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E Sivridis

Publications and source records attributed to E Sivridis.

At least 37 records · Page 2Linked to original sources
PubMed2002

Thymidine phosphorylase expression in normal, hyperplastic and neoplastic prostates: correlation with tumour associated macrophages, infiltrating lymphocytes, and angiogenesis.

Thymidine phosphorylase is an angiogenic factor primarily expressed by cancer cells, stromal cells and tumour-associated macrophages in many human malignancies. These different types of thymidine phosphorylase-expressing cells, however, may have a distinct place in the angiogenic process, and this question was addressed in the present study. A series of 20 normal/hyperplastic prostate glands and 60 prostate carcinomas was investigated by immunohistochemistry, using specific antibodies for thymidine phosphorylase (P-GF.44C), tumour-associated macrophages (CD68), endothelium (CD31) and prostate specific antigen (ER-PR8). Thymidine phosphorylase expression by normal and hyperplastic epithelial or stromal cells occurred almost exclusively in the context of an intense lymphocytic infiltrate. High thymidine phosphorylase cancer cells and thymidine phosphorylase stromal cells expression was associated with high angiogenesis in prostate carcinomas, and this significant association was extended to include both tumour-associated macrophages and tumour-infiltrating lymphocytes. Thymidine phosphorylase expression and tumour-infiltrating lymphocytes were related inversely with prostate specific antigen reactivity. In conclusion, thymidine phosphorylase is a major angiogenic factor in prostate carcinomas and its up-regulation is likely to occur in the context of a host immune response.

Cell Transformation, Neoplastic↗
PubMed2002

The significance of rapid intraoperative cytology in the evaluation of intraperitoneal and retroperitoneal spread of cervical cancer.

OBJECTIVE: To evaluate the contribution of the rapid intraoperative cytology (peritoneal washing [PW] cytology together with imprint cytology performed on lymph node samples) in the assessment of peritoneal and retroperitoneal dissemination of cervical cancer. METHODS: Seventy-nine patients with clinical Stage IA2-IIA cervical cancer underwent PW cytology and imprint cytology performed on retroperitoneal lymph node samples during primary surgical treatment. Cytologic specimens were stained with the May-Grünwald-Giemsa (MGG) and hematoxylin-eosin (HE) techniques. Pertinent histologic sections of the cervical lesions, of the cell blocks prepared from PW sediments, and of the lymph node sampling were studied and compared with the cytologic findings. RESULTS: PW cytology was positive in 2.5% of the patients, and lymph node imprints revealed metastases in 19% of the patients. Cervical adenocarcinomas presented increased rates of metastatic disease in both the peritoneal cavity and retroperitoneum. HE presented higher sensitivity in detecting malignant cells in the peritoneal fluids, while MGG gave more accurate results in the diagnosis of lymph node metastases. CONCLUSIONS: Cytologic evaluation of intraperitoneal and retroperitoneal spread of cervical cancer by use of PW cytology and imprint cytology performed on lymph node samples contributes to the assessment of the extent of disease and therefore could be useful in further treatment of the patient.

Adenocarcinoma↗
PubMed2002

Immunopathological prognostic and predictive factors in prostate cancer.

Prostate cancer is the leading male malignancy in the Western world. Patients with prostate cancer have an unpredictable clinical course, as three biologically different types of tumor exist. This review summarises some of the recent progress made in understanding the biology of prostate cancer with special reference to the prognostic and predictive role of immunohistochemical markers. The prognostic value of established prognostic variables is also discussed.

Humans↗
PubMed2002

Patterns of episialin/MUC1 expression in endometrial carcinomas and prognostic relevance.

AIMS: To investigate episialin/MUC1 expression in the normal, hyperplastic and neoplastic endometrium, and relate patterns of tumour MUC1 reactivity with histopathological characteristics, oestrogen and progesterone receptor (ER and PR) status, bcl-2 and p53 oncoproteins and with clinical behaviour. METHODS AND RESULTS: We studied 42 normally cycling endometria, 45 endometrial hyperplasias of various forms, and 111 endometrial carcinomas of endometrioid and non-endometrioid cell types with specific monoclonal antibodies employing standard immunohistochemical techniques. The follow-up period ranged from 34 to 182 months with a median of 86 months. Epithelial mucin episialin/MUC1 was consistently expressed in the normal endometrium, following a cyclical pattern: "apical membrane staining" in early and mid-proliferative endometrium; "purely cytoplasmic staining" in late proliferative endometrium; and "cytoplasmic staining with intraluminal secretions" in secretory endometrium. Immunostaining patterns in simple and complex hyperplasia were similar to late proliferative endometrium, while atypical hyperplasias and endometrial carcinomas either simulated patterns of proliferative endometrium or lacked MUC1 reactivity. Membranous MUC1 positivity was statistically more frequent in endometrioid carcinomas compared with carcinomas of non-endometrioid type (P = 0.006). Cytoplasmic MUC1 positivity was significantly associated with poor prognosis, while MUC1-negative carcinomas were associated with PR expression and an improved survival (P=0.04). There was no association of MUC1 patterns with bcl-2 and p53 immunoreactivity or with other histopathological variables. CONCLUSIONS: Episialin/MUC1 is an integral component of the normal premenopausal endometrium and is probably hormonally regulated. It is frequently expressed in endometrial hyperplasias and carcinomas. The loss of MUC1 expression from endometrial carcinomas is associated with a favourable prognosis.

Adenocarcinoma↗
PubMed2002

Spontaneous pneumothorax resulting from congenital cystic adenomatoid malformation in a pre-term infant: case report and literature review.

In the literature there are only three reported cases of spontaneous pneumothorax resulting from congenital cystic adenomatoid malformation in children under 1 year and for whom any resuscitative efforts were made. We present here a fourth case of a pre-term baby girl who was in perfect health, until she suffered a spontaneous pneumothorax as the initial manifestation of congenital cystic adenomatoid malformation of the lung at 10 weeks of age. Atypical segmentectomy with the use of stapling devices was successful. The characteristics of this particular manifestation are discussed.

Cystic Adenomatoid Malformation of Lung, Congenita↗
PubMed2002

Prognostic role of angiogenesis in operable carcinoma of the gallbladder.

The prognostic significance of intratumoral angiogenesis was investigated in 62 patients with stage I-III carcinomas of the gallbladder treated with simple cholecystectomy. Microvessel density (MVD) was assessed immunohistochemically, using the alkaline phosphatase/anti-alkaline phosphatase method and the monoclonal antibody CD31. The mean MVD was 30.5 vessels per x 200 optical field. Using the thirty-third and the sixty-sixth percentile, the patients were grouped into three MVD categories: low (MVD 9-18; 20 patients), medium (MVD 19-31; 20 patients), and high (MVD 32-86; 22 patients). A high MVD was more frequent in well-differentiated adenocarcinomas compared with moderately and poorly differentiated tumors (p = 0.04), but there was no statistically significant association between MVD and T stage, or patients' age or sex. Multivariate analysis, including MVD, T stage, and histologic grade, showed that MVD was a significant independent prognostic factor in carcinomas of the gallbladder (p = 0.001, t ratio 3.3). It is believed that the assessment of intratumoral angiogenesis in patients with operable gallbladder carcinomas may be useful in predicting prognosis and, perhaps, in decision making for postoperative adjuvant treatment.

Adult↗
PubMed2002

Malignant haemangiopericytoma of the knee joint: MR findings.

The imaging findings of intra-articular haemangiopericytomas have not been described previously. We report on a 35-year-old man with a primary malignant haemangiopericytoma of the left knee joint. MRI demonstrated joint effusion and a heterogeneous mass with haemorrhagic components and multiple peripheral serpentine signal voids, suggesting the presence of vascular channels. Multiple pulmonary metastases were seen on chest CT. These imaging findings, although not pathognomonic, might be useful in suggesting the diagnosis of intra-articular haemangiopericytoma.

Adult↗
PubMed2002

Sirenomelia in uneventful pregnancy.

A rare case of sirenomelia at 38 weeks of gestation is reported. Fusion of the lower extremities and incomplete development of the bony pelvis was associated with agenesis of the urinary and genital systems, anorectal atresia and a single large umbilical artery. There was complete situs inversus of the single lower limb. This was composed of two partially fused femurs, a common tibia without fibula, and a rudimentary foot having three metatarsal bones and their corresponding toes. The present case was also interesting for its association with hypoplasia of the lungs. The pathogenesis of sirenomelia is discussed.

Abnormalities, Multiple↗
PubMed2001

The angiogenic "vascular endothelial growth factor/flk-1(KDR) receptor" pathway in patients with endometrial carcinoma: prognostic and therapeutic implications.

BACKGROUND: Vascular endothelial growth factor (VEGF) is an important endothelial cell mitogen associated with increased angiogenesis and aggressive tumor behavior. Its stimulating effect on endothelial cells basically is dependent on the presence of specific VEGF receptors, such as the flk-1(KDR) receptor. This study investigates the roles of VEGF and of a functionally intact angiogenic pathway, "VEGF/flk-1(KDR)," in patients with endometrial carcinoma and their significance in prognosis and therapy. METHODS: A series of 121 endometrial carcinomas were studied. The expression of VEGF by endometrial tumor cells was assessed using the monoclonal antibody (MoAb) VG1. VEGF/KDR complexes on tumor endothelium or activated microvessel density (aMVD) were identified using the MoAb 11B5. In addition, the standard microvessel density (sMVD) was assessed with anti-CD31. In all tumors, the alkaline phosphatase/antialkaline phosphatase technique was employed. A Fisher exact test or an unpaired, two-tailed t test was used for testing correlations between categoric tumor variables, whereas a log-rank test was used to determine statistical differences between life tables. A Cox proportional hazards model was used to assess the effect of tumor variables on overall survival. RESULTS: Cytoplasmic VEGF expression in > 50% of tumor cells was associated significantly with aMVD (P < 0.0001) and with sMVD (P < 0.003). In univariate survival analysis, VEGF (P = 0.0002), aMVD (P = 0.001), and sMVD (P = 0.0009) were significant prognostic variables. Equally important were the histologic parameters tumor type (P = 0.03), tumor grade (P = 0.003), and disease stage (P < 0.0001). In multivariate analysis, disease stage was the most important independent prognostic factor (P < 0.0001), followed by VEGF/KDR (P < 0.01), and VEGF (P < 0.04). Furthermore, VEGF and VEGF/KDR were the only independent prognostic variables for patients with Stage I endometrioid adenocarcinoma. CONCLUSIONS: sMVD and the angiogenic factor VEGF are important indicators of a poor prognosis in patients with endometrial carcinoma. VEGF/KDR complexes define a subgroup of patients with endometrial carcinoma with an even worse prognosis.

Adult↗
PubMed2001

Expression of hypoxia-inducible carbonic anhydrase-9 relates to angiogenic pathways and independently to poor outcome in non-small cell lung cancer.

Carbonic anhydrase-9 (CA9), a transmembrane enzyme with an extracellular active site, is involved in the reversible metabolism of the carbon dioxide to carbonic acid. Up-regulation of CA by hypoxia and the hypoxia-inducible factor (HIF) pathway has been recently postulated (Wykoff et al. Cancer Res., 60: 7075-7083, 2000). In the present study we examined the expression of this enzyme in non-small cell lung cancer. Of 107 cases analyzed, 39 (36.4%) had strong membrane/cytoplasmic expression of CA9 and were grouped as positive. The staining was confined around areas of necrosis, and a significant association of CA9 expression with the extent of necrosis was noted (P = 0.004). Nevertheless, 38 of 74 cases with focal or extensive necrosis did not express CA9. CA9 expression was more frequent in the squamous cell histology (P = 0.001) and with advanced T stage (P = 0.009). A significant coexpression of CA9 with platelet-derived endothelial cell growth factor and basic fibroblast growth factor receptor expression was noted. Double staining of CA9 with anti-CD31 monoclonal antibody revealed an overall higher microvessel density in the areas expressing CA9 than in negative areas (P = 0.0005). Thirty-one of 38 CA9-positive cases were positive for HIF1a/HIF2a, but HIF positivity was a more common event (68 of 107) and their patterns of expression were diffuse (not confined in the necrotic areas). A direct association of CA9 expression with epidermal growth factor receptor, c-erbB-2, and MUC1 expression was also noted (P < 0.04). Survival analysis showed that CA9 expression is related to poor prognosis. CA9 expression in tumors with low vascularization defined a prognosis similar to the one of patients with highly angiogenic tumors. Multivariate analysis revealed that CA9 expression is a significant prognostic factor independent of angiogenesis. We conclude that CA9 is an important molecule in non-small cell lung cancer, the up-regulation of which occurs in highly hypoxic/necrotic regions of the tumors. The expression of CA9 is linked to the expression of a constellation of proteins involved in angiogenesis, apoptosis inhibition, and cell-cell adhesion disruption, which explains the strong association of CA9 with poor outcome.

Adenocarcinoma↗
PubMed2001

Relation of hypoxia inducible factor 1 alpha and 2 alpha in operable non-small cell lung cancer to angiogenic/molecular profile of tumours and survival.

Hypoxia inducible factors HIF1alpha and HIF2alpha are important proteins involved in the regulation of the transcription of a variety of genes related to erythropoiesis, glycolysis and angiogenesis. Hypoxic stimulation results in rapid increase of the HIF1alpha and 2alpha protein levels, as a consequence of a redox-sensitive stabilization. The HIFalphas enter the nucleus, heterodimerize with the HIF1beta protein, and bind to DNA at the hypoxia response elements (HREs) of target genes. In this study we evaluated the immunohistochemical expression of these proteins in 108 tissue samples from non-small-cell lung cancer (NSCLC) and in normal lung tissues. Both proteins showed a mixed cytoplasmic/nuclear pattern of expression in cancer cells, tumoural vessels and tumour-infiltrating macrophages, as well as in areas of metaplasia, while normal lung components showed negative or very weak cytoplasmic staining. Positive HIF1alpha and HIF2alpha expression was noted in 68/108 (62%) and in 54/108 (50%) of cases respectively. Correlation analysis of HIF2alpha expression with HIF1alpha expression showed a significant association (P< 0.0001, r = 0.44). A strong association of the expression of both proteins with the angiogenic factors VEGF (P< 0.004), PD-ECGF (P< 0.003) and bFGF (P< 0.04) was noted. HIF1alpha correlated with the expression of bek-bFGF receptor expression (P = 0.01), while HIF2alpha was associated with intense VEGF/KDR-activated vascularization (P = 0.002). HIF2alpha protein was less frequently expressed in cases with a medium microvessel density (MVD); a high rate of expression was noted in cases with both low and high MVD (P = 0.006). Analysis of overall survival showed that HIF2alpha expression was related to poor outcome (P = 0.008), even in the group of patients with low MVD (P = 0.009). HIF1alpha expression was marginally associated with poor prognosis (P = 0.08). In multivariate analysis HIF2alpha expression was an independent prognostic indicator (P = 0.006, t-ratio 2.7). We conclude that HIF1alpha and HIF2alpha overexpression is a common event in NSCLC, which is related to the up-regulation of various angiogenic factors and with poor prognosis. Targeting the HIF pathway may prove of importance in the treatment of NSCLC.

Adenocarcinoma↗
PubMed2001

Nuclear expression of human apurinic/apyrimidinic endonuclease (HAP1/Ref-1) in head-and-neck cancer is associated with resistance to chemoradiotherapy and poor outcome.

PURPOSE: HAP1/Ref-1 endonuclease is involved in the repair of DNA strand breaks and in the activation of DNA binding of several transcription factors. HAP1 is also a potent activator of wild type p53. It therefore has multiple possible roles in the response of human cancer to radiotherapy and chemotherapy. METHODS AND MATERIALS: The nuclear expression of HAP1 and p53 proteins was studied by immunohistochemistry in paraffin-embedded material from 95 patients with locally advanced squamous cell head-and-neck cancer (HNC) treated with radical radiotherapy (38 cases with induction platinum-based chemotherapy and 57 with concurrent platinum chemoradiotherapy). RESULTS: HAP1 was present in the nuclei of normal epithelium and stromal cells. Loss of HAP1 nuclear expression was frequently noted in cancer cells. Tumors with high HAP1 nuclear expression (% of positive cells > mean; mean = 11%) were of good differentiation (p = 0.06) and presented frequently with advanced nodal disease (p = 0.01). High nuclear HAP1 expression was significantly associated with poor complete response rate (p = 0.00001), shorter local relapse-free interval (p < 0.0001), and poorer survival (p < 0.0008). HAP1 nuclear reactivity was inversely associated with p53 nuclear accumulation (p = 0.003). The inverse correlation between HAP1 expression and prognosis was independent of p53 status. CONCLUSION: HAP1 nuclear expression in HNC is inversely associated with p53 nuclear accumulation and directly related to resistance to chemoradiotherapy and poor survival. Further clinical investigation is required to confirm these findings.

Carbon-Oxygen Lyases↗
PubMed2001

The angiogenic pathway "vascular endothelial growth factor/flk-1(KDR)-receptor" in rheumatoid arthritis and osteoarthritis.

Active angiogenesis, together with an up-regulation of angiogenic factors, is evident in the synovium of both rheumatoid arthritis (RA) and osteoarthritis (OA). The present study assessed, by immunohistochemistry, the microvessel density in the synovium of these arthritides and in normal controls, in relation to the expression of the angiogenic factors vascular endothelial growth factor (VEGF) and platelet-derived endothelial cell growth factor (PD-ECGF) and the apoptosis-related proteins bcl-2 and p53. More importantly, using the novel 11B5 MAb, the activated "VEGF/flk-1(KDR)-receptor" microvessel density was assessed. VEGF expression in fibroblasts was diffuse in both RA and OA. Diffuse PD-ECGF expression of fibroblasts was noted in all cases of RA, while fibroblast reactivity was focal in the OA material. The standard microvessel density (sMVD), as assessed with the anti-CD31 monoclonal antibody (MAb), was higher in RA (64+/-12) and in OA (65+/-16) than in normal tissues (52+/-8; p=0.008 and 0.0004, respectively). The activated microvessel density (aMVD), assessed with the 11B5 MAb, was significantly higher in RA (29+/-10) than in OA (17+/-4; p<0.0001) and than in normal tissues (14+/-2; p<0.0001). The "activation ratio" (aMVD/sMVD) was statistically higher in RA (0.46+/-0.17) than in OA and normal synovial tissues, the latter two having a similar ratio (0.28+/-0.08 and 0.26+/-0.03, respectively). Cytoplasmic bcl-2 expression was frequent in the synovial cells of OA, but rare in RA. Nuclear p53 protein accumulation was never observed. It is suggested that the angiogenic pathway VEGF/flk-1(KDR) may play an important role in the pathogenesis of RA and OA. Thus, failure of VEGF/flk-1(KDR) activation, in the presence of increased VEGF expression, may indicate a synovium with an impaired capacity to establish a viable vasculature, consistent with the degenerative nature of OA. On the other hand, the activated angiogenesis in RA shows a functional, still pathologically up-regulated VEGF/flk-1(KDR) pathway. Whether restoration of an impaired VEGF/flk-1(KDR) pathway in OA, or inhibition of this in RA, would prove of therapeutic importance requires further investigation.

Adult↗
PubMed2001

Endometrial carcinoma: association of steroid hormone receptor expression with low angiogenesis and bcl-2 expression.

In endometrial tissues, malignant change may be accompanied by a loss of hormone dependence which is, usually, reflected in a parallel loss of oestrogen and progesterone receptors (ER and PR). In this study, the steroid receptor status of 164 endometrial carcinomas was related to intratumoural angiogenesis and the apoptotic proteins bcl-2 and p53. Relationships to conventional histopathological features and patient survival were also sought. Immunohistochemistry was performed on formalin-fixed, paraffin-embedded tissues. The mean follow-up was 55 months (range 19-167 months). Specific nuclear staining for ER and PR was detected in 35% and 32% of endometrial carcinomas, respectively, and was very commonly co-expressed (P<0.0001). The failure of demonstrating a steroid receptor complement in endometrial neoplasms was, in general terms, an adverse prognostic sign. Thus, ER or PR loss was significantly associated with non-endometrioid carcinomas (ER P=0.01; PR P=0.004) and with deep myometrial invasion (ER P<0.0002), high intratumoural angiogenesis (PR P<0.01) and the absence of bcl-2 expression (PR P<0.005). There was a trend for patients with ER or simultaneous ER/PR expression to have an improved survival, but this association did not reach the level of statistical significance. In multivariate analysis (all stages), tumour cell type (endometrioid versus non-endometrioid carcinomas) and stage of disease were the only variables associated with prognosis (P=0.01 and P<0.0001, respectively), with tumour cell type retaining its independent prognostic value and within stage-I endometrial carcinomas (P=0.02). It is suggested that the loss of steroid hormone receptors in endometrial carcinomas is associated with a more aggressive phenotype and the switching-on of angiogenic pathways.

Adenocarcinoma↗
PubMed2001

Prognostic aspects on endometrial hyperplasia and neoplasia.

There are various forms of endometrial hyperplasia which, in terms of prognosis and therapy, can be subdivided into those having cytological atypia and those lacking this feature. The former may progress into invasive endometrial malignancy through a transitional non-invasive stage. This is a continuous process and, as a result, the distinction between an atypical hyperplasia and an intraepithelial adenocarcinoma (IEA) or an adenocarcinoma with stromal invasion is not histologically reproducible. The concept of endometrioid neoplasia, which includes the entire spectrum of the aforementioned proliferating endometrial lesions, was introduced. Adenocarcinomas arising from an atypical hyperplasia are invariably of the endometrioid cell type, whereas those developing from an atrophic endometrium may be either of the endometrioid or of the non-endometrioid cell type. Endometrioid adenocarcinomas arising through the hyperplasia-neoplasia sequence are oestrogen induced and tend to be well differentiated and less invasive of the myometrium, lack lymphatic and metastatic involvement and have an excellent prognosis. Oestrogen-induced adenocarcinomas are also endometrioid, arising from an atrophic or a rather weakly proliferating endometrium, but these neoplasms are frequently of higher histological grade and have a somewhat less favourable prognosis. Finally, endometrial carcinomas of the non-endometrioid cell type, mainly serous papillary and clear cell carcinomas, are non-oestrogen induced, non-hyperplasia associated and show adverse aggressive histological features and an extremely poor prognosis. The antigenic characteristics and the molecular events associated with the development of these forms of endometrial malignancy are distinct and allow the description of, at least, two pathogenetic types of endometrial carcinoma.

Biomarkers, Tumor↗
PubMed2001

Mast cell distribution and density in the normal uterus--metachromatic staining using lectins.

This study investigates the number and the distribution of mast cells in the normal human uterus. Reliability of results was ensured by prompt tissue fixation and the use of biotin-labelled lectins in conjunction with the avidin-biotin peroxidase complex (ABC) method. This design revealed that mast cells are, indeed, normal constituents of the human uterus. They occur in large numbers in the myometrium, but are only scanty in the endometrium where they tend to be confined to the stratum basalis. The mean mast cell counts per high power field (MC/HPF), after staining with Canavalia ensiformis agglutinin (Con A), were 17.9MC/HPF in the inner half of the myometrium, and 8.3MC/HPF in the outer half of the myometrium; 2.7MC/HPF in the basalis, and 0.3MC/HPF in the functionalis (P<0.05). There are no apparent differences in the number of mast cells between the normal proliferative and secretory phase endometrium, however, endometrial mast cells are considerably reduced and, apparently, depleted of metachromatic granules during the immediate pre-menstrual phase of the menstrual cycle. It is presumed that this, almost exclusive, presence of mast cells in the basal layer of the endometrial matrix, combined with the discharge of their cytoplasmic granules towards the end of the cycle, may be related with the contracting process preceding menstruation. On the other hand, the relative paucity of mast cells in the functional layer may contribute to the immune tolerance of the gestational endometrium to the implantation of the blastocyst.

Adult↗
PubMed2001

Angiogenesis and apoptosis-related protein (p53, bcl-2, and bax) expression versus response of gastric adenocarcinomas to paclitaxel and carboplatin chemotherapy.

The role of angiogenesis and apoptosis-related proteins in defining response to chemotherapy is poorly understood. We examined the microvessel density (MVD) and the expression of p53, bcl-2, and bax proteins in a series of 28 locally advanced gastric adenocarcinomas, treated with paclitaxel and carboplatin. A strong cytoplasmic reactivity in more than 10% of cancer cells was recorded in 25% of cases for p53 protein, and in 14% and 64% of cases for bcl-2 and bax proteins, respectively. Microvessel density was assigned in three categories: low (<35), medium (35-60), and high (>60). Tumors of medium MVD showed a significantly higher response rate compared with those of high or low MVD (p = 0.01 and 0.001, respectively), and prognosis was significantly better in this group of patients with medium MVD tumors (p < 0.02). Loss of bax protein expression was somewhat more frequent in tumors resistant to chemotherapy, but this difference was not of statistical significance. Nuclear p53 reactivity was associated with higher MVD (p = 0.02). The expression of p53 and bcl-2 did not influence the outcome of treatment. The present study suggests that although apoptosis-related proteins may have a role in defining response to taxanes, parameters related to tumors' vasculature, such as drug availability or angiogenic tissue regeneration, may be equally important.

Adenocarcinoma↗