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PubMed1996

Differential expression of desmosomal glycoproteins in keratoacanthoma and squamous cell carcinoma of the skin: an immunohistochemical aid to diagnosis.

The distinction between keratoacanthoma and squamous cell carcinoma is a common dermatopathological dilemma. Although the mainstay of the diagnosis is still clinico-pathological correlation, many dermatopathologists now include keratoacanthomas in the spectrum of squamous cell carcinomas. Recent reports, however, have pointed out that keratoacanthoma is "deficient squamous cell carcinoma" since it loses the expression of bcl-2 antigen, consistent with initiation of apoptosis, i.e. its involution. Electron microscope studies performed in keratoacanthomas and squamous cell carcinomas also revealed significantly reduced desmosomes in squamous cell carcinoma, but not in keratoacanthoma. A series of 38 keratoacanthomas and 62 squamous cell carcinomas of the skin (28 well-differentiated, 21 moderately differentiated and 13 poorly differentiated) were stained immunohistochemically with the monoclonal antibody 32-2B to desmosomal glycoproteins desmoglein 1 and desmoglein 3. Thirty-five keratoacanthomas showed extensive pericellular desmoglein expression. Three keratoacanthomas and 20 squamous cell carcinomas (19 well-differentiated, 1 moderately differentiated) showed focal staining, and in 11 squamous cell carcinomas (2 moderately differentiated, 9 poorly differentiated) the staining was negative. The remaining 31 squamous cell carcinomas (9 well differentiated, 18 moderately differentiated, 4 poorly differentiated) showed juxtanuclear staining. None of the squamous cell carcinomas exhibited the extensive pericellular pattern found in keratoacanthomas. Assessment of staining intensity, by 3 independent examiners, revealed a strong negative correlation between desmoglein expression and degree of dysplasia in the squamous cell carcinomas (p < 0.01). This antibody therefore clearly distinguishes these tumours and may be of value in the differential diagnosis of keratoacanthoma and squamous cell carcinomas in routine histopathology.

Autoantigens↗

PubMed2004

[Expression of cyclooxygenase-2 in esophageal squamous cell carcinogenesis].

OBJECTIVES: To investigate the expression of cyclooxygenase-2 (cox-2) protein in normal squamous epithelium, squamous dysplasia and squamous cell carcinoma of the esophagus, and to elucidate the role of cox-2 in esophageal carcinogenesis. METHODS: Biopsy specimens of atypical esophageal dysplasia (n = 47) and surgical resection of squamous cell carcinoma (n = 86) were compared with normal esophageal specimens (n = 42) and the expression of cox-2 in those specimens was analyzed by immunohistochemistry and western blotting. RESULTS: A significant elevated cox-2 expression was shown in atypical esophageal squamous dysplasia and squamous cell carcinoma, as compared to that in normal esophageal squamous epithelium, with immunohistochemical stain scores of 2.67 +/- 1.77, 2.19 +/- 1.79 and 0.71 +/- 0.46, respectively. Results of western blotting analysis confirmed those obtained by immunohistochemistry. Cox-2 expression significantly correlated with proliferation activity assessed by proliferating cell nuclear antigen index in dysplastic and carcinomous lesions, respectively, and no such correlation could be found in normal esophageal mucosa. Elevated cox-2 expression was not associated with clinical-pathological features of esophageal squamous carcinoma, including age, gender, tumor size, histological grade, lymph node metastasis and clinical stage. CONCLUSION: Elevated expression of cox-2 in atypical squamous dysplasia and squamous cell carcinoma of the esophagus, which correlated with cell proliferation activity, indicated that cox-2 may be involved in the early stage of squamous carcinogenesis of the esophagus, and may be a target of prevention and treatment for esophageal squamous cell carcinoma.

Adult↗

PubMed1997

Vascular permeability factor/vascular endothelial growth factor and its receptors in oral and laryngeal squamous cell carcinoma and dysplasia.

Increased microvessel density has been described in squamous cell carcinoma of the head and neck and is related to patient prognosis. The factors responsible for the angiogenesis have not been identified. Vascular permeability factor (VPF), also known as vascular endothelial growth factor (VEGF), is a multifunctional angiogenic cytokine expressed at high levels in many tumors. We examined 16 cases of squamous cell carcinoma, 10 cases of high-grade squamous dysplasia, and 19 cases of normal, reactive, or mildly dysplastic squamous mucosa by in situ hybridization for expression of VPF/VEGF and VPF/VEGF receptor mRNA. Strong expression of VPF/VEGF mRNA was seen in 12 of 16 squamous cell carcinomas and in 5 of 10 high-grade squamous dysplasias. In contrast, no cases of normal, reactive, or mild dysplastic squamous epithelium showed strong expression of VPF/VEGF mRNA. Furthermore, strong expression of VPF/VEGF receptor mRNA was seen in 5 of 9 cases of squamous cell carcinoma and 3 of 6 cases of high-grade squamous dysplasia but in only 2 of 14 cases of normal, reactive, or mild dysplastic squamous epithelium. Thus, expression of VPF/VEGF and its receptors is markedly increased in high-grade squamous dysplasia and invasive squamous cell carcinoma of the oral cavity and larynx and may play an important role in the angiogenesis associated with these lesions.

Bronchopulmonary Dysplasia↗

PubMed2000

Clinical significance of the qualification of atypical squamous cells of undetermined significance: An analysis on the basis of histologic diagnoses.

OBJECTIVE: This study was undertaken to evaluate the significance of further qualification of atypical squamous cells of undetermined significance in routine Papanicolaou smears. STUDY DESIGN: A retrospective medical records review was conducted on 316 women whose Papanicolaou smears yielded diagnoses of either atypical squamous cells of undetermined significance suggestive of the presence of an intraepithelial lesion or atypical squamous cells of undetermined significance suggestive of a reactive process. RESULTS: The overall incidence of a squamous intraepithelial lesion (cervical intraepithelial neoplasia grades I, II, and III) was higher in the group with atypical squamous cells of undetermined significance suggestive of the presence of an intraepithelial lesion than in the group with results suggestive of a reactive process (41.1% vs 22.3%; P =.0344). Women with atypical squamous cells of undetermined significance suggestive of the presence of an intraepithelial lesion were 9.7 times more likely to have high-grade squamous intraepithelial lesion (cervical intraepithelial neoplasia III) develop than were women with atypical squamous cells of undetermined significance suggestive of a reactive process (95% confidence interval, 1.26-74.64). The incidence of high-grade squamous intraepithelial lesion was higher among women </=35 years old than among women >35 years old (17.8% vs 6.3%; P =.0378). CONCLUSION: Women with a diagnosis of atypical squamous cells of undetermined significance suggestive of the presence of an intraepithelial lesion are more likely to have intraepithelial lesions develop than are those with atypical squamous cells of undetermined significance suggestive of a reactive process. Aggressive evaluation of cases of atypical squamous cells of undetermined significance suggestive of the presence of an intraepithelial lesion with colposcopy and cervical biopsies may be appropriate. Age should be considered as an independent factor in the plan of management.

Adult↗

PubMed2006

Immunohistochemical detection of GLUT1, p63 and phosphorylated histone H1 in head and neck squamous intraepithelial neoplasia: evidence for aberrations in hypoxia-related, cell cycle- and stem-cell-regulatory pathways.

AIM: Most epithelial malignancies are characterized by multistep progression from preinvasive/intraepithelial neoplasia to invasive malignancy. Detection and grading of early squamous intraepithelial neoplasia may at times be problematic. The aim of this study was to examine the ability of immunomarkers GLUT1, phospho-histone H1 and p63 to detect such early lesions. METHODS: Sections of formalin-fixed paraffin-embedded tissue from 27 cases of squamous intraepithelial neoplasia, 26 associated with invasive carcinoma, were immunostained with anti-p63 (4A4; Santa Cruz), anti-GLUT1 (Chemicon) and anti-phospho-histone H1 (monoclonal 12D11) and compared with normal, hyperplastic and immature squamous metaplastic epithelium. RESULTS: Normal epithelium displayed phospho-histone H1 in scattered parabasal cells; p63 in the basal one-quarter to one-half of epithelium; and GLUT1 negativity or weak/equivocal mid-epithelial GLUT1+ foci. In hyperplasia phospho-histone H1+ cells were also limited to the parabasal layer; p63 positivity was essentially identical to that in normal epithelium; GLUT1 characteristically stained basal cells in rete-like areas. p63 staining in squamous intraepithelial neoplasia (grade 1) was indistinguishable from normal epithelial staining; in contrast, squamous intraepithelial neoplasia (grade 3) was readily apparent, with up to full-thickness p63 positivity. Squamous intraepithelial neoplasia (grade 1) was readily distinguishable from normal epithelium with both phospho-histone H1 and GLUT1 immunostaining; both markers were detected in cell layers above the parabasal layer. With both, progressively higher cell layers stained in proportion to the severity of the intraepithelial neoplasia, up to full thickness positivity in grade 3 squamous intraepithelial neoplasia. Squamous metaplasia and grade 3 squamous intraepithelial neoplasia were not distinguishable with p63 (both showed full-thickness staining) but were readily distinguishable with GLUT1 and phospho-histone H1 stains. GLUT1 appeared to be the most sensitive marker for all grades of intraepithelial neoplasia. CONCLUSION: Altered expression of all three markers was a common finding in squamous intraepithelial neoplasia, hence, dysregulation of cell cycle-promoting cyclin-dependent kinases (phospho-histone H1), altered stem cell regulatory pathways (p63) and enhancement of hypoxia-sensing pathways (GLUT1) are all early alterations in the progression of squamous malignancy of head and neck origin. A panel of all three may be a useful means of detecting squamous intraepithelial neoplasia.

Biomarkers, Tumor↗

PubMedDate not supplied

Ultrastructural distinction of basaloid-squamous carcinoma and adenoid cystic carcinoma.

Basaloid-squamous carcinoma is a unique and infrequent variant of squamous cell carcinoma with a predilection for occurring in the upper aerodigestive tract. The cardinal diagnostic criteria are the presence of basaloid cells arranged in lobules or cords and a squamous component. Another feature that distinguishes basaloid-squamous carcinoma from conventional squamous cell carcinoma is the development of multiple foci of amorphous, eosinophilic, or mucinous materials among the basaloid tumor cells. It is this feature in basaloid-squamous carcinoma that causes confusion with adenoid cystic carcinoma, especially the solid variant of adenoid cystic carcinoma. To clarify the distinctive features of these two types of tumors, the ultrastructural findings in three basaloid-squamous carcinomas from the head and neck region were compared with three adenoid cystic carcinomas, one from the head and neck region and one each from trachea and bronchus. Widened intercellular spaces, tonofilaments, and replicated basal lamina were present in both types of tumor. However, the ultrastructural features of glandular differentiation were present only in adenoid cystic carcinoma, whereas the ultrastructural features of squamous cell differentiation were present only in basaloid-squamous carcinoma. The distinction between basaloid-squamous carcinoma and adenoid cystic carcinoma is important since basaloid-squamous carcinoma is a clinically aggressive, high-grade form of squamous cell carcinoma, generally with a worse prognosis than adenoid cystic carcinoma.

Adult↗

PubMed1996

Human papillomavirus DNA in uterine cervix squamous cell carcinoma and adenocarcinoma detected by polymerase chain reaction.

BACKGROUND: Substantial clinical, epidemiologic, and experimental evidence has reinforced the role of high risk human papillomavirus (HPV) types in the development of cervical carcinoma. The authors investigated HPV in the uterine cervix squamous cell carcinomas and adenocarcinomas of Finnish patients. METHODS: Specimens from 352 patients with uterine cervix squamous cell carcinomas and 108 with adenocarcinoma were examined for HPV DNA by polymerase chain reaction. The authors used consensus primers located in the L1 region, as well as HPV16, 18, and 33 type-specific primers located in the E6 region. RESULTS: HPV DNA was detected in 324 of 352 squamous cell carcinomas (92%), and 81 of 108 adenocarcinomas (75%). Two-hundred seventy-four of 352 squamous cell carcinomas (78%) and 18 of 108 adenocarcinomas (17%) contained HPV16 DNA, whereas 55 of 352 squamous cell carcinomas (16%) and 60 of 108 adenocarcinomas (56%) contained HPV18 DNA. Eight squamous cell carcinomas and 4 adenocarcinomas were positive for HPV33. Twenty-eight squamous cell carcinomas and 5 adenocarcinomas were positive for either HPV16 and HPV18 or HPV16 and HPV33. Unclassified HPV DNA was detected in 17 squamous cell carcinomas and 4 adenocarcinomas. Twenty-eight squamous cell carcinomas and 9 adenocarcinomas, which were positive for E6 DNA using type-specific primers, were negative for the L1 gene. All 460 cervical specimens were tested twice with identical results. CONCLUSIONS: HPV DNA was highly prevalent in both uterine cervix squamous cell carcinoma and adenocarcinoma. HPV16 was detected more often in squamous cell carcinoma and HPV18 was detected more often in adenocarcinoma. Both consensus structural L1 gene-derived primers and type-specific viral E6 oncogene-derived primers were necessary to detect HPV DNA in cervical carcinoma.

Adenocarcinoma↗

PubMed1991

Barrett's mucosa in conjunction with squamous carcinoma of the esophagus.

Fifty esophagectomies (32 specimens with squamous cell carcinoma and 18 with adenocarcinoma) were reviewed for the presence of Barrett's mucosa. The whole resected specimens were cut, and a total of 1677 blocks (measuring up to 4.0 x 0.5 cm) were obtained. In resections with squamous cell carcinoma, a mean of 33.6 sections (range, 16 to 55 sections) were excised, and in those with adenocarcinomas, a mean of 33.4 sections (range, ten to 60 sections) were cut. Barrett's mucosa (without or with dysplasia) was present in all 18 specimens with an adenocarcinoma (100%) and in 13 of the 32 specimens (40.6%) with squamous cell carcinoma. In ten of the 13 specimens with squamous cell carcinoma, adjacent areas with high-grade squamous cell dysplasia were found. The squamous cell carcinoma and/or the adjacent squamous cell dysplasia were found separated from the Barrett's mucosa by normal squamous epithelium, supporting the view that these two lesions are not related to one another. Early clinical and experimental data showed that squamous cell dysplasia antedated the development of squamous cell carcinoma in that organ. One possible suggestive of these findings is that the detection of a Barrett's esophagus (without or with dysplasia) should prompt the endoscopist also to examine carefully the rest of the esophagus to exclude mucosal alterations possibly connected with squamous cell carcinogenesis in that organ.

Adenocarcinoma↗

PubMed2001

Outcome analysis of HIV-positive patients with anal squamous cell carcinoma.

PURPOSE: With improved antiretroviral therapy, HIV-positive patients are achieving a longer life expectancy. An increased incidence of anal squamous cell carcinomas has been noted in these patients. The purpose of this study was to determine the outcome of HIV-positive patients with anal squamous cell carcinomas. METHODS: We conducted a review based on our tumor registry from 1980 through 1999. We identified 73 patients with anal squamous cell carcinoma treated at the University of Texas Southwestern Medical Center affiliated hospitals; 23 were HIV positive (18 had AIDS). In the HIV-positive group, 9 had in situ squamous carcinomas and 14 had invasive squamous cell carcinomas. Data collected included age, CD4 count, treatment, complications, and survival; these data were analyzed by Student's t-test. RESULTS: All patients were male. Those with squamous cell cancer of the anus were offered radiation therapy and chemotherapy. Beginning in 1998, all patients received highly active antiretroviral therapy before treatment. Seven of 14 anal squamous cell carcinoma patients had their therapy adjusted owing to toxicity. Morbidity included proctocolitis and diarrhea (n = 2) requiring diversion (n = 1), hemorrhagic cystitis (n = 1), neutropenic fever (n = 3), bone marrow suppression (n = 1), and urethral stricture (n = 1). Mean age was 42 years for anal squamous cell carcinoma patients and 36 years for squamous cell carcinoma in situ patients (P = 0.05). Mean CD4 count was 222 cells/ml in patients with infiltrating carcinoma and 200 in the in situ patients (P = NS). One-year and five-year mortality rates, respectively, were 40 percent and 80 percent for infiltrating carcinoma patients and 17 percent and 50 percent for the in situ patients. Both of the in situ patients who died had CD4 counts <20 cells/ml at diagnosis, whereas the rest had CD4 counts >100 cells/ml and are currently without anal disease. Mean CD4 count at diagnosis for all patients who died was 133 cells/ml, whereas for those surviving, it was 261 cells/ml (P = 0.03). Eight (all with infiltrating carcinoma) of the 10 patients who died had persistent anal disease, but none had metastasis. CONCLUSION: HIV-positive patients with in situ carcinomas present at an earlier age than those with infiltrating lesions. In situ patients with CD4 counts as low as 105 cells/ml do well with local excision. A low CD4 count at diagnosis without highly active antiretroviral therapy predicts a poor prognosis. Because these patients appear to succumb to their HIV status and not the anal disease, anal squamous cell carcinoma should be included with cervical squamous cell carcinoma as an AIDS-defining illness. HIV-positive patients, particularly AIDS patients, with invasive anal cancers and without effective antiretroviral therapy obtain little benefit and significant toxicity from current radiation therapy and chemotherapy. Initiation of highly active antiretroviral therapy in HIV-positive patients before radiation therapy and chemotherapy are begun may decrease toxicity and improve survival. Additional clinical trials are warranted to test this theory.

Adult↗

PubMed1998

[Primary squamous cell carcinoma of female mammary gland].

Squamous metaplasia can be demonstrated in about 4% of all invasive carcinomas of the breast. Primary squamous cell carcinomas of the breast are rare, since they occur in less than 1% of all primary invasive breast carcinomas. In order to classify a breast tumor as a primary squamous cell carcinoma one must exclude an epidermal origin, especially from the nipple region and the possibility of metastatic infiltration of the breast by a squamous cell carcinoma from a different location. Causative and formal pathogenesis of primary squamous cell carcinoma of the breast is not clear. A pluripotent embryonal stem cell origin is discussed, considering the phylogenetic descent of the mammary gland from skin appendages. Squamous metaplasia is also suggested to be a precursor of squamous cell carcinoma. Here endocrine stimulation and chronic inflammation may both play an inductive role. The number of published cases of squamous cell carcinomas developing years and decades after implantation of silicon prostheses has increased in recent years. These tumors probably develop on top of squamous metaplasia induced by the inflammatory pseudocapsule. Estimating the prognosis and therapeutic management in patients with squamous cell carcinoma of the breast should follow the same guidelines as for other squamous cell cancers.

Biomarkers, Tumor↗

PubMed1996

Angiogenesis in squamous cell carcinoma in situ and microinvasive carcinoma of the uterine cervix.

OBJECTIVE: To evaluate angiogenesis in squamous cell carcinoma in situ (CIS) and microinvasive squamous cell carcinoma of the uterine cervix and to investigate the relations among angiogenesis, stromal inflammation, and depth of invasion. METHODS: Three groups of women were studied: 22 controls who had undergone hysterectomy for benign conditions; 18 with squamous cell CIS of the cervix who underwent cone biopsy, hysterectomy, or both; and 14 with microinvasive squamous cell carcinoma who underwent conization of the cervix and subsequent surgical management according to depth of invasion. All specimens were stained immunohistochemically for factor VIII-related antigen. Areas below the basement membrane with the highest angiogenic density were selected. The degree of stromal inflammatory reaction was assessed. Statistical analyses included Kruskal-Wallis, analyses of variance and covariance, Scheffe and Bonferroni-Dunn post hoc procedures, and Pearson correlation analysis. P < .05 was considered statistically significant. RESULTS: Microvessel counts per high-power field (x 400) of microinvasive squamous cell carcinoma of the cervix differed significantly from those of controls and squamous cell CIS (median 34.5 per high-power field, range 9-76 versus median 17, range 7-47, and median 19, range 8-39, respectively; P < .005). Microvessel counts per high-power field in squamous cell CIS did not differ significantly from those of controls (P = .91). Among patients with microinvasive squamous cell carcinoma of the cervix, no significant correlation was found between microvessel counts per high-power field and the depth of invasion (r = 0.19, P = .51). Stromal inflammatory reaction (graded 0-3) differed significantly among controls, squamous cell CIS, and microinvasive carcinoma (mean 0.40, 0.83, and 1.64, respectively; P < .005). CONCLUSIONS: Microinvasive squamous cell carcinoma of the uterine cervix is angiogenic, but depth of invasion is not associated with increased angiogenicity. Squamous cell CIS is not angiogenic.

Adult↗

PubMed2004

Correlations among neural cell adhesion molecule, nerve growth factor, and its receptors, TrkA, TrkB, TrkC, and p75, in perineural invasion by basal cell and cutaneous squamous cell carcinomas.

BACKGROUND: Neural cell adhesion molecule; nerve growth factor; and its receptors TrkA, TrkB, TrkC, and p75(NGFR) regulate unique survival pathways in the cells of different noncutaneous malignancies exhibiting a perineural invasive phenotype. Their expression is currently unknown in basal cell carcinoma and cutaneous squamous cell carcinoma exhibiting perineural invasion. OBJECTIVE: The objective was to evaluate neural cell adhesion molecule, nerve growth factor, TrkA, TrkB, TrkC, and p75(NGFR) expression when perineural invasion occurs in basal cell carcinoma and cutaneous squamous cell carcinoma. METHODS: Four basal cell carcinomas and five cutaneous squamous cell carcinomas that were perineural invasion-positive and four basal cell carcinomas and three cutaneous squamous cell carcinomas that were perineural invasion-negative were evaluated for the expression of neural cell adhesion molecule, nerve growth factor, TrkA, TrkB, TrkC, and p75(NGFR) by immunohistochemical staining. RESULTS: For neural cell adhesion molecule, six of eight basal cell carcinomas and two of eight cutaneous squamous cell carcinomas stained positive. For nerve growth factor, seven of nine perineural invasion-positive and six of seven perineural invasion-negative tumors stained moderately or greater. For TrkA, B, and C, the perineural invasion-positive cutaneous squamous cell carcinomas generally stained darker than the perineural invasion-negative cutaneous squamous cell carcinomas. For p75(NGFR), four of five perineural invasion-positive cutaneous squamous cell carcinoma stain patterns indicated that p75(NGFR) expression was higher perineurally than elsewhere in the tumor. CONCLUSION: In basal cell carcinoma and cutaneous squamous cell carcinoma, the presence of neural cell adhesion molecule may determine tumor aggression and increased levels of nerve growth factor and TrkA, B, and C may reflect unique survival pathways. Higher levels of expression of Trk receptors in cutaneous squamous cell carcinoma cells may predict perineural invasion and the increased p75(NGFR) expression found in cutaneous squamous cell carcinoma perineurally may allow p75(NGFR) immunohistochemical staining to be used for detecting sites of perineural invasion.

Aged↗

PubMed1994

Squamous cell carcinoma antigen as an adjunct tumour marker in primary carcinoma of the lung.

AIMS: To determine (1) the detection rate of primary carcinoma of the lung by serological assay of CEA (carcinoembryonic antigen); and (2) whether addition of seroassay of squamous cell carcinoma related antigen before treatment improves detection sensitivity. METHODS: A prospective study spanning 27 months was conducted at the University Hospital, Kuala Lumpur. Serum CEA (Abbott IMx) and serum squamous cell carcinoma antigen (Abbott IMx) from patients clinically suspected of having primary carcinoma of the lung, were assayed using the microparticle enzyme immunoassay method. RESULTS: Thirty seven cases of histologically confirmed primary lung carcinoma were studied. Of these, 17 were squamous cell carcinomas, 10 adenocarcinomas, nine small cell carcinomas, and one large cell carcinoma. The patients' ages ranged from 34-82 years. The male:female ratio was 3.6:1. Squamous cell carcinoma antigen was raised above the cutoff value of 1.5 ng/ml in 94.1% of squamous cell carcinomas, 20.0% of adenocarcinomas, and 11.1% of small cell carcinomas. By comparison, CEA was raised above the cutoff value of 3.0 ng/ml in 70.6% of squamous cell carcinomas, 77.8% of small cell carcinomas, and 100% of adenocarcinomas. CEA and squamous cell carcinoma antigen were not raised in the patient with large cell carcinoma and in 14 healthy volunteers. None of 15 patients with a variety of benign lung diseases showed a rise of CEA, while two patients--a 25 year old Indian woman with pneumonia and a 64 year old Malay man with bronchial asthma--had raised squamous cell carcinoma antigen values above the cutoff. Serum CEA and squamous cell carcinoma antigen values did not seem to correlate with stage or degree of differentiation of the tumours. CONCLUSIONS: The findings suggest that CEA is a good general marker for carcinoma, particularly adenocarcinoma. In contrast, squamous cell carcinoma antigen is more specific for squamous carcinoma.

Adenocarcinoma↗

PubMed2001

Expression of cyclo-oxygenase-2 in naturally occurring squamous cell carcinomas in dogs.

Squamous cell carcinoma is one of the most common cancers in humans and is also a frequently diagnosed neoplasm in dogs. Induction of cyclo-oxygenase-2 (COX-2), a key rate-limiting enzyme in prostaglandin biosynthesis, has been implicated in the oncogenesis of various cancers in humans, including squamous cell carcinomas. However, expression of COX-2 has not been reported in spontaneous squamous cell carcinomas of non-human species. Canine squamous cell carcinomas share several similarities with the human disease. Therefore, the objective of this study was to determine whether COX isoenzymes were expressed in naturally occurring cases of squamous cell carcinomas in dogs. Canine normal skin (n=4) and squamous cell carcinomas (n=40) were studied by immunohistochemistry and immunoblotting analysis using polyclonal antibodies selective for COX-1 or COX-2. COX-2 was strongly expressed by neoplastic keratinocytes in all cases of squamous cell carcinomas, whereas no COX-2 was detected in normal skin and in the non-neoplastic skin and oral mucosa included in the tumor tissue samples (p<0.01). Immunoblotting analysis confirmed the restricted expression of COX-2 (72,000--74,000 molecular weight doublet) in squamous cell carcinomas only. In contrast, faint COX-1 staining was found in normal skin and in squamous cell carcinomas. This study demonstrates for the first time that COX-2 is induced in canine squamous cell carcinomas, and provides a new model to investigate the role and regulation of COX-2 gene expression in naturally occurring squamous cell carcinomas. (J Histochem Cytochem 49:867-875, 2001)

Animals↗

PubMed1989

[Immunohistochemical study of dysplasia and squamous cell carcinoma of the larynx].

Formalin- or alcohol-fixed, paraffin-embedded laryngeal specimens were stained immunohistochemically with several kinds of monoclonal anti-Keratin antibody (KL-1, PKK-1, PKK-2, PKK-3), polyclonal anti-Keratin antibody, and epithelial membrane antigen. Immunohistochemical technique was used by Avidin-Biotin Complex method with the following subjects; normal epithelium 6 cases, dysplasia 15 cases, inflammation and polyp 12 cases, squamous cell carcinoma 47 cases. 6 specimens of squamous cell carcinoma were totally resected and alcohol-fixed, and other specimens were all biopsied and formalin-fixed. Comparing these two methods, the alcohol-fixed specimen gave superior result to those obtained with formalin-fixed in its staining. Non-staining area was recognized around basal layer by KL-1 stain in the normal epithelium. Enlargement of non-staining area was recognized in the dysplasia. Also, KL-1 staining showed positive staining with the keratinizing squamous cell carcinoma, and weak staining with the non-keratinizing squamous cell carcinoma. And, PKK-3 showed weak staining in the keratinizing squamous cell carcinoma. The results indicate that high molecular weight keratin (56 kilodalton) hardly localize around the basal layer in the squamous epithelium, and also in the non-keratinizing squamous cell carcinoma. The other way, this also suggests that low molecular weight keratin (45 kilodalton) hardly localize in the keratinizing squamous cell carcinoma. It is supposed that intracellular localization of keratin of dysplastic epithelium and squamous cell carcinoma varies from that in the normal squamous epithelium. Accordingly, monoclonal keratin stain is thought to be an useful method for the diagnosis of dysplasia and squamous cell carcinoma.

Antibodies, Monoclonal↗

PubMed2004

[Loss of heterozygosity in esophageal squamous cell carcinoma and its precursor lesion].

OBJECTIVE: To detect the loss of heterozygosity (LOH) in esophageal squamous cell carcinoma and adjacent high-grade squamous dysplasia, and to evaluate possible tumor suppressor genes in the development and progression of invasive malignancy. METHODS: LOH was detected in normal esophageal mucosa, high grade squamous dysplasia and esophageal squamous cell carcinoma using microdissection and polymerase chain reaction technology. The changes of LOH at seven microsatellite markers and the relationship between LOH rate and clinicopathologic parameters were analyzed. RESULTS: In high grade squamous dysplasia, LOH was detected at D13S802 (40%), D13S267 (32%), D13S221 (31%), D9S942 (30%), D17S520 (24%) and D9S171 (33%). However, D17S1798 LOH was not detected. In invasive squamous cell carcinoma, LOH was detected as follows: D13S267 (71%), D13S802 (58%), D17S520 (55%), D13S221 (45%), D9S942 (43%), D9S171 (33%) and D17S1798 (11%). The frequency of LOH in the seven microsatellite markers, the pathologic grade, clinical stage and occurrence of lymph node metastasis did not show any statistically significant correlation (P > 0.05). CONCLUSIONS: The progression from normal squamous epithelium to high grade squamous dysplasia and subsequently to invasive squamous cell carcinoma of the esophagus was associated with accumulation of genetic errors. Possible tumor suppressor genes related to the development of esophageal squamous cell carcinoma may exist near D13S802 (13q12.12). Possible tumor suppressor genes near D13S267 (13q13.1), D17S1798 (17p13.3) and D17S520 (17p13.1) may be related to the progression of esophageal squamous cell carcinoma.

Adult↗

PubMed1987

Antigenic epitopes of three tumor-associated antigens of well-differentiated squamous cell carcinoma of the larynx for use in monitoring patients in specific active immunochemotherapy trials.

Laryngeal tumor-associated antigen (LX-TAA-1) monoclonal antibody-derived epitopes were tested by enzyme immunoassay (ELISA) against a coded series of 30 non-laryngeal squamous cancer sera, 32 laryngeal squamous cancer sera and 36 non-squamous cancer sera. Epitope LX-TAA-1 a62 cross-reacted with 46% of non-laryngeal squamous and with 16% non-squamous cancer sera. Epitope i5 cross-reacted with 50% non-laryngeal squamous cancer sera and with 11% non-squamous cancer sera. LX-TAA-1 epitope f18 cross-reacted with 26% of non-laryngeal squamous cancer sera but with only one, at weaker titer, of the non-squamous cancer serums (2%). Preliminary screening had ruled out any reactivity to 92 normal, age- and sex-matched sera. One hundred percent of laryngeal squamous cancer sera showed reactivity to one or more of the three epitopes. These results from highly sensitive testing imply that epitope f18 protein is probably a unique gene product of certain squamous cancer cells in the body. Serial titrations of immunized patient sera indicated that epitope f18 produces a strong but very early reactivity and appears to be a marker for early post-immunization response in patients on immunotherapy, with epitope i5 showing a low but continuing positive response starting at 7 months post-immunization. This is in contrast to our studies in other cancer systems where earlier responses are usual.

Antigens, Neoplasm↗

PubMed1994

Cytokeratin 19 fragment CYFRA 21-1 compared with carcinoembryonic antigen, squamous cell carcinoma antigen and neuron-specific enolase in lung cancer. Results of an international multicentre study.

The diagnostic value of the water-soluble cytokeratin 19 fragment CYFRA 21-1 in lung cancer was assessed in comparison with carcinoembryonic antigen, squamous cell carcinoma antigen, and neuron-specific enolase. The cut-off value, defined as 95% specificity versus a group of 526 patients suffering from benign chest diseases, was set at 3.3 micrograms/l for cytokeratin 19 fragment CYFRA 21-1 (carcinoembryonic antigen: 7.8 micrograms/l, squamous cell carcinoma antigen: 1.9 micrograms/l, neuron-specific enolase: 13.7 micrograms/l). Elevated pretreatment cytokeratin 19 fragment CYFRA 21-1 concentrations were recorded: in 112 of 244 (46%) patients with all histological types of lung cancer (carcinoembryonic antigen: 32%, squamous cell carcinoma antigen: 25%, neuron-specific enolase: 28%), in 89 of 177 (50%) patients with non-small cell lung cancer (carcinoembryonic antigen: 33%, squamous cell carcinoma antigen: 24%, neuron-specific enolase: 12%), in 47 of 81 (58%) patients with squamous cell carcinoma (carcinoembryonic antigen: 23%, squamous cell carcinoma antigen: 32%, neuron-specific enolase: 14%), in 27 of 63 (42%) patients with adenocarcinoma (carcinoembryonic antigen: 44%, squamous cell carcinoma antigen: 14%, neuron-specific enolase: 9%), in 15 of 33 (45%) patients with other non-small cell lung cancer (carcinoembryonic antigen: 36%, squamous cell carcinoma antigen: 24%, neuron-specific enolase: 14%), and in 20 of 55 (36%) patients with small cell lung cancer (carcinoembryonic antigen: 32%, neuron-specific enolase: 77%). Three of 12 patients with undefined histological type showed cytokeratin 19 fragment CYFRA 21-1 elevations. The best performance in terms of sensitivity and diagnostic accuracy was attained with the cytokeratin 19 fragment CYFRA 21-1 test in squamous cell carcinoma. In small cell lung cancer neuron-specific enolase was confirmed to be superior to the other markers. Cytokeratin 19 fragment CYFRA 21-1 concentrations increased with the extent of the malignant disease in non-small cell lung cancer. The positivity rate of cytokeratin 19 fragment CYFRA 21-1 in tumour stage TNM I was only 23% (carcinoembryonic antigen: 23%, squamous cell carcinoma antigen: 14%), i.e. the markers under study cannot be used for the diagnosis of early stage disease. Cytokeratin 19 fragment CYFRA 21-1 differentiated significantly between squamous cell carcinoma and the other histological types (p < 0.01). In addition, cytokeratin 19 fragment CYFRA 21-1 distinguished significantly the operable group TNM I-IIIa from inoperable TNM IIIb-IV (p < 0.05), but not TNM IIIa from IIIb. Out of 177 patients with non-small cell lung cancer, 90 individuals were monitored after surgery.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗