis and to support the concept of "field cancerization" [1, 2, 4]. That an apparently polyclonal origin was a particular feature of SCCs of the head, neck, and skin remained a possibility, but could not be verified by reference to studies on direct chromosome preparations owing to the extreme paucity of such studies on these types of tumor. Cytogenetic studies on series of malignant tumors using direct techniques generally show: i) evidence of monoclonality; ii) modal chromosome numbers that in the majority of tumors are below 45 or above 47; and iii) a lack of reciprocal translocations [5]. This is true of SCCs of the cervix uteri [6]; our studies to date suggest that it is also true of extragenital SCCs. We have previously published a direct chromosome study of an SCC of the forehead [7]. The modal chromosomal number was 42 and there were several unbalanced clonal structural chromosome changes. Clonal changes (unpublished data) have also been found in another SCC of the skin (mode, about 88 chromosomes), in one of the larynx (mode, 42), and in two of probable nasopharyngeal origin (modes, 44 and 70). Moreover, our earlier cytophotometric studies of 14 extragenital SCCs (unpublished data), including three of the tongue, five of the larynx, and three of the esophagus, showed a discrete DNA mode in all, which was compatible with 4 5 - 4 7 chromosomes in only one (esophagus); of the others, one was equivalent to 40 chromosomes (larynx), while the remainder were in the hypotriploidohypertetraploid range. How can the data on cultures of SCCs be reconciled with those obtained on uncultured tumor material? The chromosomal findings on cultures are certainly intriguing and merit further investigation. Are the dividing cells neoplastic but at an earlier, preinvasive, stage? Or, are they normal epithelial or stromal cells? We have recently commented [8] on a report [9] in which it was claimed that a basal cell carcinoma was of polyclonal origin, on the basis of cytogenetic findings on cultures of the tumor. Unless the nature of the cells that are dividing in cultures of malignant tumors is known, it does not seem justified to conclude that their karyotypes are those of the tumor. 135 © 1991 Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010
Cancer Genet Cytogenet 54:135-136 (1991) 0165-4608/91/$03.50
136
N . B . Atkin and M. C. Baker
This work was supported by a grant from the Association for International Cancer Research. We thank Margaret F. Fox for assistance with the chromosome studies. NIELS B. ATKIN MARION C. BAKER
Department of Cancer Research Mount Vernon Hospital Northwood, Mi d d l esex HA6 2RN, United Kingdom
REFERENCES 1. Jin Y, Heim S, Mandahl N, Bi6rklund A, Wennerberg J, Mitelman F (1988): Multiple apparently unrelated clonal chromosome abnormalities in a squamous cell carcinoma of the tongue. Cancer Genet Cytogenet 32:93-101. 2. Heim S, Mertens F, Jin Y, Mandahl N, Johansson B, Bi6rklund A, Wennerberg J, Jonsson N, Mitelman F (1988): Diverse chromosome abnormalities in squamous cell carcinomas of the skin. Cancer Genet Cytogenet 39:69-76. 3. Jin Y, Helm S, Mandahl N, Bi6rklund A, Wennerberg J, Mitelman F (1990): Multiple clonal chromosome aberrations in squamous cell carcinomas of the larynx. Cancer Genet Cytogenet 44:209-216. 4. Heim S, Mandahl N, Mitelman F (1988): Genetic convergence and divergence in tumor progression. Cancer Res 48:5911-5916. 5. Atkin NB (19861: Lack of reciprocal translocations in carcinomas. Cancer Genet Cytogenet 21:275-278. 6. Atkin NB, Baker MC, Fox MF (1990): Chromosome changes in 43 carcinomas of the cervix uteri. Cancer Genet Cytogenet 44:229-241. 7. Atkin NB, Baker MC, Petkovic I (1988): Squamous cell carcinoma of the skin with an unusual marker chromosome. Cytobios 54:161-166. 8. Atkin NB, Baker MC (1990): Cytogenetic studies of basal cell carcinomas. Cancer Genet Cytogenet 49:281-282. 9. Scappaticci S, Fraccaro M, Orecchia G (1989): Multiple clonal chromosome abnormalities in a superficial basal cell epithelioma. Cancer Genet Cytogenet 42:309-311.
