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PubMed1996

Bladder squamous cell carcinomas express psoriasin and externalize it to the urine.

PURPOSE: To report a single biomarker, psoriasin (Mr 11.0 kd, pI 6.2), a calcium binding protein which is expressed largely by stratified squamous epithelia and is externalized to the urine of bladder squamous cell carcinoma (SCC) bearing patients. MATERIALS AND METHODS: Protein expression profiles of SCCs obtained immediately after surgery were analyzed by two-dimensional gel electrophoresis and Coomassie blue staining. Protein identity was determined by microsequencing and immunoblotting. Protein expression in cryosections was studied by immunofluorescence. RESULTS: Four patients with SCC were identified from 100 samples of patients with suspected transitional cell carcinoma (TCC). The protein profiles of the 4 SCCs (56-1, grade III, T4; 181-1, grade I, T3; 219-1, grade III, T3 and 239-1, grade not determined, T2-4) resembled that of keratinocytes, suggesting that these cells express an early developmental pattern of gene expression. Besides expressing markers characteristic of keratinizing stratified squamous epithelia, the SCCs exhibited psoriasin, a protein externalized to the medium by keratinocytes. Immunohistochemistry of 3 of the SCCs with psoriasin antibodies showed that the positive cells were confined chiefly to the "squamous pearls." The presence of psoriasin in the urine of the 4 SCC patients was demonstrated by two-dimensional gel immunoblotting. Similar analysis of 43 urines from patients with bladder tumors other than SCC revealed 7 positives, some of which may reflect squamous differentiation. Analysis of the urine of 13 control individuals (12 males matched by age and a 42-year-old female) revealed 2 positives. Immunoblotting of the SCC patients' serum proteins with psoriasin antibodies failed to reveal the protein. CONCLUSION: The results point towards psoriasin, alone or as part of a biomarker profile, as a potential marker for the noninvasive follow-up of patients with SCC.

Adult↗

PubMed1996

Transactivation of the PTHrP gene in squamous carcinomas predicts the occurrence of hypercalcemia in athymic mice.

Humoral hypercalcemia of malignancy (HHM) is caused by the secretion of parathyroid hormone-related protein (PTHrP) by tumor cells, and tumors of squamous histology are the ones most commonly complicated by HHM. To determine why some squamous tumors cause HHM and others do not, we quantitated the levels of PTHrP mRNA expression and PTHrP secretion in a series of eight squamous tumor lines. As anticipated, we found that the level of PTHrP mRNA expression in individual lines correlated with their PTHrP secretion rates. However, PTHrP mRNA levels varied widely in individual lines, and only those tumor lines with the highest levels of PTHrP gene expression were able to cause hypercalcemia in athymic mice. We found that a specific segment of the PTHrP promoter could reproduce the relative pattern of PTHrP gene expression when cloned in front of a chloramphenicol acetyltransferase reporter gene and transiently transfected into these squamous lines. Deletional analysis confirmed that specific sequences within the PTHrP gene promoter appeared to be involved in the transactivation of the gene in tumor lines expressing high levels of PTHrP mRNA. These data suggest that the ability of a given squamous tumor to cause HHM is ultimately a function of its level of PTHrP gene expression, which in turn appears to be a function of the ability of specific transcription factors to transactivate PTHrP gene expression.

Animals↗

PubMed1996

[Primary squamous cell carcinoma of the prostate: a case report].

The patient was a 77-year-old man who visited our clinic with a chief complaint of dysuria. Digital rectal examination suggested prostatic carcinoma, but prostatic tumor marker levels were within normal limits. Transrectal needle biopsy was performed and histology was squamous cell carcinoma. Radical prostatectomy and pelvic lymph node dissection were performed with the diagnosis of T3N0M0 primary squamous cell carcinoma of the prostate. The 127 gm. tumor was moderately differentiated pT3N2M0 squamous cell carcinoma. Metastasis to the bilateral internal iliac arterial lymph nodes was confirmed histologically. Therefore, four courses of chemotherapy were performed using methotrexate, cisplatin, and pepleomycin. However, local recurrence was observed 11 months postoperatively and multiple pulmonary metastasis was developed at 13 months. The patient died of the disease 14 months after the operation. In Japan, seven cases of primary squamous cell carcinoma of the prostate have been reported, but none of these patients were treated by radical prostatectomy when the diagnosis was established by preoperative biopsy. In this case, changes in the squamous cell carcinoma antigen level in the blood corresponded to the effect of postoperative chemotherapy.

Aged↗

PubMed1996

[Expression of CD44 variant 6 and its metastatic potential in squamous cell carcinoma of the oral cavity].

Using antihuman CD44 variant 6 monoclonal antibody (2F10), immunohistochemical screenings were performed for 38 oral squamous cell carcinoma cases and 10 oral mucosa in healthy cases as normal counterpart. Normal epithelium in the oral surface was stained intensely by the antibody. The reactivity was particularly strong in the spinous layers of stratified squamous epithelium. Cells in the basal layers exhibited moderate staining. In contrast, expression of CD44v6 tended to be downregulated in 38 oral squamous cell carcinoma materials. Interestingly, more faint or no staining by the anti-CD44v6 monoclonal antibody was found in the primary squamous cell carcinomas involving regional lymphnode metastasis. Downregulation of CD44v6 isoform was suggested to occur during regional lymphnode metastasis on oral squamous, cell carcinomas.

Carcinoma, Squamous Cell↗

PubMedDate not supplied

[Immunohistochemical characterization and ultrastructural features of cervical squamous cell carcinoma of ectocervical and endocervical (cambial cell or metaplastic) genesis].

Among 199 invasive squamous cell carcinomas immunophenotype of ectocervical carcinoma (true squamous cell one) was found in 18 tumors. Immunophenotype of metaplastic, endocervical squamous cell carcinoma was established in 181 cases. There was a pronounced expression of cytokeratins N 1, 2, 10, 14 and negative or weak expression of N 8 and 17. Ultrastructural features of this carcinoma type were desmosomes on microprocesses, abundant bundles of cytoplasmic tonofibrils. A high level of cytokeratins N 8 and 17, carcinoembryonic antigen was found in squamous cell endocervical carcinoma; at the same time keratins N 1, 2, 10 and 14 were weakly expressed, there was also a characteristic ultrastructure of intercellular contacts (desmosomes on flat surfaces) and microvilli. The results allow to use immunohistochemical and ultrastructural methods for differential diagnosis of squamous cell carcinoma originating from different sources.

Carcinoembryonic Antigen↗

PubMed1996

Parathyroid hormone-related protein gene expression in human squamous carcinoma cells is repressed by mutant isoforms of p53.

Parathyroid hormone-related protein (PTHrP) is a normal secretory product of a variety of squamous epithelia, including epidermal keratinocytes. Only a subset of squamous carcinomas, however, express the gene at levels sufficient to cause humoral hypercalcemia. In the present study, comparison of PTHrP expression levels with p53 functional status in a series of squamous carcinoma lines has revealed an association between expression of specific mutant isoforms of p53 and very low levels of PTHrP mRNA. Evaluation of p53 isoforms with mutations in codons 248 and 273 showed them to be capable of repressing PTHrP gene expression in a high-expressing, p53-negative squamous line by approximately 50%. Conversely, inactivation of an endogenous mutant p53 with E1B proteins resulted in an increase in PTHrP expression in a low-expressing cell line. Subsequent analysis of promoter-specific PTHrP transcripts in a p53-negative squamous line transfected with mutant p53 isoforms suggested that down-regulation occurred primarily at the two TATA-based promoters. Direct testing of a murine PTHrP reporter construct in transient transfection assays confirmed the capacity of the 248 and 273 mutants to repress this TATA-based promoter, although only about half as effectively as wild-type p53.

Adenovirus E1B Proteins↗

PubMed1995

Application of the AgNOR method to distinguish pseudoepitheliomatous hyperplasia from squamous cell carcinoma.

The AgNOR stain was performed on seventeen cases of pseudoepitheliomatous hyperplasia of the oral cavity and genital tract, seventeen cases of squamous cell carcinomas of the same regions, and nineteen cases of squamous cell carcinoma of the cervix, to determine whether the stain could help to distinguish pseudoepitheliomatous hyperplasia from squamous cell carcinoma. No constant relationship of the AgNOR score to the grade of the lesion could be determined. Follow up of some of the cases was possible. Here, too, it was seen that the AgNOR score could not reliably predict which cases of pseudoepitheliomatous hyperplasia would progress to squamous cell carcinoma, and which cases of squamous cell carcinoma would suffer a relapse.

Carcinoma, Squamous Cell↗

PubMed1997

[A case of primary squamous cell carcinoma of the ureter: biochemical modulation with cisplatin and 5-fluorouracil].

A case of primary squamous cell carcinoma of the ureter is reported. A 62-year-old male presented with gross hematuria and paralysis of the left leg. Abdominal computed tomographic (CT) scan and ultrasonography revealed left hydronephrosis, a massive tumor (8 x 7 cm) in the left distal ureter which invaded the pelvic bone (T4), and left obturator lymph node metastasis (N2). Pathologic examination of the biopsy specimen revealed poorly differentiated squamous cell carcinoma. Cisplatin (100 mg/m2, day 1) and 5-fluorouracil (960 mg/m2/day, days 2-6) were administered systemically in accordance with biochemical modulation regimen for head and neck squamous cell carcinoma, and a minor response was obtained (tumor regression rate 38%, serum SCC antigen regression rate 64%). Thereafter, resection of residual tumor was performed, resulting in noncurative operation because of direct invasion to the pelvic bone. Four months after tumorectomy, liver metastasis appeared, and the patient died of disease 14 months after the initial visit. Combination therapy with cisplatin and 5-fluorouracil is widely used for head and neck squamous cell carcinoma, and the response rate has been reported to be 46-94%. This regimen may also be effective against urological squamous cell carcinoma.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1997

Multiple squamous cell carcinomas in a psoriatic patient following high-dose photochemotherapy and cyclosporin treatment: response to long-term acitretin maintenance.

Cumulative toxicity is a well known limitation of antipsoriatic treatments. In particular, the induction of multiple squamous cell carcinomas following long-term PUVA treatment is well established. In the present report, a psoriatic patient is described who was treated for more than 14 years with photochemotherapy (PUVA) and who received excessive amounts of topical corticosteroids. The patient developed, in total, 34 squamous cell carcinomas. In all, three squamous cell carcinomas developed during long-term PUVA treatment, and 21 carcinomas appeared during 16 months of treatment with cyclosporin. Subsequently, a marked inhibition of the occurrence of new tumours occurred during prolonged treatment with acitretin, and no new tumours have appeared during the last 4 years of continuous treatment with this retinoid at a dose of 60 mg/day. Modulation of the expression of PUVA-induced squamous cell carcinomas by cyclosporin and acitretin are discussed. The present report lends support to the hypothesis that cyclosporin causes an increased occurrence of PUVA-induced carcinomas, whereas acitretin (60 mg/day) is of value in preventing the occurrence of new squamous cell carcinomas in patients who were treated with long-term PUVA.

Acitretin↗

PubMed1997

Amplification of the genes BCHE and SLC2A2 in 40% of squamous cell carcinoma of the lung.

Gene amplification is a common genetic change in human cancer cells. Previously, we provided the first evidence for gene amplification at chromosome band 3q26 in squamous cell lung carcinoma. In this study, the following analyses were performed: (a) we evaluated biopsies and paraffin-embedded tissues of 16 additional squamous cell lung carcinomas for gene amplification using reverse chromosome painting. Of the 16 tumors, 3 tumors showed an amplification of the entire long arm of chromosome 3, and 3 tumors showed various amplifications on 3q, all of which involved chromosome band 3q26; (b) we tested eight genes encompassing region 3q25-qter in two different tumors to identify amplified genes on chromosome 3q. The genes SI, BCHE, and SLC2A2 were amplified in both tumors; and (c) we analyzed 15 additional paraffin-embedded tissues to determine the amplification frequency of these genes. Of the 15 squamous cell lung carcinomas, 6 showed amplification for at least 1 of the genes, with BCHE and SLC2A2 as the genes most frequently amplified. Together, our reverse chromosome painting data and our PCR analysis indicate gene amplification at 3q26 in 40% of all squamous cell lung carcinomas with BCHE and SLC2A2 as possible target genes of the amplification unit in squamous cell lung carcinoma.

Blotting, Southern↗

PubMed1998

Retinoic acid receptor beta induces terminal differentiation of squamous cell carcinoma lines in the absence of cyclin-dependent kinase inhibitor expression.

The chemotherapeutic agent and vitamin A metabolite retinoic acid (RA) has been used to treat many tumor types. The effects of RA are mediated by a family of ligand-dependent transcription factors, the retinoic acid receptors (RAR) and the retinoid X receptors. Alterations in RAR expression have been implicated in tumorigenesis. We showed previously that loss of RARbeta expression and target gene responsiveness to RA were consistent features of head and neck squamous cell carcinoma lines. To begin to elucidate the role of RARbeta in the malignant transformation of stratified squamous epithelia, we reexpressed RARbeta in squamous cell carcinoma (SCC) lines by stable transfection. SCC lines expressing RARbeta produced large numbers of flat cells with abundant cytoplasm that died and detached from the culture dish. These cells morphologically resembled the differentiated cells of normal stratified squamous epithelium in culture. These cells did not exhibit the characteristic DNA fragmentation pattern of apoptotic cells, nor did they label in a fluorescent apoptosis assay. Northern and Western blotting revealed induction of terminal differentiation markers in these cells. RARbeta produced alterations in levels of RA-responsive gene expression in these cells, and terminal differentiation occurred in the absence of detectable cyclin-dependent kinase inhibitor expression. We concluded that RARbeta expression induced terminal differentiation in SCC lines, suggesting a role for this transcription factor in the normal maturation of stratified squamous epithelium.

Apoptosis↗

PubMed1997

Mucosal changes in the upper gastrointestinal tract in Sri Lankan patients with squamous carcinoma of the oesophagus.

BACKGROUND: Squamous carcinoma of the oesophagus, is a common tumour in Sri Lanka. A thickened and pale appearance of the oral, hypopharyngeal and oesophageal mucosa, has been observed during endoscopy. The aim of this study was to document the histological changes of the mucosa thus affected in 93 patients with squamous carcinoma of the oesophagus. METHOD: 93 patients with oesophageal carcinoma had mucosal biopsies done from the left cheek, hypopharynx and 2.5 cm. and 5 cm above the tumour, during endoscopy for biopsy of the tumour. Paraffin sections of the biopsy stained with Haematoxylin and Eosin were examined. 25 specimens of oesophageal tissue, and tissue from the mucosa and hypopharyngeal mucosa obtained at coroners' autopsies from a comparable group served as controls (15 males, 10 females). RESULTS: The tumours were squamous carcinoma of varying grades of differentiation. The mucosal biopsies showed, acanthosis, basal cell hyperplasia, intra epithelial neoplasia (IEN) grades I-III, chronic oesophagitis, koilocytosis and papillomatosis. The mucosa of the control group only showed koilocytosis and papillomatosis in two cases. CONCLUSION: Pathological changes such as acanthosis, basal cell hyperplasia, intra epithelial neoplasia, chronic oesophagitis koilocytosis and papillomatosis occur in the oral hypopharyngeal and other areas of the oesophageal squamous mucosa, in association with squamous carcinoma of the oesophagus.

Adult↗

PubMed1998

Expression of Bcl-X(L), an antiapoptotic member of the Bcl-2 family, in esophageal squamous cell carcinoma.

Bcl-X, a Bcl-2-related protein, is a potent antagonist of apoptosis in its long splice variant (Bcl-X(L)). The present study was performed to determine its expression in preneoplastic and neoplastic lesions of the esophagus, its correlation with other members of the Bcl-2 family, and its impact on the outcome of surgically treated esophageal cancer patients. Samples of normal esophageal squamous epithelium (n = 10), severe squamous cell dysplasias (n = 19), carcinomas in situ (n = 14), invasive squamous cell carcinomas (n = 172), and lymph node metastases (n = 21) were immunohistochemically analyzed for Bcl-X(L) expression using a polyclonal anti-Bcl-X(L) antibody. The immunostaining was evaluated according to a score system (0-12 points) based on the percentage of positive tumor cells and the relative immunostaining intensity. Cytoplasmic staining for Bcl-X(L) protein was invariably found in all cell layers of the normal esophageal squamous epithelium. In contrast, a considerable portion of preneoplastic and neoplastic lesions display a decreased Bcl-X(L) expression as compared with that in the normal esophageal epithelium. On comparison of the amount of Bcl-X(L) expression between the different types of lesions, however, no significant differences were found between severe squamous cell dysplasias (mean immunoreactive score +/- SD, 5.2 +/- 1.8), carcinomas in situ (5.2 +/- 2.2), invasive carcinomas (4.5 +/- 2.8), and lymph node metastases (4.2 +/- 2.6). In invasive carcinomas, Bcl-X(L) expression decreased continuously with decreasing tumor differentiation (P = 0.0001) and was also directly correlated with bcl-2-associated X protein expression (P = 0.0001). On the contrary, an inverse correlation was found between Bcl-X(L) expression and Bcl-2 protein expression (P = 0.0001). No correlation was found between Bcl-X(L) expression and the parameters pT category, pN category, and tumor size. In the univariate survival analysis, patients with low immunoreactive scores (< or = 4) of Bcl-X(L) expression in the tumor tissue showed lower 2-year and 5-year survival rates than patients with high immunoreactive scores (> 4; P = 0.0485). In multivariate survival analysis, however, only the parameters pN category and pT category, but not Bcl-X(L) expression, could be verified as independent prognostic factors. This tendency of decreasing levels of an antiapoptotic protein toward unfavorable outcome is supported by an increasing number of studies on the role of Bcl-2, another antiapoptotic protein, and must be interpreted against the backdrop of apoptosis as a result of the interaction of many cell death-promoting and protecting proteins.

Apoptosis↗

PubMed1998

DNA gains in 3q occur frequently in squamous cell carcinoma of the lung, but not in adenocarcinoma.

We performed a comparative genomic hybridization study on 25 samples of adenocarcinoma and 19 samples of squamous cell carcinoma of the lung to detect recurrent changes in the genetic material. DNA copy number changes were found in 16 squamous cell carcinoma samples and 17 adenocarcinoma samples. The most common changes were gains of DNA sequences in 3q (43%), 1q (34%), 8q (32%), 5p, (30%), 7p (25%), and 12p (25%). Of the squamous cell carcinoma samples with DNA copy number changes, 94% (15/16) had a gain in 3q (minimal common region of overlap q24-qter), whereas only 24% (4/17) of the adenocarcinoma samples with DNA copy number changes showed a gain in 3q (q22-qter) (P < 0.001). Six high-level amplifications in 3q (q26.2-q26.3) were detected in the squamous cell carcinoma samples but none were observed in the adenocarcinoma samples. Our results suggest that amplification of genes in 3q may be important in the tumorigenesis of squamous cell carcinoma but not necessarily of adenocarcinoma.

Adenocarcinoma↗

PubMed1998

Granulocyte-macrophage-colony stimulating factor stimulates tumor invasiveness in squamous cell lung carcinoma.

BACKGROUND: Bronchial epithelial cells produce a significant amount of granulocyte-macrophage-colony stimulating factor (GM-CSF), which is believed to mediate both the host defense and inflammation. Recently, GM-CSF has been demonstrated to be produced by several tumor cells and also to be associated with tumor growth and metastasis. In the current study, the authors investigated the biologic role of GM-CSF produced by squamous cell lung carcinoma. METHODS: The production of GM-CSF from 17 human lung carcinoma cell lines was determined by an enzyme-linked immunoabsorbent assay. In vitro invasiveness was investigated by using a Biocoat Matrigel (Collaborative Biomedical Products, Bedford, MA) precoated invasion chamber. The activity of the matrix metalloproteinases (MMPs) were examined by gelatin zymography. The expression of GM-CSF in 113 cases of resected nonsmall cell lung carcinoma was analyzed immunohistochemically, and the association between the expression of GM-CSF and clinicopathologic features was investigated. RESULTS: The production of GM-CSF by squamous cell carcinoma cell lines was closely related to the in vitro invasiveness and MMP activity of the cancer cells. Recombinant GM-CSF stimulated the invasiveness of less invasive LK-2 and LC-1 cells in a dose-dependent manner, and this stimulation was abrogated by the neutralizing anti-GM-CSF antibody. Furthermore, anti-GM-CSF antibody decreased the invasiveness of highly invasive EBC-1 and NCI-H157 cells. GM-CSF also increased the MMP activity of LK-2 and LC-1 cells. Of 113 resected nonsmall cell lung carcinomas, 30 of 71 squamous cell carcinomas (42.3%), and 24 of 42 adenocarcinomas (57.1%) stained positively for GM-CSF. The expression of GM-CSF in squamous cell carcinomas was associated with the local invasion by the primary tumor. CONCLUSIONS: These results suggest that the production of GM-CSF is involved in both the in vitro invasiveness and the local progression of squamous cell carcinoma of the lung.

Carcinoma, Squamous Cell↗

PubMed1998

A c-rasHa mutation in the metastasis of a human papillomavirus (HPV)-18 positive penile squamous cell carcinoma suggests a cooperative effect between HPV-18 and c-rasHa activation in malignant progression.

BACKGROUND: Human papillomaviruses (HPV) have been implicated in the etiology of anogenital squamous epithelial tumors. Of the 65 HPV strains, subtypes HPV-16 and HPV-18 frequently are associated with malignant conditions and are capable of transforming keratinocytes in vitro. However, additional cellular changes are necessary to confer tumorigenicity to HPV-infected cells. Secondary events implicated in the progression to malignancy include loss of tumor suppressor genes such as p53 and/or activation of cellular oncogenes such as c-rasHa. METHODS: Polymerase chain reaction (PCR) was used to identify HPV-16 or HPV-18 genetic sequence in primary penile squamous cell carcinoma and two inguinal lymph node metastases. p53 and c-rasHa loci were analyzed by sequencing of PCR-amplified genomic DNA. RESULTS: HPV-18 but not HPV-16 infection was found in the primary carcinoma and in inguinal metastases occurring 5 and 7 years after the initial lesion. Sequence analysis did not identify any p53 mutations in the primary carcinoma or its metastases. However, although the primary lesion and the 5-year metastasis encoded wild-type c-rasHa, the 7-year metastasis had a missense mutation within c-rasHa codon 61. CONCLUSIONS: To the authors' knowledge, this is the first report of an activating c-rasHa mutation associated with squamous cell carcinoma of the penis. The presence of activated c-rasHa in the second metastasis but not in the first metastasis or the primary lesion suggests that activation of c-rasHa may be a late event in the malignant progression of HPV-18-associated penile squamous cell carcinoma. Analysis of additional samples from primary lesions and their resultant metastases is necessary to elucidate the incidence and significance of c-rasHa activation in penile squamous cell carcinoma.

Carcinoma, Squamous Cell↗

PubMed1998

Squamous and basal cell carcinoma in heart transplant recipients.

BACKGROUND: Cutaneous malignancies are frequent in organ transplant recipients. We retrospectively reviewed a large series of heart transplant recipients and report on the prevalence and risk factors for development of cutaneous squamous and basal cell carcinoma. METHODS: Between Dec. 4, 1985, and Dec. 27, 1996, 299 heart transplantations were performed at the Oregon Health Sciences University. Heart transplant recipients with more than 6 months survival or follow-up were investigated for squamous and basal cell carcinoma (n = 248). RESULTS: Forty-one patients (17%) were found to have 192 squamous or basal cell carcinomas. Squamous cell carcinoma was the predominate skin malignancy, constituting 172 (90%) of the lesions. The mean number of skin malignancies per patient was 4.7 +/- 0.81 (range 125). Patients with development of a skin malignancy were 8 years older on average, with a male-to-female ratio of 19.5:1. The predominant skin type and eye color were fair (59%) and blue (59%), respectively. Cumulative risk, based on actuarial survival analysis for development of a squamous or basal cell carcinoma at 1 year, was 3% and increased to 21% and 35% at 5 and 10 years, respectively. In addition, cumulative risk increased in patients who received treatment with OKT3. CONCLUSION: Cumulative risk of development of a skin malignancy increased with time and use of OKT3. Additional patient risk factors included older age, male sex, fair skin, and blue eyes.

Actuarial Analysis↗

PubMed1998

Nucleolar organiser regions and morphologic subtypes of squamous cell carcinoma of cervix.

Nucleolar organiser regions (NOR) are chromosomal segments coding for ribosomal RNA. The number of nucleolar organiser regions correlates with cellular proliferation and has a diagnostic and prognostic value in neoplastic diseases. The aim of this study was to study the morphologic subtypes of squamous cell carcinoma of the uterine cervix in biopsy and hysterectomy specimens and to determine the AgNOR counts in these morphologic subtypes. One hundred and seventy-nine cases of squamous cell carcinoma of the uterine cervix were classified into three morphological subtypes namely large cell non keratinising squamous cell carcinoma (113), keratinising squamous cell carcinoma (64) and small cell carcinoma (2). A correlation of histologic typing on biopsy and hysterectomy specimens was done in 142 cases with a complete correlation in 90.5%. Fifty-eight of these tumours were stained with silver nitrate to demonstrate Nucleolar organiser regions (AgNORS). The mean AgNOR count was higher (3.66) in keratinising squamous cell carcinoma, which is known to have a worse prognosis as compared to 3.04 in large cell non keratinising carcinoma and (3.45) in the two cases of small cell carcinoma of the uterine cervix.

Adult↗