DigitalUM :: Browsing by Subject "Carcinoma"

Browsing by Subject "Carcinoma"

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Open Access
17p13 (p53 locus), 5q21 (APC locus) and 9p21 (p16 locus) allelic deletions are frequently found in oral exfoliative cytology cells from smoker patients with non-small-cell lung cancer
(Murcia : F. Hernández, 2007) Sanz Ortega, J.; Roig, F.; Al-Mousa, M.M.; Saez, M.C.; Muñoz, A.; Sanz Esponera, J.; Callol, L.
Molecular cytogenetic and LOH analyses of non-small cell lung cancer (NSCLC) have shown frequent allelic deletions in a variety of chromosomes where tumour suppressor genes are located. Allelic loss at 9p21 (p16 locus), 17p13 (p53) and 5q21(APC) has been frequently described in NSCLC and has also been described in premalignant epithelial lesions of the bronchus and normal bronchial cells. These findings suggest that a tissue field of somatic genetic alterations precedes the histopathological phenotypic changes of carcinoma. Similar changes have been described in oral and laryngeal epithelial tumours associated with smoke exposure. We previously reported frequent LOH at 5q21, 9p21 and TP53 in tumor cells and peritumoral normal bronchial cells from surgically resected NSCLC. We now analyze 96 cases of normal oral exfoliative cytology in which normal epithelial cells were obtained: 43 cases from smoker patients with NSCLC diagnosis, 33 smoker patients with no evidence of malignancy and 20 nonsmoker patients with no evidence of tumour. All groups had a similar age and sex distribution. PCR amplification was performed utilising the specific markers D5S346, D9S157 and TP53. In normal oral mucosae cells from patients with NSCLC, we found that 21% of the informative cases showed LOH at any of the informative cases showed LOH at 5q21, 7.7% at 9p21 and 22.2% at TP53. Within the smoker risk group only one case (4% of the informative cases) showed LOH at TP53, while no LOH was found at 5q21 or 9p21. No LOH was found in non-smokers. In conclusion, our results show that a significant number of patients with NSCLC have LOH at TP53, 5q21 and 9p21 in normal oral mucosae, while LOH at these loci is unusual in similar cells obtained from patients with no evidence of malignancy. Our study demonstrates that LOH studies can detect smoker patients with a mutated genotype in normal epithelial cells. Further prospective studies may confirm whether LOH studies can detect patients with a higher risk of NSCLC.
Open Access
3p21, 5q21, 9p21 and 17p13 allelic deletions accumulate in the dysplastic spectrum of laryngeal carcinogenesis and precede malignant transformation
(Murcia : F. Hernández, 2003) Sanz Ortega, J.; Valor, C.; Saez, M.C.; Ortega, L.; Sierra, E.; Poch, J.; Hernández, S.; Sanz-Esponera, J.
A tissue field of somatic genetic alterations precede the histopathological phenotypic changes of carcinoma. Loss of Heterozygosity (LOH) at the sites of known or putative tumor suppressor genes is a common genetic abnormality detected in precancerous conditions. These genomic changes could be of potential use in the diagnosis and prognosis of pre-malignant laryngeal lesions. Recently the concept of laryngeal intraepithelial neoplasia (LIN) was introduced. To evaluate patients with an increased risk of developing invasive laryngeal carcinoma via a dysplasia-carcinoma progression we investigated 102 microdissected cell populations. Cell populations were procured from 15 laryngectomy specimens with different peritumoral histological changes adjacent to the squamous cell carcinoma cells and 15 laryngeal endoscopic biopsies with no evidence of malignant transformation in a 6-10-year follow-up period. Histological diagnoses were subdivided into keratosis without dysplasia (KWD), with mild dysplasia (LIN 1), with moderate dysplasia (LIN 2), and with severe dysplasia or carcinoma in situ (LIN 3). Microsatellite analysis was performed with the aim of studying LOH of 5q21 (APC), 9p21 (p16), 3p21 and 17p13 (p53) chromosomal regions. Frequent allelic losses were found in carcinoma cells at p53 (54%), p16 (66%), 3p21(87%) and 5q21(58%). Identical LOH patterns were determined in 100% of the LIN3 peritumoral cells, 60% of LIN2, 50% of LIN 1 and 25% of KWD. In contrast, histologically normal mucosae, KWD and LIN1 lesions without malignant progression showed no allelic loss. These results show that dysplasia correlates with LOH at 3p21, 5q21, 9p21 and 17p13 in early laryngeal carcinogenesis. These genomic changes in pre-malignant laryngeal lesions could be of potential use as markers for cancer risk assessment.
Open Access
A review of neoplasms with MITF/MiT family translocations
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Wei, Shuanzeng; Testa, Joseph R.; Argani, Pedram
Microphthalmia-associated transcription factor (MITF/MiT) family is a group of basic helix-loophelix leucine zipper (bHLH-LZ) transcription factors including TFE3 (TFEA), TFEB, TFEC and MITF. The first described neoplasms involving MITF family translocation were renal cell carcinomas with chromosome translocations involving ASPLTFE3/t(X;17)(p11.23;q25) or MALAT1-TFEB/t(6;11) (p21.1;q12), and now it is known as MiT family translocation RCC in 2016 WHO classification. Translocations involving MITF family genes also are found in other tumor types, such as perivascular epithelioid cell neoplasm (PEComa), alveolar soft part sarcoma (ASPS), epithelioid hemangioendothelioma, ossifying fibromyxoid tumor (OFMT), and clear cell tumor with melanocytic differentiation and ACTINMITF translocation. In this review, we summarize the features of different types of neoplasms with MITF family translocations.
Open Access
Akt pathway as a target for therapeutic intervention in HNSCC
(Murcia : F. Hernández, 2008) Moral, Marta; Paramio, Jesús M.
Head and neck squamous cell carcinoma (HNSCC) is the sixth most common form of cancer worldwide. One frequent alteration found in this type of cancer is overactivation of the PI3K/PTEN/mTOR pathway, of which protein kinase B (PKB)/Akt is a central key element, controlling important cellular processes such as metabolism, cell size, proliferation and apoptosis, ultimately regulating cell growth and survival. Thus, drugs that target Akt directly or elements of the pathway are plausible candidates for cancer treatment. Accordingly, numerous clinical trials in various phases are being performed for these drugs. In this review, we discuss the tumorigenic capacity of Akt and focus on its role in HNSCC, paying special attention to the current efforts in treating this cancer in a more specific, Akttargeted way, based on its primordial role in this type of cancer.
Open Access
Apoptosis in gallbladder carcinomas and dysplasias, its relation to the expression of caspases 3,6 and 8 and apoptosis regulating proteins bcl-2, mcl-l and bax
(Murcia : F. Hernández, 2000) Turunen, N.; Paakko, P.; Solni, Y.
In this study we investigated apoptosis and the expression of caspases 3, 6 and 8 and bcl-2, mcl-l and bax in 39 gallbladder carcinomas and 7 epithelia1 dysplasias. The average apoptotic index was 0.68+0.91%. The extent of apoptosis was higher in grade 11-111 than grade I tumours or epithelial dysplasias (p=0.003). Also, tumours invading beyond serosa or into other organs (T3-T4) had a higher apoptotic index than other tumours (p=0.05). Caspase 3 expression was found in 37 (95%) and caspase 6 and 8 expression each in 30 (77%) carcinomas. Their expression associated with each other and tended to increase along with the progression of the lesions. Bcl-2 expression was found in only 4 (10%) tumours. In contrast, mcl-l positivity was found in 34 (87%) and bax positivity in all cases. The results show that apoptosis is increased along with progression of the neoplastic lesion of the gallbladder epithelium. Caspases 3,6 and 8 are strongly expressed in gallbladder carcinomas suggesting that they contribute to the increased apoptosis observed in them. Of the bcl-2 family proteins, bcl-2 was expressed infrequently suggesting that it does not play any significant role in apoptosis inhibition in gallbladder tumours.
Open Access
Bcl-2 protein in normal, hyperplastic and neoplastic breast tissues. A metabolite of the putative stem-cell subpopulation of the mammary gland
(Murcia : F. Hernández, 2004) Luna-Moré, S.; Weil, B.; Bautista, D.; Garrido, E.; Florez, P.; Martínez, C.
This investigation, though initially designed to examine the possible influence of the Bcl-2 protein on the node-metastasizing capacity of breast carcinomas, was amplified to study the expression of this antiapoptotic protein in normal breast lobules and hyperplastic lesions. We examined paraffin sections of 508 breast carcinomas, stained for Bcl-2, estrogen (ER) and progesterone receptors (PgR) and epithelial membrane antigen, and occasionally for other antigens as well. Only a few cells showing a strong Bcl-2 positivity spotted the tubulo-lobular units of normal resting glands, whereas such cells were relatively numerous in atrophic lobules, and very scarce in the terminally differentiated lactating breast. Columnar and usual types of hyperplasia were exclusively, or almost exclusively, composed of Bcl-2(+), ER(+) and PgR(+) cells. The foci of carcinoma in situ and those of invasive carcinomas were respectively 83% and 66% positive for Bcl-2 in at least 25% of their cells. Even among the invasive carcinomas, Bcl-2(+) cases included 83% and 87% of the ER(+) and PgR(+) cases, respectively (p=0.0001). Though there was a statistically significant inverse relation between Bcl-2 and tumor grade (p=0.0001), no significant association was found between Bcl-2 and lymph node stage. In conclusion, we suggest that normal, hyperplastic and neoplastic breast epithelial cells expressing the anti-apoptotic protein Bcl- 2 are immature cells that ought to form part of the stemcell subpopulation, which is committed to the development and to the maintenance of the normal gland and which gives rise to hyperplastic and neoplastic disorders when its proliferation is deregulated. In ductal proliferative changes Bcl-2 assays may be useful for diagnostic but not for prognostic purposes.
Open Access
Breast carcinoma vascularity, A comparison of manual microvessel count and Chalkley count
(Murcia : F. Hernández, 2009) Dhakal, Hari Prasad; Bassarova, A.V.; Naume, Bjørn; Synnestvedt, Marit; Borgen, Elin; Kaaresen, Rolf; Schlichting, Ellen; Wiedswang, Gro; Giercksky, Karl- Erik; Nesland, Jahn M.
. Manual counting of microvessels as intratumoral microvessel density (MVD) and Chalkley counting have been used in several studies to assess the prognostic impact of vascularity in invasive breast carcinomas. In our present study, the aim was to evaluate the prognostic value of angiogenesis in invasive breast carcinoma assessed by MVD and Chalkley techniques in the same series of patients. A total of 498 breast carcinoma patients with median follow up time 85 months were evaluated. The tumour vascularity was quantified by both manual microvessel count (MVD) and Chalkley count in CD34 stained breast carcinoma slides by a single investigator blinded to clinical information. Other relevant clinicopathological parameters were noted, including breast cancer related death and both loco-regional and systemic relapse. The patients were stratified by converting MVD and Chalkley counts to categorical variables to assess prognostic impact, and results were compared. High vascular grades using MVD count did not demonstrate any prognostic significance for breast cancer specific survival (BCSS) or distant disease free survival (DDFS) either in whole patient group (BCSS, p=0.517, DDFS, p=0.301) or in non-treated node negative patients (p>0.05). Chalkley count showed prognostic significance for both DDFS and BCSS in whole patient group (p<0.001) and also in untreated node negative patient group (p<0.05). In multivariate analysis, Chalkley count, but not MVD, retained the prognostic value for BCSS (p=0.007) and DDFS (p=0.014). The Chalkley count for assessing angiogenesis in invasive breast carcinomas demonstrated prognostic value. The Chalkley method appears to be the better method in estimating the prognostic impact of vascularity in invasive breast carcinomas.
Open Access
C-erb-B-2 oncoprotein and epidermal growth factor receptor in human hepatocellular carcinoma: An immunohistochemical study
(Murcia : F. Hernández, 1994) Nakopoulou, Lydia; Stefanaki, K.; Filaktopoulos, D.; Giannopoulou, I.
The aim of this study was to evaluate the irnmunohistochemical expression of epidermal growth factor (EGFR) and c-erb-B-2 oncoprotein in a series of 71 hepatocellular carcinomas as well as in the adjacent hepatic tissue and to assess any correlation with HBsAg expression. The total of the 71 hepatocellular carcinomas (HCCs) was classified into 17 low grade and 54 high grade cases with adjacent non-neoplastic liver parenchyma, observed in 14 and 28 cases respectively. Coexisting cirrhosis or fibrosis was noticed in the adjacent non-neoplastic parenchyma in 12 cases of low grade and 22 cases of high grade HCC. The immunohistochemical avidin-biotin-peroxidase complex (ABC) method was performed on formalin-fixed paraffin sections for the detection of EGFR, c-erb-B-2 oncoprotein and HBsAg using monoclonal antibodies. The expression of c-erb-B-2 was observed in 29.5% (21171) of the HCCs showing no statistically significant correlation with histological grade. The c-erb-B-2 was also detected in the adjacent non-neoplastic parenchyma in 7/14 low grade HCCs, and in 9/28 high grade HCCs. No statistically significant differences in c-erb-B-2 oncoprotein expression were observed between the HCCs and the adjacent non-neoplastic parenchyma. In addition, HBsAg was detected in 10142 examined cases of HCC with adjacent non-neoplastic parenchyma, while only 4 cases of HCCs were simultaneously positive for c-erb-B-2 and HBsAg. EGFR was detected in only 3171 cases of HCC, while the antigen was not detected at al1 in the adjacent non neoplastic parenchyma. HBsAg expression was not observed in any of the EGFR-positive HCCs. Our results suggest that both c-erb-B-2-oncoprotein and EGFR do not seem to be predorninantly involved in the transformation of hepatocytes to the malignant phenotype.
Open Access
Challenging diagnosis in pulmonary NUT carcinoma: A report of two cases with different histopathologic and molecular features and a novel SPECC1 :: NUTM1 gene fusion
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Xie Ling; Chen Jie; Ke Fei; Zheng YanYing; Li Hui; Biología Celular e Histología
Background. NUT carcinoma (NC), formerly known as NUT midline carcinoma, is a rare but highly aggressive cancer. It is a poorly differentiated carcinoma characterized by rearrangements of the NUTM1 (nuclear protein in Testis) gene with a member of the bromodomain-containing protein (BRD) family gene, usually BRD4. There is limited knowledge about primary pulmonary NC till now. It is probably underestimated or underdiagnosed because of its poorly differentiated character, misleading immunophenotype, and wide range of differential diagnoses. Method. We report here two cases of pulmonary NC with different clinicopathological and molecular presentations to draw attention to some atypical clinicopathologic features that can help clinicians and pathologists consider this rare entity. Results. The first case shows a nested pattern with small, uniform, blue epithelioid cells and aberrant expression of neuroendocrine markers, which has a known BRD3::NUTM1 fusion accompanied by a novel IGR (downstream ROR2)::NUTM1 fusion. The second case demonstrates solid sheets and cords of eosinophilic epithelioid-polygonal cells with a mucoid stroma and TTF1 expression, which has a novel SPECC1::NUTM1 gene fusion accompanied by TP53 and JAK1 gene oncogenic variants. Conclusion. As a result, our study contributes to expanding the variant spectrum of the NUTM1 gene. NUT carcinoma with different fusion partners seems to have unique clinicopathological characteristics, yet more cases need to accumulate experience
Open Access
Cohort migration of carcinoma cells.Differentiated colorectal carcinoma cells move as coherent cell clusters or sheets
(Murcia : F. Hernández, 1999) Nabeshima, K.; Inoue, T.; Shimao, Y.; Kataoka, H.; Koono, M.
Active migration of tumor cells is usually assessed as single cell locomotion in vitro using Royden chamber-type assays. In vivo, however, carcinoma cells, malignant cells of epithelial origin, frequently invade the surrounding tissue as coherent clusters or nests of cells. We have called this type of movement "cohort migration". In our work, the invasion front of colon carcinomas consisted of compact tumor glands, partially resolved glands or markedly resolved glands with scattered tumor cell clusters or single cells lying ahead. In the former two types, which constituted about a half of all cases, cohort migration seems to be the predominant mechanism, whereas both cohort migration and single cell locomotion may be involved in the last one. In this light, it is very advantageous to investigate the mechanisms involved in the cohort migration. In this review, we present a two-dimensional motility assay as a cohort migration model, in which human colorectal carcinoma cells move outwards from the cell islands mainly as localized coherent sheets of cells when stimulated with 12-0-tetradecanoylphorbol- 13-acetate (TPA) or hepatocyte growth factorlscatter factor (HGFISF). Within the migrating cell sheets, wide intercellular gaps occur at the lower portion of the cells to allow the cells to extend leading lamellae forward while close cell-cell contacts remain at the upper portion of the cells. This localized modulation of cell-cell adhesion at the lower portion of the cells is associated with increased tyrosine phosphorylation of the Ecadherin- catenin complex in TPA-induced cohort migration and with reduced a-catenin complexed with E-cadherin in HGFISF-induced cohort migration. Furthermore, fibronectin deposited by migrating cells is essential for their movement, and on the gelatin-coated substrate even degradation and remodeling of the substrate by matrix metalloproteinases are also needed. Thus, in cohort migration it is likely that cells are released from cell-cell adhesion only at the lower portion Offprint requests to: Dr. Kazuki Nabeshima, Department of Pathology, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan. e-mail: KAZNABES@post.miyazaki-med.ac.jp Histology and Histopathology of the cells via modulation of E-cadherin-catenin-based mechanism, and this change allows the cells to extend leading lamellae onto the extracellular matrix substrate remodeled by deposition of fibronectin and organized digestion.
Open Access
Concordance of lymphovascular invasion diagnosed in penile carcinoma with and without the immunohistochemical markers ERG and CD31
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Feng, Megan A.; Ebe, Joshua J.; Shabsigh, Ahmad; Zynger, Debra L.
Lymphovascular invasion (LVI) is an independent predictor of metastatic lymph node disease in penile carcinoma and is one factor used to guide clinical management. The presence of LVI with and without the use of the endothelial immunohistochemical (IHC) markers, ERG and CD31, was retrospectively assessed in 46 penectomy cases containing invasive penile carcinoma (43 squamous cell carcinoma and 3 non-squamous cell carcinoma). Concordance for the detection of LVI between the original report, upon pathology review, and with the use of IHC was determined and histologic pitfalls were identified. For penile squamous cell carcinoma, LVI was diagnosed in 27.9% of tumors in the original reports, 16.3% upon pathology review, and in 16.3% with use of ERG and CD31. Concordance of LVI identification in the original report compared to IHC was 74.4% while concordance of review compared to IHC was 95.3%. Using IHC data as the reference, false positive LVI diagnoses were more common in the original report than false negatives. Histologic mimickers of LVI including involvement of the penile corpora cavernosum or spongiosum vasculature, seromucinous colonization, and a nested pattern of tumor invasion were identified. We demonstrated that it was not uncommon for LVI in penile carcinoma to be overdiagnosed or underdiagnosed. The use of endothelial IHC markers, such as ERG or CD31, or additional pathology consultation is recommended for penectomy cases in which LVI is difficult to histologically discern.
Open Access
Crumbs3: Expression and biological significance in normal and neoplastic tissues
(2026) Akane Kitta-Kunihiro; Chiemi Ikude; Eisaku Kondo; Hidekazu Iioka; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e Histiologia
Cellular polarity plays a fundamental role in tissue organization and homeostasis, and its disruption is closely linked to tumorigenesis. Crumbs3 (CRB3), a conserved polarity protein, is essential for epithelial morphogenesis, tight-junction formation, and barrier function. This review summarizes current knowledge regarding CRB3 expression in normal and malignant human tissues and its dual roles in cancer progression. Systematic immunohistochemical analyses revealed strong CRB3 expression in non-neoplastic glandular epithelia of the gastrointestinal, hepato-pancreato-biliary, renal, and respiratory tracts, as well as in fetal tissues, suggesting its importance in organ development and maintenance. In neoplastic tissues, represented by colorectal adenocarcinoma and oral squamous cell carcinoma, CRB3 expression is preserved or even enhanced compared with normal tissues, which promotes tumor cell migration, triggering invasion/ metastasis as well as cellular proliferation through signaling pathways involving FGFR and RhoA activation. Conversely, previous studies reported that CRB3 functions as a tumor suppressor, based on findings that CRB3 expression induces loss of epithelial mesenchymal transition, whereas loss of CRB3 expression attenuates the integrity of tight junctions, resulting in significantly poorer prognosis in certain cancers. Current data thus suggest that the biological role of CRB3 in tumors is complex. Whether CRB3 acts as a tumor accelerator or suppressor may depend on the individual-specific, unique characteristics of tumor cells. Understanding these dual functions may contribute to the development of novel polarity-targeted therapeutic strategies for cancers of differing origin.
Open Access
Expression of checkpoint kinase 2 in breast carcinomas, correlation with key regulators of tumor cell proliferation, angiogenesis, and survival
(Murcia : F. Hernández, 2006) Ribeiro-Silva, A.; Koyota Moutinho, M.A.; Becker de Moura, H.; Ribeiro do Vale, F.; Zucoloto, S.
Checkpoint kinase 2 (Chk2) is a cell-cyclecheckpoint kinase that may act as a tumor suppressor gene due to its important role in DNA damage signaling and cell cycle regulation. The role of Chk2 expression in mammary tumorigenesis, however, is still poorly understood. This study was designed to assess the relationship between the expression of Chk2 and wellestablished prognostic factors, including disease-freesurvival and overall survival; and several regulators of cell proliferation and invasiveness in breast carcinomas, including oncogenes, tumor suppressor genes, apoptosisrelated proteins, and angiogenesis-related markers. Immunohistochemistry with 27 primary antibodies was performed in 100 formalin-fixed paraffin-embedded samples of not otherwise specified invasive ductal carcinomas. Clinical data were retrieved from medical files. In normal mammary parenchyma adjacent to the tumors Chk2 stained the nuclei of epithelial cells. Downexpression of Chk2 protein was observed in 23 carcinomas and correlated with advanced disease. Among the regulators of tumor cell proliferation and invasiveness analyzed, the downexpression of Chk2 correlated only with reduced expression of p27 and telomerase. There was no difference between the overall survival and disease-free survival rates according to Chk2 status. In conclusion, Chk2 correlated with reduced expression of h-TERT and p27, but not with angiogenic factors. Chk2 expression also did not interfere in the outcome of the patients.
Open Access
Expression of MAL and MAL2, two elements of the protein machinery for raft-mediated transport, in normal and neoplastic human tissue
(Murcia : F. Hernández, 2004) Marazuela, M.; Alonso, M. A.
Polarized transport of lipids and proteins to the apical and basolateral membrane subdomains is essential for the functioning of epithelial cells. Apical transport is mediated by a direct route from the Golgi and an indirect route, referred to as transcytosis, involving the transport of the protein to the basolateral membrane followed by its internalization and subsequent transcellular transport to the apical subdomain. MAL and MAL2 have been demonstrated to be essential components of the machinery for the direct and indirect routes, respectively. Herein, we review the range of expression of MAL and MAL2 in normal human tissue and compare it with that of neoplastic tissue. Our analysis provides insight into the potential use of MALand MAL2-mediated pathways in many types of epithelial cells as well as in nonepithelial cells. In addition, the specific alterations in MAL and/or MAL2 expression observed in specific types of carcinoma provides a basis to understand the loss of the polarized phenotype that frequently accompanies the neoplastic transformation process. This points out potential applications of MAL and MAL2 as markers for tumor characterization.
Open Access
Expression of vascular endothelial growth factor (VEGF) and association with microvessel density in small-cell and non-small-cell lung carcinomas
(Murcia : F. Hernández, 2004) Stefanou, D.; Batistatou, Anna; Arkoumani, E.; Ntzani, E.; Agnantis, N.J.
Recent studies have demonstrated that tumor angiogenesis is a prognostic factor for various malignant neoplasms. Specifically, in non-small-cell lung carcinomas (NSCLCs) most reports show an association between neovascularization and vascular endothelial growth factor (VEGF) expression as well as the presence of metastases and survival, although a few reports do not agree with these findings. Angiogenesis is not clearly characterized in small-cell lung carcinomas (SCLCs), since they are rarely treated by surgery, and thus the available tissue for biological characterization is sparse. The aim of the present study was to investigate angiogenesis and the expression of VEGF in lung tumors. We examined 88 non-small-cell and 39 smallcell lung carcinomas. Angiogenesis was estimated by determining microvessel counts, with the use of anti- CD31 and anti-factor VIII antibodies and expression of VEGF was also evaluated immunohistochemically. Our data showed that in NSCLCs angiogenesis was more prominent in poorly-differentiated neoplasms and correlated with VEGF expression, therefore it is at least in part mediated by the latter. Interestingly, in SCLCs a higher vascularization was noted. However, there was no strong association with VEGF expression. Thus, smallcell lung carcinoma may represent a suitable neoplasm for testing antiangiogenic drugs in combination with chemotherapy. Nevertheless, antiangiogenic therapy should not be targeted specifically to the VEGF pathway, since in SCLCs other mediators of angiogenesis may be important as well.
Open Access
Fascin in ovarian epithelial tumors
(Murcia : F. Hernández, 2008) Kostopoulou, Evanthia; Daponte, Alexandros; Terzis, Anastasios; Nakou, María; Chiotoglou, Ioanna; Theodosiou, Dimitrios; Chatzichristodoulou, Christos; Messinis, Ioannis E.; Koukoulis, George
Fascin contributes to the formation of actinbased protrusions involved in cell migration. Fascin has emerged as a prognostic marker in some carcinomas. We examined ovarian neoplasms to check any correlation between fascin expression and established clinicopathologic parameters. Fascin immunoreactivity was semiquantitavely scored in 100 ovarian tumors (62 carcinomas, 15 borderline tumors and 23 cystadenomas). Double staining for fascin and Ki-67 was performed in selected carcinomas. Western Blotting was done in frozen samples. Fascin immunoreactivity was highest in carcinomas, lowest in cystadenomas and intermediate in borderline tumors; these results were in accordance with those from Western blotting analysis. Fascin was statistically increased in carcinomas of advanced stage and in serous carcinomas. It was also increased in metastatic foci and in tumor foci with lower Ki-67 labeling. We conclude that in ovarian tumors fascin is associated with certain features of increased tumor aggressiveness. Future studies could determine if fascin may become a routinely helpful marker in gynecological pathology or clinical oncology.
Open Access
Frequent expression of neuroendocrine markers in mucinous tubular and spindle cell carcinoma of the kidney
(Murcia : F. Hernández, 2006) Kuroda, Naoto; Hes, O.; Miyazaki, E.; Shuin, T.; Enzan, H.
Mucinous tubular and spindle cell carcinoma (MTSCC) is a new tumorous entity which has been recently established. In this article, we examined the expression of neuroendocrine markers including neuron specific enolase (NSE), chromogranin A and synaptophysin in 16 cases of MTSCC using immunohistochemistry. The sex ratio (male: female) of the patients was 4:12. In normal kidney, distal tubules or collecting ducts were positive for NSE, but no structures were positive for chromogranin A or synaptophysin. All MTSCCs showed a positive reaction for NSE. Additionally, fifteen of sixteen neoplasms (93.8%) with MTSCC showed the expression of either chromogranin A or synaptophysin or both. Finally, it is possible that MTSCC may be one of renal neoplasms which frequently exhibit the neuroendocrine differentiation
Open Access
Galectin-7, will the lectinrsquos activity establish clinical correlations in head and neck squamous cell and basal cell carcinomas?
(Murcia : F. Hernández, 2009) Câda, Z.; Chovanec, M.; Smetana, K. Jr.; Betka, J.; Lacina, L.; Plzák, J.; Kodet, R.; Stork, J.; Lensch, M.; Kaltner, H.; André, S.; Gabius, H.J.
The human lectin galectin-7 (Gal-7; p53- induced gene-1) has anti- and pro-malignant features in different in vitro models. We tried to clarify relation of its expression to cellular and clinical parameters in head and neck squamous and basal cell carcinomas. Using a non-cross-reactive antibody, immunohistochemical staining in squamous cell epithelia (epidermis, epithelium of oropharynx and larynx) (n = 57), squamous cell carcinomas (n = 47) and lymph node metastases (n = 25), as well as basal cell carcinomas (n = 10) were studied. This monitoring was flanked by processing to assess the level of differentiation (cytokeratins 10 and 14), proliferation (Ki67) and basal lamina formation (collagen IV). The results were correlated with clinical and pathological findings (grading, TNM-staging, extracapsular spread, angio- and lymphangioinvasion, perineural invasion, recurrence and survival). Gal-7 resides in all layers of epithelia with cytoplasmic and nuclear localization in normal specimens. Basal cell carcinomas were devoid of the Gal-7 respective signal. Squamous cell carcinomas were positive, presenting different staining profiles. Intense staining was predominantly found in squamous cell cancers with high degrees of differentiation and keratinization. Fittingly, poor level of differentiation (P = 0.0009), absence of keratinization (P = 0.0105) and significant discontinuity or absence of collagen IV expression in the peritumoral basal lamina (P = 0.0024). was found in Gal-7-negative tumors. Gal-7 presence was not related to gender, primary tumor site, T-stage, Nstage, clinical stage, extracapsular spread, angio- and lymphangioinvasion, perineural spread or treatment outcome at a statistically significant level. Immunohistochemical analysis revealed a positive correlation for differentiation and keratinization to Gal-7 presence in squamous cell carcinomas. Absence of Gal-7 expression was detected in basal cell carcinomas. These clinical data delineate Gal-7 influence on differentiation in vivo, without evidence for a role in dissemination reported for lymphoma.
Open Access
Grading of the prostate carcinoma, cyto-histological correlations on 100 cases
(Murcia : F. Hernández, 1986) Dalla Palma, P.; Dante, S.; Costantin, G; Rebuffi, A.; Zattoni, F.; Plazza, R.
From January 1980 to December 1983, 154 patients underwent prostatic FNAB and histological control. The sensitivity of cytology was 85070, the specificity 68% and the predictive value of positive cases 83%. The cyto-histological correlation of the grading of the 100 prostatic carcinomas histologically confirmed (85 cytologically positive for carcinoma and 15 negative or uncertain) showed a predictive value of positive results of 58%, ranging from 42% for G3, 50% for G1 and 69% for G2. The usefulness of cytological grading is stressed to monitor the follow-up of those patients treated for prostatic carcinoma who, because of the advanced stage or age, were not surgically treated. Key words: Prostate cancer - FNAB - Cytohistological grading correlation
Open Access
High prevalence of human papillomavirus 16 in penile carcinoma
(Murcia : F. Hernández, 2007) Pascual, A.; Pariente, M.; Godínez, J.M.; Sánchez-Prieto, R.; Atienzar, M.; Segura, M.; Poblet Martínez, Enrique
f Human Papillomavirus (HPV) in penile carcinoma, we studied 49 patients with penile carcinoma. Formalin-fixed, paraffin-embedded tissue samples were collected from 64 samples of penile carcinoma from the Hospital General Universitario (Albacete, Spain). Cases were histologically classified and the polymerase chain reaction (PCR) method was used to detect the presence of HPV. Two sets of consensus primers were used, the My09/My11, and the GP5+/GP6+. All positive cases were sequenced in order to establish the implicated genotype. Our results showed that 38 of the 49 cases were positive for HPV (77,5%). HPV16 appeared in 32 (84,2 %) of the 38 positive cases and HPV18 in 4 (10,5%). Our data demonstrate that the My09/My11 primers are more sensitive than GP5+/GP6+ primers, although the combination of the two sets of primers notably increased the total number of HPV positive cases detected.