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PubMed1999

A possible involvement of aberrant expression of the FHIT gene in the carcinogenesis of squamous cell carcinoma of the uterine cervix.

To investigate involvement of an aberrant expression of the FHIT (fragile histidine triad) gene in the process of carcinogenesis and progression in cervical carcinoma, we examined its expression by the reverse transcriptase polymerase chain reaction (RT-PCR) and cDNA sequence method in 32 cervical invasive carcinomas (25 squamous cell carcinomas and seven adeno- or adenosquamous carcinomas) and 18 of its precursor lesions [four low-grade and 14 high-grade cervical intraepithelial neoplasias (CINs)]. We also examined a link between the occurrence of the aberrant expression and human papillomavirus (HPV). We detected the aberrant FHIT transcripts in 11 of 25 (44%) cervical invasive squamous cell carcinomas and in 5 of 14 (36%) high-grade CINs (CIN 2 or 3), whereas they were not found in seven non-squamous type and four low-grade CINs (CIN 1). The alteration patterns of the FHIT gene expression in high-grade CINs were virtually similar to those found in invasive carcinomas, such that the exons 5-7 were consistently deleted associated or unassociated with loss of the exon 4 and/or 8. The incidence of the aberrant expression was not related to the presence of HPV and its type. These data indicate that the aberrant expression of the FHIT gene is observed in precursor lesions of cervical carcinoma as well as invasive carcinomas, with its incidence not increasing with advance of clinical stage. Given the squamous cell type dominant expression, the aberrant expression may play a critical role in the generation of squamous cell carcinoma of the uterine cervix, but not the consequence of the progression of the cancer.

Adult↗

PubMed2006

Photodynamic therapy does not prevent cutaneous squamous-cell carcinoma in organ-transplant recipients: results of a randomized-controlled trial.

A randomized-controlled trial with paired observations was performed with 40 organ-transplant recipients to assess the preventive effect of photodynamic therapy (PDT) on the development of new squamous-cell carcinomas and to evaluate the effect of PDT on the number of keratotic skin lesions. The treatment area consisted of a randomly assigned forearm and the corresponding hand, whereas the other forearm and hand served as the control area. After the initial visit, follow-up visits were scheduled at 3-monthly intervals during 2 years. No statistically significant difference was found in the occurrence of new squamous-cell carcinomas between the treated and untreated arms: after 2 years of follow-up, we observed 15 squamous-cell carcinomas in nine out of 40 PDT-treated arms and 10 squamous-cell carcinomas in nine out of 40 control arms. The number of keratotic skin lesions increased in both arms, but was less pronounced in the PDT-treated arm. After 1 year of follow-up, a trend in favor of the PDT-treated arm was observed, but statistical significance was not reached. Nearly 80% of the patients reported mild to severe adverse effects consisting of pain and a burning sensation, immediately after the treatment. No long-term adverse events were noted. In conclusion, PDT does not appear to prevent the occurrence of new squamous-cell carcinomas in organ-transplant recipients, but to some degree, reduces the increase of keratotic skin lesions.

Adult↗

PubMed2005

Centromeric chromosomal translocations show tissue-specific differences between squamous cell carcinomas and adenocarcinomas.

Structural chromosomal aberrations are common in epithelial tumors. Here, we compared the location of centromeric breaks associated with whole arm translocations in seven adenocarcinoma cell lines and nine squamous cell carcinoma cell lines using SKY, microarray-based comparative genomic hybridization (array CGH) and fluorescence in situ hybridization (FISH). Whole arm translocations were more frequent in squamous cell carcinomas (112 in nine cell lines and nine in one short-term culture) than in adenocarcinomas (13 in seven cases) and most often resulted in copy number alterations. Array CGH analysis demonstrated that in all squamous cell carcinomas and in most adenocarcinomas, the breakpoints of unbalanced whole arm translocations occurred between the two clones on the array flanking the centromeres. However, FISH with centromeric probes revealed that in squamous cell carcinomas, the marker chromosomes with whole arm translocations contained centromeres comprised of material from both participating chromosomes, while in adenocarcinomas centromeric material from only one of the chromosomes was present. These observations suggest that different mechanisms of centromeric instability underlie the formation of chromosomal aberrations in adenocarcinomas and squamous cell carcinomas.

Adenocarcinoma↗

PubMed1999

Multimodal therapy for squamous carcinoma of the oesophagus.

BACKGROUND: The results of surgical treatment for oesophageal squamous cell cancer have improved over recent decades, but the long-term prognosis for patients with tumours of stage II or higher is still unsatisfactory. While uncontrolled series of adjuvant or neoadjuvant treatment have reported favourable survival rates, the true benefit of multimodal treatment can be determined only by randomized controlled trials. METHODS: The literature was searched for prospective randomized controlled trials (PRCTs) examining the effect of neoadjuvant or adjuvant treatment on the long-term survival of patients with squamous cell cancer of the oesophagus. RESULTS: More than 30 PRCTs studying multimodal treatment concepts aimed at improving the prognosis of squamous cell carcinoma of the oesophagus were identified. These trials have not documented improved survival by adjuvant radiotherapy or chemotherapy. Following neoadjuvant radiotherapy or chemotherapy (or a combination of both), resectability of squamous cell carcinoma is not increased, the postoperative mortality rate appears to be higher and survival is not prolonged. CONCLUSION: Past multimodality protocols have not improved the prognosis of squamous carcinoma of the oesophagus. Careful design and reporting, together with strict control of surgical procedures, should allow more meaningful analysis of future multimodal treatment studies. At present, neoadjuvant or adjuvant treatment cannot be recommended outside such clinical protocols.

Carcinoma, Squamous Cell↗

PubMed2003

Differential expression of p53, p63 and p73 proteins in human buccal squamous-cell carcinomas.

Abnormalities in the p53 gene are regarded as the most consistent of the genetic abnormalities in oral squamous-cell carcinoma. Two new members of the p53 gene family, p73 and p63, have recently been identified, with the three sharing considerable sequence homology at the acidic N-terminal transactivation, central DNA-binding and C-terminal oligomerization domains, indicating possible functional and biological interactions. The differential expression of p73, p63 and p53 genes in human oral squamous-cell carcinoma does not yet appear to be completely understood, however. In this study, therefore, immunohistochemical analysis of protein expression was performed for 40 samples of well-differentiated human buccal squamous-cell carcinomas, with 10 specimens of normal buccal mucosa employed as controls. Differential expressions of p63, p73 and p53 proteins in the carcinoma samples were: p63+/p73+/p53 + (n = 28; 70%); p63+/p73+/p53- (n = 4; 10%); p63+/p73-/p53- (n = 8; 20%), respectively; and p63+/p73+/p53- for normal mucosa (n = 10; 100%). A significant correlation between p53, p63 and p73 immunoexpression was demonstrated for the buccal squamous-cell carcinoma samples (P < 0.0001; Fisher's exact test). Significance was not achieved for the correlation between p73 and p53 immunoexpression and clinicopathological parameters for buccal carcinomas (P > 0.05; Fisher's exact test). Our results indicate that both p73 and p63 may be involved in the development of human buccal squamous-cell carcinoma, perhaps in concert with p53.

Adult↗

PubMed1996

Cytokeratin immunolocalization and lectin binding studies in oesophageal squamous dysplasia.

We examined full thickness specimens of oesophageal squamous dysplasia from both cancer-free and cancer patients using immunohistochemical labelling for cytokeratin subtypes 10/13 and 14 and for involucrin, binding studies for various lectins, and PAS/D staining before and after diastase treatment. We studied specimens from patients with oesophageal carcinoma (52 normal epithelia, and 49 with mild, 38 with moderate, and 32 with severe dysplasia), and 32 specimens from cancer-free patients (five normal epithelia and 16 with mild and 11 with moderate dysplasia). Abnormal cytokeratin expression patterns in atypical cells, i.e. both cytokeratin 10/13 and cytokeratin 14 immunoreactivity in the same cells was detected in 41 of 99 specimens with dysplasias in cancer patients. Helix aspersa, Erythrina cristagalli and Robinia pseudoacacia binding was consistently negative in atypical cells in squamous dysplasia. The non-atypical layer of squamous dysplasia, which was morphologically indistinguishable from the corresponding layer of normal oesophageal squamous epithelium, showed abnormal involucrin expression in 39/ 101 specimens, Helix aspersa binding in 74/106, diastase sensitive PAS staining in 52/110, Erythrina cristaglli binding in 28/107, and Robinia pseudoacacia binding in 16/100. There were no significant differences in the expression of these markers in dysplasia between cancer patients and cancer-free individuals with the exception of increased Robinia pseudoacacia binding in the non-atypical layer in cancer-free patients. The results indicate that abnormal patterns of cytokeratin expression and lectin binding occur not only in atypical cells but also in non-atypical cells in oesophageal squamous dysplasia.

Adult↗

PubMed2000

Basaloid squamous carcinoma of the oesophagus: a distinct neoplasm with multipotential differentiation.

AIMS: Basaloid squamous carcinoma (BSC) is an uncommon variant of squamous cell carcinoma, with its prevalent sites being the hypopharynx, tongue base and larynx. In the oesophagus, BSC is rarer than in the head and neck region. This study was aimed to document the clinicopathological features of BSCs of the oesophagus, and to present their relative incidence and immunohistochemical findings. METHODS AND RESULTS: Eighteen cases of BSC of the oesophagus, comprising 3.6% of 502 oesophageal carcinomas, were reviewed for their pathological and clinical features, and examined for the immunohistochemical expression of neuroendocrine markers, cytokeratins, p53, pRb and bcl-2. Oesophageal basaloid squamous carcinomas tended to be biphasic or multiphasic carcinomas, most commonly with basaloid and squamous components (eight cases), or with additional adenocarcinoma (three cases) or with small cell carcinoma (two cases). Each component was microscopically clearly distinguishable from the others, and metastasized separately, chiefly the basaloid component. The remaining five cases were apparently pure basaloid carcinomas, being characterized by lobules and nests of monotonous round undifferentiated cells with frequent comedo necrosis. They resembled, but were differentiated from, the small cell carcinoma on the basis of neuroendocrine markers and cytokeratin expression. p53, pRb and bcl-2 oncoprotein, which are known to normally present in the basal/parabasal cells of the oesophageal epithelium, were detected in 40-50% of cases, with a heterogeneous expression pattern. The patients were all male, with the age ranging 47-74 years (median 57) and presented at variable stages. The plotted 3 years survival rate was 51%, and the immunohistochemical expression of p53, pRb and bcl-2 was not related to the survival of the patients. CONCLUSION: Basaloid squamous carcinoma of the oesophagus is a peculiar neoplasm with a capacity of multidirectional differentiation, often with heterogeneous oncogene expression, probably reflecting the pluripotential stem cell origin.

Aged↗

PubMed2000

Ber EP4 and epithelial membrane antigen aid distinction of basal cell, squamous cell and basosquamous carcinomas of the skin.

AIMS: Seventy-five skin tumours were studied to investigate the value of immunohistochemistry in differentiating basal cell, squamous cell and basosquamous carcinomas of the skin. METHODS AND RESULTS: Archived paraffin-embedded tissue samples of basal cell carcinomas (n = 39), squamous cell carcinomas (n = 23) and basosquamous carcinomas (n = 13) were stained immunohistochemically using a panel of antibodies. All of the basal cell carcinomas stained positively for Ber EP4, in contrast to the group of squamous cell carcinomas, that showed no staining. Basosquamous carcinomas all showed at least some areas of Ber EP4 positivity. None of the basal cell carcinomas, but most of the squamous cell carcinomas (22 of 23) expressed epithelial membrane antigen (EMA). Only one of the basosquamous carcinomas expressed EMA positivity focally. CAM 5.2, carcinoembryonic antigen (CEA) and 34betaE12 antibodies lacked specificity in relation to the different tumour types. CONCLUSION: Distinction of basal and squamous cell carcinomas of the skin can be readily achieved with routine immunohistochemistry using Ber EP4 and EMA. Identification of basosquamous carcinoma is also facilitated with this method.

Adolescent↗

PubMed2000

Microsatellite instability and alteration of E2F-4 gene in adenosquamous and squamous cell carcinomas of the stomach.

Microsatellite instability (MSI) due to defective DNA mismatch repair (MMR) is a form of genomic instability underlying the tumorigenesis of various human neoplasms. To evaluate the roles of MSI in the pathogenesis of gastric carcinomas with squamous differentiation, 17 primary stomach cancer patients (15 adenosquamous and two squamous cell carcinomas) were examined for MSI frequency using five microsatellite markers and the criteria for MSI recommended by the National Cancer Institute Workshop. The molecular causes and consequences of MSI in these neoplasms were further researched through the immunohistochemistry of MMR proteins and the mutational analysis of cancer-associated genes targeted by MSI, respectively. Two of the 17 (12%) cases demonstrated MSI at the most examined loci and were classified as having high level MSI (MSI-H). These tumors also exhibited frame-shift mutations at mononucleotide repeats in the target genes, including TGFbetaRII, IGFIIR, BAX, and hMSH6. It is interesting to note that the mutations of the serine (AGC)13 repeats within the E2F-4 gene were found only in the squamous cell carcinoma portions of them, whereas such alterations were not detected in any of the adenocarcinomatous portions. This suggests that E2F-4 might be implicated in the transformation of adenocarcinoma into squamous cell carcinoma and further studies are needed to understand its role in squamous differentiation.

Carcinoma, Adenosquamous↗

PubMed2003

Immunohistochemical demonstration of 14-3-3 sigma protein in normal human tissues and lung cancers, and the preponderance of its strong expression in epithelial cells of squamous cell lineage.

In order to confirm 14-3-3 sigma (sigma) protein distribution in human tissues, immunohistochemistry was performed using various paraffin-embedded human tissues. In normal human tissues, the strongest immunoreactivity for 14-3-3sigma protein was observed in squamous epithelia at various sites, followed by basal cells of the trachea, bronchus and basal or myoepithelial cells of various glands. Moderate to weak 14-3-3sigma immunoreactivity was seen in the epithelial cells of the alimentary tract, gall bladder, urinary tract and endometrium. In the lung, 14-3-3sigma immunoreactivity was also observed in hyperplastic type II alveolar cells and metaplastic squamous cells. Immunohistochemical study using non-small-cell lung cancers revealed that 14-3-3sigma immunoreactivity was stronger in squamous cell carcinomas than in adenocarcinomas. The present study revealed that 14-3-3sigma expression was exclusively present in various epithelial cells and had a tendency to be stronger in cells destined for squamous epithelium or differentiating toward squamous cells in human normal and neoplastic cells.

14-3-3 Proteins↗

PubMed1999

Regulation of guanylate-binding protein expression in interferon-gamma-treated human epidermal keratinocytes and squamous cell carcinoma cells.

Interferon-gamma is a potent inducer of growth arrest and squamous differentiation of human epidermal keratinocytes in vitro. In order to understand the proximate events regulating interferon-gamma action we studied the relationship between interferon-gamma-mediated induction of a cytoplasmic guanylate-binding protein and the expression of growth and differentiation marker genes in normal and transformed keratinocytes. Induction of guanylate-binding protein mRNA by interferon-gamma was detectable at 4 h, was transcription dependent, and preceded changes in the expression of markers of growth arrest (E2F-1 mRNA downregulation) and differentiation (SQ37 mRNA induction). The Ec50 value for guanylate-binding protein induction (4 units interferon-gamma per ml) was lower than previously reported for SQ37 (40 units interferon-gamma per ml). Guanylate-binding protein mRNA appeared to be only moderately downregulated by modulators of the squamous phenotype such as retinoic acid and transforming growth factor-beta1. In addition, mRNA levels of E2F-1 or SQ37 were not altered in several squamous carcinoma cell lines treated with interferon-gamma. In contrast, guanylate-binding protein mRNA was highly induced in all these cell lines following interferon-gamma treatment. Further analysis of the signal transduction pathway mediating interferon-gamma responses using protein kinase inhibitors indicated that guanylate-binding protein induction in normal human epidermal keratinocyte cells was most likely protein kinase C independent. Our data suggest that more than one postreceptor interferon-gamma signaling pathway exists in keratinocytes and that at least one of these pathways is defective in squamous carcinoma cells. Furthermore, our data demonstrated that the failure of the squamous carcinoma cells to undergo interferon-gamma-induced growth arrest and differentiation is not due to an inherent defect in interferon-gamma receptor activation, but most likely is due to a defect in a non-guanylate-binding protein-dependent signaling pathway.

Carcinoma, Squamous Cell↗

PubMed2003

Presence of human papillomavirus DNA in plucked eyebrow hairs is associated with a history of cutaneous squamous cell carcinoma.

A role for cutaneous human papillomaviruses (HPV) has been proposed in the development of skin cancer. Well-designed epidemiologic studies to demonstrate an association between HPV infection and skin cancer are extremely rare. To identify HPV infection as a potential risk factor, we investigated the association between the presence of HPV DNA in eyebrow hairs and a history of cutaneous squamous cell carcinoma. A case-control study was designed consisting of 155 immunocompetent individuals with a history of squamous cell carcinoma and 371 controls without skin cancer. DNA extracted from plucked eyebrow hairs collected from the study population was analyzed with a cutaneous HPV subgroup polymerase chain reaction and newly designed HPV type specific polymerase chain reactions for HPV 2, 5, 8, 15, 16, 20, 24, and 38. HPV DNA was detected in 63.1% of the total study population. The presence of HPV DNA was associated with age (p=0.0002) and male sex (p=0.02), but not with sun exposure, skin type, and smoking. After adjustment for age and sex, the presence of HPV DNA in eyebrow hairs was associated with a history of squamous cell carcinoma (odds ratio 1.7, 95% confidence interval 1.1; 2.7). HPV type specific analysis revealed that no HPV type stood out. The high-risk mucosal type HPV 16 and the skin wart type HPV 2 were rarely found in this study (<0.2%). The positive association found between the presence of HPV DNA in eyebrow hairs and a history of squamous cell carcinoma warrants further research into the role that HPV infection plays in the development of cutaneous squamous cell carcinoma.

Age Distribution↗

PubMed2002

Does human papilloma virus have a role in squamous cell carcinoma of the colon and upper rectum?

AIM: To determine if Human Papilloma Virus (HPV) has a role in the aetiology of adenosquamous and squamous cell carcinoma of the colon and upper rectum, and to describe the clinical features seen in our patients with this condition. METHODS: Patients were identified with squamous cell carcinoma (SCC), adenosquamous carcinoma (Ad-SCC), or adenocarcinoma with squamous metaplasia (AA) of the colon and upper rectum over the 10 years from 1/1/1990 to 31/12/1999. Patients were identified from a prospective pathology database. All tumours were at least 5cm above the dentate line. Pathology blocks were stained using the Peroxidase labelled Streptavidin technique using mouse monoclonal antibody NCL-HPV-4C4, which identifies HPV 6, 11, 16 and 18. Age, gender and site matched controls (colorectal adenocarcinomas) were also stained. The clinical presentation and management was reviewed from the case notes. RESULTS: Twenty patients were identified from a pathological database of 2351 colorectal cancers (0.85% of colorectal cancers). 0/20 of the study patients (SCC, Ad-SCC, AA) or adenocarcinoma controls stained positively for HPV 6, 11, 16, 18. The clinical presentation was similar to patients presenting with adenocarcinomas. CONCLUSIONS: The peroxidase labelled streptavidin technique is an immunohistochemical technique with high specificity but lower sensitivity. There was no apparent association between HPV 6, 11, 16, 18 and squamous cell and adenosquamous carcinoma of the colon and rectum using this technique. Clinical features are similar in squamous and adenosquamous colorectal carcinomas to colorectal adenocarcinomas.

Aged↗

PubMed1996

[Monoclonal antibodies against squamous epithelial carcinomas of the upper aerodigestive tract].

BACKGROUND: Squamous cell carcinoma is the most common cancer of the head and neck. The application of monoclonal hybridoma technology to the identification and characterization of molecules preferentially expressed in carcinoma cells may provide potentially important diagnostic and therapeutic tools. METHODS: After immunization of mice with viable squamous cell carcinoma cells derived from human tumors of the upper aerodigestive tract hybridomas were selectively grown for production of monoclonal antibodies. Monoclonal antibodies produced by 690 hybridoma clones were tested on immunoreactions with frozen sections of human squamous cell carcinoma and reactive tonsils. RESULTS: Immunohistochemical trials showed that monoclonal antibodies produced by hybridoma clone K-640 are strongly accumulated at the plasma membrane whereas no immunoreaction in squamous epithelium of the tonsil could be detected. By means of ELISA it could be shown that these antibodies belong to the class of IgM. Immunoblotting revealed that the antibodies recognize antigenes with approximate molecular weights of 52 and 54 kD. CONCLUSIONS: The experiments suggest that the hybridoma clone K-640 produces antibodies which bind to the plasmamembrane of the tumor cells. Further recloning steps of this hybridoma clone could possibly enhance the specificity of these antibodies for squamous cell carcinoma.

Animals↗

PubMed1995

[Establishment and characterization of 2 cell lines of squamous epithelial carcinoma of the mouth floor and tongue].

OBJECTIVE: The cultivation of squamous cell carcinoma cells of the upper aerodigestive tract is more difficult compared to other malignancies because of microbial contamination. The establishment of new squamous cell carcinoma cell lines is absolutely necessary to further characterize this tumor entity. METHODS: Two squamous cell carcinoma cell lines of the floor of the mouth and the tongue were established from tumor biopsies. They were examined by light and electron microscopy. Furthermore immunocytochemical and DNA cytofluorometric studies were performed. The growth features were tested in a tumor-stem cell assay and through transplantation in thymusless nude mice. RESULTS: The epithelial character of the cells was determined morphologically, immunocytochemically, and immunologically. Both cell lines shaved an aneuploid DNA Index of 1.92 for the tongue carcinoma cell line (HCTK-1) and 1.77 for the floor of the mouth cell line (HCFMK-1). The plating efficiency was 0.008 and 0.01%. Cell differentiation in the original tumor and the nude mice tumor was identical. HCTK-1 is in the 25th passage and HCFMK-1 in the 42nd. CONCLUSIONS: The two new squamous cell carcinoma cell lines HCFMK-1 and HCTK-1 may serve as a basis for various in vitro investigations and may help to further characterize squamous cell carcinomas of the upper aerodigestive tract.

Aged↗

PubMed1995

Association between cigarette smoking and mutation of the p53 gene in squamous-cell carcinoma of the head and neck.

BACKGROUND: Although epidemiologic studies have long associated tobacco and alcohol use with the development of squamous-cell carcinoma of the head and neck, the molecular targets of these carcinogens have yet to be identified. We performed a molecular analysis to determine the pattern of mutations in the p53 gene in neoplasms from patients with squamous-cell carcinoma of the head and neck and a history of tobacco or alcohol use. METHODS: Sequence analysis of the conserved regions of the p53 gene was performed in tumor samples from 129 patients with primary squamous-cell carcinoma of the head and neck. We then used statistical analysis to identify any patient characteristics associated with mutation of the p53 gene. RESULTS: We found p53 mutations in 42 percent of the patients (54 of 129). Fifty-eight percent of the patients who smoked cigarettes and used alcohol (37 of 64; 95 percent confidence interval, 45 to 70 percent), 33 percent of the patients who smoked but abstained from alcohol (13 of 39; 95 percent confidence interval, 19 to 50 percent), and 17 percent of the patients who neither smoked nor drank alcohol (4 of 24, 95 percent confidence interval, 5 to 37 percent) had p53 mutations (P = 0.001). (Two patients used alcohol but did not smoke, and neither had a p53 mutation.) Furthermore, 100 percent of the mutations in the patients who neither drank nor smoked occurred at sites containing cytidine phosphate guanosine dinucleotides (potentially representing endogenous mutations) within the p53 gene (5 of 5 mutations; 95 percent confidence interval, 48 to 100 percent), whereas only 23 percent of those in cigarette smokers consisted of such changes (12 of 53 mutations; 95 percent confidence interval, 12 to 36 percent; P = 0.001). CONCLUSIONS: In our study, a history of tobacco and alcohol use was associated with a high frequency of p53 mutations in patients with squamous-cell carcinoma of the head and neck. Preliminary evidence linked cigarette smoking to p53 mutations at nonendogenous mutation sites. Our findings suggest a role for tobacco in the molecular progression of squamous-cell carcinoma of the head and neck and support the epidemiologic evidence that abstinence from smoking is important to prevent head and neck cancer.

Base Composition↗

PubMed2003

The predictive value of cytologic testing in women with the human immunodeficiency virus who have low-grade squamous cervical lesions: a substudy of a randomized, phase III chemoprevention trial.

OBJECTIVE: The purpose of this study was to determine whether the progression of low-grade squamous intraepithelial lesions of the cervix in women with the human immunodeficiency virus can be predicted reliably by standard cytologic testing. STUDY DESIGN: As part of a previously reported trial, 288 biopsy specimens were collected from 117 women with the human immunodeficiency virus. These specimens underwent central and local interpretation, which were compared and correlated with cytologic results. Ninety-two subjects had matched cytologic/histologic pairs at study termination, which were compared to determine whether cytologic testing was predictive of progression. RESULTS: Of the central histologic interpretations, 26 of 288 interpretations (9%) differed from local results, 97 of 246 cytologic/histologic pairs (39%) were discordant, and 21 subjects had progression to high-grade squamous intraepithelial lesions by histologic evidence. Cytologic testing showed high-grade squamous intraepithelial lesions in 4 of 21 specimens (sensitivity, 19%). The remaining cytologic specimens were either low-grade squamous intraepithelial lesions or were normal. CONCLUSION: This substudy of pathologic results from a randomized clinical trial suggests that, although the risk of progression of low-grade squamous intraepithelial lesions is low, follow-up cytologic testing is unreliable. Colposcopic evaluation with directed biopsies should be continued.

Antineoplastic Agents↗

PubMed1989

Differential DNA sequence deletions from chromosomes 3, 11, 13, and 17 in squamous-cell carcinoma, large-cell carcinoma, and adenocarcinoma of the human lung.

Activation of protooncogenes and inactivation of putative tumor suppressor genes are genetic lesions considered to be important in lung carcinogenesis. Fifty-four cases of non-small-cell lung cancer (23 adenocarcinomas, 23 squamous-cell carcinomas, and 8 large-cell carcinomas) were examined for loss of DNA sequences at 13 polymorphic genetic loci. Loss of heterozygosity was seen more frequently in squamous-cell carcinoma than in adenocarcinoma. The loss of DNA sequences from the short arm of chromosome 17 (D17S1 locus) was detected in 8 of 9 heterozygous cases of squamous-cell carcinoma and in only 2 of 11 heterozygous cases of adenocarcinomas. Furthermore, in 7 of these 8 squamous-cell carcinomas, loss of heterozygosity from chromosome 17 was accompanied by loss of DNA sequences from chromosome 11. The spectrum of allelic sequences lost from chromosome 11 was, however, similar in every type of carcinoma studied, and the data show two regions commonly deleted from chromosome 11 (11pter-p15.5 and 11p13-q13) that may have a role in the pathogenesis of all these types of non-small-cell bronchogenic carcinoma. Loss of DNA sequences from chromosome 3 was seen in 16 of 31 cases where the constitutive DNA was heterozygous-i.e., informative. These data included only 6 of 16 cases where loss of heterozygosity involved a chromosomal locus previously shown to be lost consistently in small-cell lung cancer (DNF15S2). Loss of heterozygosity at the chromosome 13q locus, D13S3, was seen in 9 of 21 informative cases, and in 2 cases, both adenocarcinomas, duplication of the intact DNA sequences suggested the possibility that mitotic recombination had occurred. Frequent DNA sequence deletions, including those from chromosome 17, in squamous-cell carcinomas may reflect the extensive mutagenic and clastogenic effects of tobacco smoke that may lead to inactivation of putative tumor-suppressor genes.

Adenocarcinoma↗