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PubMed2000

Composite tumor with papillary adenocarcinoma and squamous cell carcinoma of the esophagus: report of a case.

Papillary adenocarcinoma is extremely rare in the squamous epithelium-lined esophagus. The histopathologic and immunohistochemical characteristics were examined in a composite tumor showing distinct papillary adenocarcinoma and squamous cell carcinoma of the esophagus resected from a 66-year-old man. The esophageal tumor consisted both grossly and histologically of two distinct components: an ulcerative part showing a squamous cell carcinoma, and a polypoid part corresponding to a papillary adenocarcinoma. In addition, the in situ squamous cell carcinoma was contiguous with the esophageal tumor. Mucin secretion was found only in the papillary adenocarcinoma component. Immunohistochemically, tumor cells of the papillary adenocarcinoma component were positive for carcinoembryonic antigen, secretory component, and lactoferrin. These staining patterns were similar to those of the normal esophageal gland proper. These histologic, mucin-histochemical, and immunohistochemical findings suggest that the papillary adenocarcinoma originated from the submucosal esophageal gland and the squamous cell carcinoma from the squamous epithelium lining the esophagus.

Adenocarcinoma, Papillary↗

PubMed2001

Expression of epithelial growth factor receptor and its two ligands, transforming growth factor-alpha and epithelial growth factor, in normal and neoplastic squamous cells in the vulva: an immunohistochemical study.

Epithelial growth factor receptor (EGFR) sends signals to the proliferation signal transduction system, receiving two ligands: epithelial growth factor (EGF) and transforming growth factor-alpha (TGF-alpha). This immunohistochemical study examined the roles of EGFR and its ligands in the proliferation of normal and neoplastic vulvar squamous cells in 25 patients with vulvar squamous cell carcinoma (VSCC), 10 patients with vulvar condyloma acuminata (VCA), 15 patients with vulvar intra-epithelial neoplasm I-II or III (VIN I-II or III), and 5 subjects with vulvar normal squamous cells (VNSC). EGFR was detected in a few basal cells in 40% of the VNSC, in highly dysplastic cells in 40% of the VIN III, in many neoplastic cells in 80% of the VCA, and in some malignant cells in 64% of the VSCC. EGF was seen in the cytoplasm in 20% of the VIN I-II, 100% of the VIN III, 100% of the VCA, and 100% of the VSCC. Diffuse TGF-alpha was weakly expressed in the cytoplasm in 100% of the VNSC, more intensely in 100% of the VIN and 100% of the VCA, and intensely in 100% of the VSCC. These findings led to the suggestion that the TGF-alpha-EGFR system maintains the growth of normal squamous cells and, in part, maintains the growth of dysplastic and neoplastic squamous cells in the vulva. EGF expression was an early sign of neoplasia. The expression of EGFR with overexpression of its two ligands contributed to the proliferation of dysplastic and neoplastic squamous cells in VIN III and VCA. EGFR expression appeared to contribute to essential neoplastic abnormalities in 64% of the VSCC.

Carcinoma in Situ↗

PubMed2001

Implications of adrenomedullin expression in the invasion of squamous cell carcinoma of the uterine cervix.

BACKGROUND: Adrenomedullin (AM) is a multifunctional peptide involved in a variety of physiological functions, including vasodilatation, growth regulation, and carcinogenesis. To elucidate the possible role of AM in the growth and invasion of uterine cervical carcinoma, the presence and distribution of AM and AM mRNA was examined in the neoplastic changes of squamous epithelium of the uterine cervix. METHODS: The expression of AM mRNA by CaSki, a uterine squamous cell carcinoma cell line, was examined by reverse transcriptase-polymerase chain reaction (RT-PCR). The presence and distribution of AM and AM mRNA in sections of normal cervical tissues, cervical intraepithelial neoplasia (CIN), and invasive squamous cell carcinomas were evaluated by immunohistochemical staining with a specific antibody against AM and by in situ RT-PCR, respectively. RESULTS: AM mRNA expression in CaSki cells was demonstrated by RT-PCR. Immunohistochemical staining for AM and in situ RT-PCR revealed that AM and AM mRNA were expressed in invasive squamous carcinoma cells, but not in normal cervical epithelium or in CIN lesions. Abundant expression of AM and AM mRNA was localized in the cytoplasm of carcinoma cells of bulky invasive carcinomas, while in early invasive carcinoma, the expression of AM and AM mRNA was more prominent in stromal cells adjacent to the early invasive carcinoma cells than in the carcinoma cells themselves. CONCLUSIONS: Because AM expression was evident only in invasive cervical squamous carcinoma cells and the stromal cells adjacent to early invasive carcinomas, it is likely that AM may play an important role in the growth and invasion of squamous cell carcinoma of the uterine cervix.

Adrenomedullin↗

PubMed2006

Expectant management of anal squamous dysplasia in patients with HIV.

PURPOSE: Anal squamous dysplasia is commonly found in patients with HIV infection. There is no satisfactory treatment that eradicates this premalignant lesion with low morbidity and low recurrence. This study reviews a series of patients with HIV and an abnormal anal examination who had squamous dysplasia and who have been followed with physical examination alone and with repeat biopsies as necessary for new or suspicious lesions. METHODS: We reviewed the charts of 40 HIV-positive men who had squamous dysplasia of the anal canal and anal margin, focusing on history, physical findings, histologic diagnosis, and the occurrence of invasive squamous-cell carcinoma. RESULTS: Forty HIV-positive men (mean age, 39 years) were followed for anal squamous dysplasia. Biopsies revealed dysplasia, which was usually multifocal. The grade of dysplasia varied, but 28 of 40 patients had at least one area of severe dysplasia. All patients had a follow-up period greater than one year (mean, 32 months; range, 13-130 months). Three patients developed invasive carcinoma while under surveillance, and these were completely excised or cured with chemoradiation. CONCLUSIONS: Extensive excision for dysplasia in the context of HIV confers high morbidity and questionable benefit, and other treatments are of uncertain value. In a group of patients followed expectantly, most did not develop invasive cancer, and in those who did, early cancers could be identified and cured. Physical examination surveillance for invasive carcinoma may be acceptable for following patients with HIV and biopsy-proven squamous dysplasia.

Adult↗

PubMed1988

Thrombospondin binding by human squamous carcinoma and melanoma cells: relationship to biological activity.

Human squamous carcinoma cells attach and spread on thrombospondin (TSP)-coated culture dishes but exhibit significant variability among individual cell lines in their degree of responsiveness. Using a highly responsive squamous carcinoma line and a cell line which is much less responsive (as well as a human melanoma cell line which does not respond at all in the adhesion assay), we have examined binding of exogenous radiolabeled TSP. The cells which were the most responsive to TSP in the adhesion assay bound the greatest amount of radiolabeled ligand. Binding was time- and dose-dependent, saturable, inhibitable with excess unlabeled TSP, reversible, and specific. The less-responsive squamous carcinoma cells bound only 25-30% of the amount of TSP bound by the highly responsive cells while the nonresponsive melanoma cells bound less than 10% of the amount bound by the highly responsive squamous carcinoma cells. Our previous studies (J. Varani et al. (1986) Exp. Cell Res. 167, 376) have shown that the highly responsive squamous carcinoma cells also synthesized the greatest amount of TSP as indicated by biosynthetic labeling studies. The less-responsive squamous carcinoma cells were intermediate in synthetic activity and no synthetic activity was seen with the melanoma cells. These findings suggest that the amount of ligand bound may determine the degree of biological responsiveness and that endogenously synthesized TSP may be the source of that ligand.

Antibodies, Monoclonal↗

PubMed1996

Heterogeneous etiology of squamous carcinoma of the vulva.

OBJECTIVE: To correlate various previously identified risk factors, different histologic types, and the presence of human papillomaviruses (HPV) in squamous vulvar carcinomas and intraepithelial precursor lesions. METHODS: Cases of squamous vulvar carcinomas and intraepithelial precursor lesions from a case-control study were analyzed by histologic type, the presence of HPV, and HPV type. These findings were correlated with demographic and interview data. RESULTS: Significant differences (P < .001) in the prevalence of HPV DNA were noted between the following: 1) patients with high-grade vulvar intraepithelial neoplasia (VIN) (48 of 54 [88.9%]), 2) different types of squamous carcinomas, designated basaloid and warty carcinomas (18 of 21 [85.7%]), and 3) keratinizing squamous carcinoma (three of 48 [6.3%]). When the risk factor profiles for basaloid or warty carcinoma and keratinizing squamous carcinoma were compared, it was found that basaloid and warty carcinoma was significantly associated with the classical cervical cancer risk factors (lifetime number of sexual partners, age at first intercourse, abnormal Papanicolaou smears, venereal warts, low socioeconomic status, and cigarette smoking) whereas keratinizing squamous carcinoma was less strongly linked to these factors and in some cases not at all. The risk profile for VIN was similar to that of basaloid and warty carcinoma (with respect to sexual and reproductive history and smoking), although effects were weaker for some factors. CONCLUSION: The results of this study further support the view that vulvar carcinoma has two different etiologies, one related to HPV infection and one that is not.

Adult↗

PubMed1990

Comparison between squamous cell carcinoma-associated antigen and CA-125 in patients with carcinoma of the cervix.

Serum levels of CA-125 and squamous cell carcinoma-associated antigen (SCC) were measured in 30 patients with squamous cell carcinoma and 12 patients with adenocarcinoma of the uterine cervix. SCC was elevated in 67% of patients with squamous cell carcinoma but in only 25% of patients with adenocarcinoma. In contrast, CA-125 was elevated in 75% of patients with adenocarcinoma but in only 26% of patients with squamous cell carcinoma. These data demonstrate the applicability of the measurement of CA-125 as a tumor marker for cervical adenocarcinoma and confirm the value of the measurement of SCC antigen in patients with cervical squamous cell carcinoma. Moreover, we show that measurement of SCC antigen in adenocarcinoma and measurement of CA-125 in squamous cell carcinoma are of insufficient clinical value.

Adenocarcinoma↗

PubMed1991

Cutaneous squamous cell carcinomas and papillomaviruses in renal transplant recipients: a clinical and molecular biological study.

Papillomaviruses are strongly implicated in squamous cell carcinomas arising on mucosal surfaces of normal individuals, and in the skin carcinomas of epidermodysplasia verruciformis suffers. Renal transplant recipients often have numerous skin warts and, in Australia particularly, a very high risk of developing cutaneous squamous cell carcinoma. To determine the magnitude of this risk, and to test whether papillomaviruses are specifically associated with these cancers, we examined 188 renal transplant recipients for skin cancers and tested 235 biopsy specimens of (histologically proven) squamous cell carcinomas for the presence of viral DNA. The risk of developing squamous cell carcinoma increased with duration of transplant: the probability being 25% after 9.5 years (standard error = 1.3 years) rising to 50% at 20.6 years (standard error 6.8 years). Factors which did not appear to affect the risk of tumour development included the patients sex and their skin type. However the age at transplant significantly altered the risk with patients transplanted at greater than 35 years developing tumours about four times more rapidly than patients less than or equal to 35 years. Extensive hybridisation tests for the presence of papillomavirus DNA in squamous cell carcinomas were negative, as was the polymerase chain reaction amplification method using general L1 gene oligonucleotide primers. Our data do not support a role for papillomavirus in the maintenance of cutaneous squamous cell carcinoma.

Adolescent↗

PubMed2007

An audit of surgical outcomes of esophageal squamous cell carcinoma.

OBJECTIVE: Esophageal squamous cell carcinoma and adenocarcinoma were increasingly recognized as two entities with different biologic behaviors and prognosis. Surgical risks and oncologic benefits of transthoracic and transhiatal esophagectomy for esophageal squamous cell carcinoma patients are not confessed. METHODS: Between 1994 and 2005, 216 esophageal squamous cell carcinoma patients underwent esophagectomy were enrolled and analyzed retrospectively. RESULTS: One hundred sixty-six patients underwent transthoracic esophagectomy and 50 patients underwent transhiatal esophagectomy. The overall hospital mortality and postoperative complication rates were 9.7 and 49%, respectively. The amount of intra-operative blood loss or transfusion, postoperative complication rate, lengths of hospital stay and hospital mortality rate were not significantly different between both groups. However, shorter operative time was noticed in transhiatal group (p<0.001). The overall 5-year survival rate was 16.8%. ESCC patients underwent either transthoracic or transhiatal esophagectomy had comparable long-term survival. The pTNM stage was independent prognostic factor for patients underwent transthoracic esophagectomy. However, location of tumor (p=0.009) and pathologic tumor length (p=0.012) were predictors of prognosis for patients underwent transhiatal esophagectomy. CONCLUSIONS: For esophageal squamous cell carcinoma patients, no significant differences in postoperative mortality or morbidity rates were observed between transthoracic and transhiatal esophagectomy. However, traditional pTNM staging system might underestimate the severity of esophageal squamous cell carcinoma patients who underwent transhiatal esophagectomy. The information of dissimilar prognostic factors for transhiatal or transthoracic esophagectomies will be helpful in tailoring more individualized adjuvant therapy to optimize esophageal squamous cell carcinoma patient's outcome.

Adult↗

PubMed2006

Role of glycogen synthase kinase 3 in squamous differentiation induced by cigarette smoke in porcine tracheobronchial epithelial cells.

Epidemiological evidence suggests that cigarette smoke induces squamous metaplasia in human tracheobronchial epithelium that can progress to lung squamous carcinoma. But it is not well understood how tracheobronchial epithelial cells transduce the signals that mediate cigarette smoke-induced squamous differentiation or squamous metaplasia. In the present study, we found that in vitro cigarette smoke components notably inhibited glycogen synthase kinase 3 (GSK3) and induced the expression of involucrin, a marker of squamous differentiation. The inactivation of GSK3 by two highly selective inhibitors, lithium and SB216763, also significantly enhanced involucrin expression in cultured porcine tracheobronchial epithelial cells (PTBECs). Moreover, we demonstrated that cigarette smoke components significantly promoted activator protein-1 (AP-1) binding activities to the upstream regulatory region of involucrin gene, and similar results were observed by further studies through using GSK3 inhibitors to imitate the effects of cigarette smoke components. Taken together, we conclude that GSK3 is involved in involucrin expression induced by cigarette smoke in PTBEC probably via negatively regulating AP-1 activity, implying a possible mechanism responsible for squamous differentiation induced by cigarette smoke.

Animals↗

PubMed2004

Repopulation of moderately well-differentiated and keratinizing GL human squamous cell carcinomas growing in nude mice.

PURPOSE: It has been suggested that, reminiscent of the regulated proliferative response of normal squamous epithelium, squamous cell carcinomas that have preserved characteristics of differentiation have a greater repopulation capacity during fractionated irradiation than undifferentiated tumors. The aim of the present study was to investigate repopulation in moderately well-differentiated and keratinizing GL human squamous cell carcinomas in nude mice. METHODS AND MATERIALS: GL human squamous cell carcinomas were transplanted s.c. into the right hind leg of NMRI nu/nu mice. Irradiation was performed with 5.4 Gy fractions under clamp hypoxia or with 2 Gy fractions under ambient conditions. Six, 12, or 18 fractions were given daily, every second day, or every third day. Graded top-up doses were applied under clamp hypoxia to determine the tumor control dose 50% (TCD(50)). A total of 20 TCD(50) assays were performed and analyzed using maximum-likelihood techniques. RESULTS: With an increasing number of daily 5.4 Gy fractions under clamp hypoxia, the top-up TCD(50) values decreased significantly from 50.9 Gy (95% CI: 47, 54) after single doses to 0 Gy after 18 fractions. For the same number of fractions, the top-up TCD(50) increased with increasing overall treatment time. The results are consistent with a constant repopulation rate with a clonogenic doubling time (T(clon)) of 12.7 days (8.6, 16.8). Under ambient blood flow, the top-up TCD(50)s for daily 2 Gy fractions decreased significantly, but were less pronounced than for 5.4 Gy fractions under clamp hypoxia. For a given number of fractions under ambient conditions, the top-up TCD(50)s did not increase significantly with overall treatment time, except for irradiation with 12 fractions in 36 days compared to 12 and 24 days. The T(clon) value from these data was 24.0 days (11.6, 36.4). CONCLUSION: Our data demonstrate a slow but significant rate of repopulation of clonogenic tumor cells during fractionated irradiation of GL human squamous cell carcinomas under clamp hypoxia without indication of a change of the repopulation rate during treatment. Less pronounced repopulation was observed for irradiation under ambient conditions, which might be explained by preferential survival of hypoxic and therefore nonproliferating cells. Taken together with our previous studies on poorly differentiated FaDu tumors (Petersen et al., IJROBP 2001;51:483-493), the results support important heterogeneity of kinetics and mechanisms of repopulation, in particular of the influence of the oxygenation status of surviving clonogenic cells on the repopulation rate during fractionated irradiation, in different experimental squamous cell carcinoma.

Algorithms↗

PubMed2006

Elevated risk of squamous-cell carcinoma of the lung in heavy smokers carrying the variant alleles of the TP53 Arg72Pro and p21 Ser31Arg polymorphisms.

Alterations in cell cycle regulation and apoptosis leading to malignant transformation could be caused by common genetic variants in tumor suppressor genes. The effects of the TP53 polymorphism Arg72Pro on lung cancer risk have been investigated in numerous studies with, however, conflicting results. In many studies, important risk modifiers such as smoking or tumor histology were not taken into account. We therefore investigated the combined effects of polymorphisms in TP53 (Arg72Pro) and p21/CDKN1A (Ser31Arg) and smoking on lung cancer risk. Our case-control study consisted of 405 patients with lung cancer, mainly squamous-cell carcinoma (185) and adenocarcinoma (177) and 404 unmatched tumor-free hospital controls. Multivariate regression analysis showed a moderate but statistically significant risk of lung cancer overall and especially of squamous-cell carcinoma (OR, 1.65; CI, 1.10-2.47) for TP53 72Pro allele carriers. The risk was markedly increased in heavy smokers (>20 pack-years) with squamous-cell carcinoma (OR, 2.80 in patients homozygous for 72Pro; CI, 1.19-6.58), but not in light smokers (<or=20 pack-years). The results for the p21 Ser31Arg polymorphism suggested that 31Ser is a moderate-risk allele for squamous-cell carcinoma. Analysis of the combined effects of the two polymorphisms revealed a higher OR for TP53 72Pro carriers homozygous for p21 31Ser than for 72Pro carriers in general; this effect being most pronounced in heavy smokers with squamous-cell carcinoma (OR, 3.84; CI, 1.46-10.1). Our data indicate that the TP53 Arg72Pro polymorphism increases the risk for squamous-cell carcinoma mainly in heavy smokers. The observed interaction with smoking is biologically plausible as, for the 72Pro p53 variant, decreased apoptosis and extended G1 cell cycle arrest is reported after carcinogen exposure. Nevertheless, confirmation by further molecular and epidemiological studies is warranted.

Adenocarcinoma↗

PubMed2004

Expression of adenomatous polyposis coli (APC) in tumorigenesis of human oral squamous cell carcinoma.

The product of the adenomatous polyposis coli (APC) tumor suppressor gene has been observed to regulate the Wnt signaling pathway through beta-catenin. In the present study, we attempted to clarify the relation between APC and the canceration of oral squamous epithelium. Each target tissue of normal squamous epithelium, epithelial dysplasia, and squamous cell carcinoma (SCC) was recovered the oral SCC case by laser microdissection. In recovered cells, we examined the change in expression of APC and beta-catenin gene transcription products, as well as the existence of mutations in APC gene. We analyzed the localization of each protein of APC and beta-catenin by immunohistochemical study. We found a clear change in the expression level of the gene transcription product of APC in canceration of oral squamous epithelium and the differentiation of oral SCC. In addition, there was some change in the localization of the APC protein in canceration. It was not clear, however, whether the APC was mutated. A change was also observed in the expression level of the beta-catenin gene transcription product during the differentiation of oral SCC. Our results suggest that the changes in the expression level and the intracellular localization of APC are related to the canceration of oral squamous epithelium, and in malignant characterization of oral SCC. Mutations of the APC gene might not be indispensable, however, in canceration of oral squamous epithelium.

Adenomatous Polyposis Coli Protein↗

PubMed2005

Squamous cell carcinoma of the oral cavity, maxillary antrum and lip in a Zimbabwean population: a descriptive epidemiological study.

Squamous cell carcinoma accounts for approximately 90% of oral malignancies. The objective of this study was to document the gender, age, sub-site distribution and histologic differentiation of squamous cell carcinoma of the oral cavity, maxillary antrum and lip in a Zimbabwean population. Hospital records of patients with a histologic diagnosis of squamous cell carcinoma of the oral cavity, maxillary antrum and lip seen at Harare Central Hospital and Parirenyatwa Hospital in Zimbabwe during the period January 1982-December 1991 were reviewed. 20.8% (n = 358/1723) were squamous cell carcinoma of the oral cavity, maxillary antrum and lip. Age ranged from 3 to 70years with a 2:1 male:female ratio. Peak incidence in both sexes were in the 41-50 and 51-60years age groups. Sub-site distribution was mandibular gingiva 18.4%, tongue 17.9%, floor of the mouth 16.2%, maxillary gingiva 9.2%, buccal mucosa 9.2%, maxillary antrum 12.6%, hard palate 7.8%, soft palate 4.8%, lower lip 2.8% and upper lip 1.1%. 64.8% were well differentiated, 24.8% moderately differentiated and 10.4% poorly differentiated. The mandibular gingiva, floor of the mouth and tongue were most commonly affected. Lip squamous cell carcinoma was uncommon. Well-differentiated squamous cell carcinoma was most common in the 41-60 years age group.

Adolescent↗

PubMed2006

Overexpression of p16INK4 is a reliable marker of human papillomavirus-induced oral high-grade squamous dysplasia.

OBJECTIVE: Human papillomavirus (HPV) infection has been implicated in the development of high-grade squamous dysplasia and carcinoma of the oral cavity in the absence of other known risk factors such as smoking. HPV-induced oral dysplasia or carcinoma may be a unique tumor entity in terms of biologic behavior and treatment decisions. In detecting such cases, most reported studies have used techniques that are less sensitive than DNA amplification. Recent reports have suggested that overexpression of the p16INK4 protein is a surrogate marker of HPV-induced high-grade dysplasia or carcinoma. However, the correlation between expression of p16INK4 and the presence of HPV DNA as determined by polymerase chain reaction (PCR) amplification has not been previously reported. The purpose of this research was to determine if immunohistochemistry for p16 would serve as a marker of HPV-associated high-grade oral squamous dysplasia. STUDY DESIGN: Archival formalin-fixed, paraffin-embedded tissue sections from 41 cases of high-grade oral squamous dysplasia were randomly selected. Expression of p16INK4 protein was assessed by immunohistochemical analysis (16P04 Neomarkers, Fremont, CA). Strong and diffuse nuclear staining restricted to the dysplastic region in the epithelium was scored as positive for protein expression, whereas focal or weak nuclear or cytoplasmic staining was scored as negative. The presence of HPV was determined by microdissection, DNA extraction, and PCR DNA amplification using elongated primers that align with corresponding sequences of the L1 region of 23 mucosotropic HPV genotypes. The HPV type was determined by direct sequencing of the PCR product. Normal squamous epithelium was used as an internal negative control, and cases of severe cervical high-grade squamous dysplasia were used as a positive control for immunohistochemical staining and PCR. RESULTS: The results of immunohistochemical analysis for overexpression of p16INK4 were positive in 6 of the 41 tissue sections. The results of PCR DNA amplification were also positive for these 6 sections. HPV-16 was identified in 5 of the positive cases; in the other case, the viral strain could not be determined. CONCLUSIONS: Immunohistochemical detection of p16INK4 is a technically simple and potentially reliable assay for diagnosing cases of HPV-induced oral high-grade squamous dysplasia. Detecting such lesions may influence future therapeutic decisions.

Adult↗

PubMed2002

Expression of heat shock protein 70 in grossly resected esophageal squamous cell carcinoma.

BACKGROUND: The aim of the present study was to use immunohistochemical methods to clarify the clinical implication of heat shock protein (HSP) 70 expression in esophageal squamous cell carcinoma and to investigate the function of HSP70 as a chaperone for p53. METHODS: Seventy-one patients with esophageal squamous cell carcinoma were admitted in the present study. Expression of HSP70 was analyzed by immunohistochemistry and correlated with TNM classification, vessel invasion, p53 expression, and clinical outcome after operation. RESULTS: Overexpression of HSP70 was related to sex (p < 0.05), tumor configuration (p < 0.05), lymph node metastasis (p < 0.01), and lymphatic vessel invasion (p < 0.05). Expression of p53 and HSP70 were not correlated with each other (p = 0.824). Esophageal squamous cell carcinoma with HSP70 expression exhibited a significantly better prognosis compared with HSP70-negative esophageal squamous cell carcinoma in univariate analysis (p < 0.05), but no significance was found in multivariate analysis. CONCLUSIONS: We suggest that HSP70 expression might be of use to assess the progression, lymph node metastasis, and lymphatic vessel invasion of esophageal squamous cell carcinoma. Inasmuch as both lymph node metastasis and HSP70 expression are prognostic variables in esophageal squamous cell carcinoma, examination of HSP70 expression may be of use to assess clinical outcome after operation.

Adult↗

PubMed1997

Squamous cell carcinoma arising from mature cystic teratoma of the ovary: a clinicopathologic analysis.

OBJECTIVE: There have been few studies concerning the clinical pathology of squamous cell carcinoma arising from ovarian mature cystic teratoma. Thus, the objective of this study is to determine clinicopathologic factors affecting survival in this rare tumor. METHODS: From September 1979 to June 1996, 37 patients with squamous cell carcinoma arising from ovarian mature cystic teratoma were treated by the Tokai Ovarian Tumor Study Group. A retrospective clinicopathologic and survival analysis of these patients was performed. The mode of infiltration was classified into expansive, moderately diffused, and diffused patterns. RESULTS: Although the 5-year survival rate was 94.7% and 80.0% for stage I and II patients, respectively, 12 of 13 patients with stage III died within 20 months (P = .0001). A significant difference was also observed between the survival of the groups with and without residual tumor at surgery (P = .0001). Pathologic features, grade, mode of infiltration, and vascular involvement were significant factors by univariate analysis. Multivariate analysis showed significant differences in survival related to grade (P = .0154) and mode of infiltration (P = .0053). The preoperative squamous cell carcinoma antigen level was significantly higher in the patients with squamous cell carcinoma arising from mature cystic teratoma than in patients with mature cystic teratoma (P < .0001). CONCLUSION: This study suggests that pathologic factors, grade, and mode of infiltration can provide valuable information for predicting the survival of patients with squamous cell carcinoma arising from mature cystic teratoma. In addition, squamous cell carcinoma antigen may be a useful marker to detect this disease preoperatively.

Adult↗

PubMed1985

Involucrin in intraepithelial and invasive squamous cell carcinomas of the cervix: an immunohistochemical study.

Immunohistochemical staining for involucrin, a cytoplasmic protein synthesized during squamous maturation, was assessed in histologic sections from hysterectomy and cone biopsy specimens from patients with cervical neoplasia. In normal and condylomatous squamous epithelium, diffuse cytoplasmic staining was seen in the suprabasal layers, with no staining of the basal cells. Staining was absent in two cases of cervical intraepithelial neoplasia (CIN), grade III, in which the lesions were composed entirely of undifferentiated cells and markedly decreased in cases involving large numbers of basal cells. In 19 of 23 cases (83 per cent) of CIN, however, focal staining for involucrin was seen in large differentiated cells in the more superficial layers, and in two cases of keratinized CIN diffuse suprabasal staining was observed. Similarly, strong staining for involucrin was present in differentiated areas in one case of microinvasive squamous cell carcinoma and in 93 per cent of cases of infiltrating squamous cell carcinoma. These findings suggest that involucrin is a marker for maturation in cervical squamous epithelial neoplasms. Patterns of immunohistochemical staining for involucrin in keratinized dysplasia and differentiated squamous carcinomas should be taken into consideration if loss of involucrin staining is used as a criterion for neoplastic transformation of cervical epithelium, as has been proposed.

Carcinoma, Squamous Cell↗