Invasive Tumors (invasive + tumor)

Distribution by Scientific Domains


Selected Abstracts


High-resolution comparative genomic hybridization detects extra chromosome arm 12p material in most cases of carcinoma in situ adjacent to overt germ cell tumors, but not before the invasive tumor development

GENES, CHROMOSOMES AND CANCER, Issue 2 2003
Anne Marie Ottesen
High-resolution comparative genomic hybridization (HR-CGH) analysis was performed on DNA purified from laser-capture microdissected carcinoma in situ (CIS) cells from nine cases of CIS, either from tissue without any invasive tumor or from testicular parenchyma adjacent to seminoma, nonseminoma, or a combined germ cell tumor. Before CGH analysis, DNA was amplified by degenerate oligonucleotide primed PCR (DOP-PCR) and directly labeled with a mixture of FITC-dUTP and FITC-dCTP. CGH analysis revealed extra chromosome arm 12p material in six out of seven cases with CIS adjacent to overt tumors, but only a diminutive gain of 12q was noted in one of the two cases of CIS without invasive elements. In addition, gains of parts of chromosome 8 (3/7) and losses of chromosome 5 (2/7) were demonstrated in CIS adjacent to invasive tumors. Gains of parts of chromosome 7 were found in CIS adjacent to seminoma (4/4), whereas relative gains of chromosome 15 were identified in some cases of CIS adjacent to seminoma and in isolated CIS in comparison to CIS adjacent to nonseminoma. Our data seem to indicate that extra 12p material is not present in the "dormant" CIS cell before development of an invasive tumor. The gain of extra chromosome 12 material may not be an early event in the neoplastic transformation, but is most likely associated with a more malignant progression of the CIS cell. © 2003 Wiley-Liss, Inc. [source]


Actinic cheilitis: histopathology and p53

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 8 2006
Dalva Regina Neto Pimentel
Background:, Chronic actinic cheilitis (AC) is a precursor of squamous cell carcinoma (SCC) of the lip. Objectives:, To evaluate the histopathological characteristics that may help to identify AC more susceptible to carcinomatous transformation, to assess the p53 protein expression in AC, and to determine the value of the p53 expression as a marker of transformation into SCC of the lip. Methods:, Seventy cases of chronic AC were reviewed, 31 of which were associated with SCCs. The samples were obtained from pathology reports of AC and SCC of the lip. Histopathology and immunohistochemical expression of the p53 protein were evaluated in isolated AC and in AC adjacent to SCC. Results:, The intensity of the inflammatory infiltrate in the corium was the only histopathological finding significantly associated both with the presence of an invasive tumor and with the degree of epithelial atypia. Most AC (85%) were immunoreactive to the p53 protein. The p53 protein expression in cheilitis was not statistically associated with any other histopathological criteria. Conclusions:, An intense inflammatory infiltrate in AC was predictive of an adjacent invasive SCC. In this study, the p53 protein immunoreactivity was not a marker of malignant transformation. [source]


The World Health Organization histologic classification system reflects the oncologic behavior of thymoma,

CANCER, Issue 3 2002
A clinical study of 273 patients
Abstract BACKGROUND Although the histologic classification of thymic epithelial tumors has been confusing and controversial, an agreement on the universal classification system for thymic epithelial tumors was achieved by the World Health Organization (WHO) in 1999. The authors previously reported that the WHO histologic classification system reflects invasiveness and immunologic function of thymic epithelial tumors. In this subsequent study, they examined the prognostic significance of this classification system. METHODS Clinical features as well as postoperative survival of patients with thymoma, but not thymic carcinoma, were examined with reference to WHO histologic classification based on an experience with 273 patients over a 44-year period. RESULTS There were 18 type A tumors, 77 type AB tumors, 55 type B1 tumors, 97 type B2 tumors, and 26 type B3 tumors. In patients with type A, AB, B1, B2, and B3 tumors, the respective proportions of invasive tumor were 11.1%, 41.6%, 47.3%, 69.1%, and 84.6%; the respective proportions of tumors with involvement of the great vessels were 0%, 3.9%, 7.3%, 17.5%, and 19.2%; and the respective 20-year survival rates were 100%, 87%, 91%, 59%, and 36%. According to the Masaoka staging system, the 20-year survival rates were 89%, 91%, 49%, 0%, and 0% in patients with Stage I, II, III, IVa, and IVb disease, respectively. By multivariate analysis, the Masaoka staging system and the WHO histologic classification system were significant independent prognostic factors, whereas age, gender, association with myasthenia gravis, completeness of resection, or involvement of the great vessels were not significant independent prognostic factors. CONCLUSIONS This study showed that histologic appearance reflects the oncologic behavior of thymoma when the WHO classification system is adopted. The WHO classification system may be helpful in clinical practice for the assessment and treatment of patients with thymoma. Cancer 2002;94:624,32. © 2002 American Cancer Society. DOI 10.1002/cncr.10225 [source]


High-resolution comparative genomic hybridization detects extra chromosome arm 12p material in most cases of carcinoma in situ adjacent to overt germ cell tumors, but not before the invasive tumor development

GENES, CHROMOSOMES AND CANCER, Issue 2 2003
Anne Marie Ottesen
High-resolution comparative genomic hybridization (HR-CGH) analysis was performed on DNA purified from laser-capture microdissected carcinoma in situ (CIS) cells from nine cases of CIS, either from tissue without any invasive tumor or from testicular parenchyma adjacent to seminoma, nonseminoma, or a combined germ cell tumor. Before CGH analysis, DNA was amplified by degenerate oligonucleotide primed PCR (DOP-PCR) and directly labeled with a mixture of FITC-dUTP and FITC-dCTP. CGH analysis revealed extra chromosome arm 12p material in six out of seven cases with CIS adjacent to overt tumors, but only a diminutive gain of 12q was noted in one of the two cases of CIS without invasive elements. In addition, gains of parts of chromosome 8 (3/7) and losses of chromosome 5 (2/7) were demonstrated in CIS adjacent to invasive tumors. Gains of parts of chromosome 7 were found in CIS adjacent to seminoma (4/4), whereas relative gains of chromosome 15 were identified in some cases of CIS adjacent to seminoma and in isolated CIS in comparison to CIS adjacent to nonseminoma. Our data seem to indicate that extra 12p material is not present in the "dormant" CIS cell before development of an invasive tumor. The gain of extra chromosome 12 material may not be an early event in the neoplastic transformation, but is most likely associated with a more malignant progression of the CIS cell. © 2003 Wiley-Liss, Inc. [source]


Genome-wide amplification and allelotyping of sporadic pituitary adenomas identify novel regions of genetic loss

GENES, CHROMOSOMES AND CANCER, Issue 3 2003
D. J. Simpson
Through the use of a candidate gene approach, several previous studies have identified loss of heterozygosity (LOH) at putative tumor-suppressor gene (TSG) loci in sporadic pituitary tumors. This study reports a genome-wide allelotyping by use of 122 microsatellite markers in a large cohort of tumors, consisting of somatotrophinomas and non-functioning adenomas. Samples were first subject to prior whole genome amplification by primer extension pre-amplification (PEP) to circumvent limitations imposed by insufficient DNA for whole-genome analysis with this number of microsatellite markers. The overall mean frequency of loss in invasive tumors was significantly higher than that in their non-invasive counterparts (7 vs. 3% somatotrophinomas; 6 vs. 3% non-functioning adenomas, respectively). Analysis of the mean frequency of LOH, across all markers to individual chromosomal arms, identified 13 chromosomal arms in somatotrophinomas and 10 in non-functioning tumors, with LOH greater than the 99% upper confidence interval calculated for the rate of overall random allelic loss. In the majority of cases, these losses were more frequent in invasive tumors than in their non-invasive counterparts, suggesting these to be markers of tumor progression. Other regions showed similar frequencies of LOH in both invasive and non-invasive tumors, implying these to be early changes in pituitary tumorigenesis. This genome-wide study also revealed chromosomal regions where losses were frequently associated with an individual marker, for example, chromosome arm 1q (LOH > 30%). In some cases, these losses were subtype-specific and were found at a higher frequency in invasive tumors than in their non-invasive counterparts. Identification of these regions of loss provides the first preliminary evidence for the location of novel putative TSGs involved in pituitary tumorigenesis that are, in some cases, subtype-specific. This investigation provides an unbiased estimate of global aberrations in sporadic pituitary tumors as assessed by LOH analysis. The identification of multiple "hotspots" throughout the genome may be a reflection of an unstable chromatin structure that is susceptible to a deletion or epigenetic-mediated gene-silencing events. © 2003 Wiley-Liss, Inc. [source]


Odontogenic ghost cell carcinoma

HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 4 2004
David Goldenberg MD
Abstract Background. Odontogenic ghost cell carcinoma (OGCC), a malignant counterpart of the calcifying odontogenic cyst (COC), is exceedingly rare. Previous descriptions of this tumor were based on identification of malignant histologic characteristics such as infiltration, cellular pleomorphism, numerous mitoses, and necrosis concurrent with classical benign COC or its solid benign variant, the odontogenic ghost cell tumor. Methods. We present a case of a young Asian man who underwent multiple local excisions of a recurring maxillary COC. After one such excision, a rapid onset of painful swelling ensued, and the patient was referred to our institution for definitive surgery. Results. The patient underwent a right subtotal maxillectomy. Intraoperatively, a 5-cm tumor was found to be extending into the right maxillary sinus and nasal cavity. The excised tumor was diagnosed as an OGCC. The tumor was excised with clear margins, and no adjunctive radiotherapy was given. The patient was free of residual or recurrent disease 18 months after surgery. Conclusions. On the basis of this case and prior cases found in the literature, OGCCs show a spectrum of growth from slow growing locally invasive tumors to highly aggressive, rapidly growing, infiltrative tumors. Wide local excision with histologically clean margins is the recommended mode of treatment. We recommend close long-term surveillance of recurrent or long-standing benign COCs and OGCC. © 2003 Wiley Periodicals, Inc. Head Neck26: 378,381, 2004 [source]


Green tea extracts decrease carcinogen-induced mammary tumor burden in rats and rate of breast cancer cell proliferation in culture

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2001
Kathryn T. Kavanagh
Abstract Epidemiological evidence suggests tea (Camellia sinensis L.) has chemopreventive effects against various tumors. Green tea contains many polyphenols, including epigallocatechin-3 gallate (EGCG), which possess anti-oxidant qualities. Reduction of chemically induced mammary gland carcinogenesis by green tea in a carcinogen-induced rat model has been suggested previously, but the results reported were not statistically significant. Here we have tested the effects of green tea on mammary tumorigenesis using the 7,12-dimethylbenz(a)anthracene (DMBA) Sprague-Dawley (S-D) rat model. We report that green tea significantly increased mean latency to first tumor, and reduced tumor burden and number of invasive tumors per tumor-bearing animal; although, it did not affect tumor number in the female rats. Furthermore, we show that proliferation and/or viability of cultured Hs578T and MDA-MB-231 estrogen receptor-negative breast cancer cell lines was reduced by EGCG treatment. Similar negative effects on proliferation were observed with the DMBA-transformed D3-1 cell line. Growth inhibition of Hs578T cells correlated with induction of p27Kip1 cyclin-dependent kinase inhibitor (CKI) expression. Hs578T cells expressing elevated levels of p27Kip1 protein due to stable ectopic expression displayed increased G1 arrest. Thus, green tea had significant chemopreventive effects on carcinogen-induced mammary tumorigenesis in female S-D rats. In culture, inhibition of human breast cancer cell proliferation by EGCG was mediated in part via induction of the p27Kip1 CKI. J. Cell. Biochem. 82:387,398, 2001. © 2001 Wiley-Liss, Inc. [source]


Activity of the matrix metalloproteinase-9 promoter in human normal and tumor cells

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2004
Cristina Morelli
Matrix metalloproteinases (MMPs) belong to a family of proteins essential for those processes involving extracellular matrix degradation, such as embryonic development, morphogenesis, and tissue resorption and remodeling. Some members of this family play a crucial role also in tumor invasion. Most notably, MMP-9 is expressed in invasive tumors, and represents a key protein in brain tumor progression, whereas it is not expressed in adult normal tissues. The expression of the MMP-9, like other members of the family, is transcriptionally regulated. We, therefore, postulated that the MMP-9 promoter could be useful in driving selective expression of exogenous genes in tumor cells. This represents a key feature for gene therapy applications, since currently employed viral promoters induce severe organ toxicity, limiting the clinical benefits. In this study, we investigated the activity of the MMP-9 promoter in driving exogenous gene expression in human cell lines. High levels of reporter gene expression were detected in tumor derived cell lines, whereas the MMP-9 promoter activity in non-tumor cells was negligible. Furthermore, we show that tumor necrosis factor alpha (TNF,) is able to enhance considerably the MMP-9 promoter activity only in tumor cells. Since recent studies have indicated that MMP-9 enzymatic activity is detectable in the blood, it would be possible to screen potential responsive patients for a tumor gene therapy approach based on the MMP-9 promoter. Taken together these data suggest that MMP-9 promoter has the characteristics for transcritpionally targeted and inducible gene therapy applications. J. Cell. Physiol. 199: 126,133, 2004© 2003 Wiley-Liss, Inc. [source]


LAPTM4B-35 is a novel prognostic factor of hepatocellular carcinoma

JOURNAL OF SURGICAL ONCOLOGY, Issue 5 2010
Hua Yang MD
Abstract Background LAPTM4B-35 is a 35-kDa tetra-transmembrane protein overexpressed in hepatocellular carcinoma (HCC) and promotes cell survival, proliferation, and tumorigenesis. However, the potential clinical implications of LAPTM4B-35 in HCC are still unclear. This study is aimed to investigate the correlations between LAPTM4B-35 expression and prognosis in patients with HCC. Methods Western blot and immunohistochemistry assays were used to determine the expression of LAPTM4B-35 in HCCs and their paired noncancerous liver tissues from 65 patients. The correlations of LAPTM4B-35 expression with clinicopathological parameters were assessed by Chi-square test. Patient survival was determined by Kaplan,Meier method and log-rank test. Cox regression was adopted for multivariate analysis of prognostic factors. Results LAPTM4B-35 overexpression occurred in 76.9% of HCC tissues, while only in 4.6% of noncancerous liver tissues. Overexpression of LAPTM4B-35 was significantly associated with TNM staging and invasive tumors. Patients with higher LAPTM4B-35 expression had significantly poorer overall survival (OS) and disease-free survival (DFS) (both P,<,0.001). On multivariate analysis, elevated expression of LAPTM4B-35 was found to be an independent prognostic factor for OS and DFS (P,=,0.009, 0.043, respectively). Conclusions LAPTM4B-35 overexpression is an independent prognostic factor for OS and DFS of HCC. J. Surg. Oncol. 2010; 101:363,369. © 2010 Wiley-Liss, Inc. [source]


LIM kinase-2 targeting as a possible anti-metastasis therapy

THE JOURNAL OF GENE MEDICINE, Issue 3 2004
Eigo Suyama
Abstract Background Metastatic properties of tumors involve movement of cancerous cells from one place to another and tissue invasion. Metastatic cells have altered cell adhesion and movement that can be examined by in vitro chemotaxis assays. The Rho/ROCK/LIM kinase pathway is one of the major signaling pathways involved in tumor metastasis. It is involved in the regulation of the actin cytoskeleton. Using the randomized ribozyme library, we initially found that metastatic human fibrosarcoma cells harboring ribozyme specific for ROCK lose their metastatic properties. In this study, we have determined the effect of ribozymes specific for LIM kinase-2 on metastatic and proliferative phenotypes of human fibrosarcoma cells. Methods We attempted to target LIM kinase-2 (LIMK-2) expression by hammerhead ribozymes (Rz) in human metastatic fibrosarcoma cells. An effective ribozyme was selected based on the expression analysis. Cells were stably transfected with Rz specifically effective for LIMK-2 and were examined for metastatic and proliferative properties. Results Analyses of cellular phenotypes such as cell proliferation, cell migration and colony-forming efficiency revealed that the suppression of LIMK-2 expression in human fibrosarcoma cells limits their migration and dense colony-forming efficiency without affecting cell proliferation rate or viability. Conclusions Specific targeting of metastatic and malignant properties of tumor cells by LIMK-2 ribozyme may serve as an effective therapy for invasive tumors with minimum effect on the surrounding normal cells. Copyright © 2004 John Wiley & Sons, Ltd. [source]


Antiangiogenic and Chemopreventive Activities of Celecoxib in Oral Carcinoma Cell,,

THE LARYNGOSCOPE, Issue 5 2002
Zhi Wang MD
Abstract Objectives Chemoprevention is a promising strategy to inhibit carcinoma before invasive tumors develop, but a new molecular target is desirable. Celecoxib is a newly developed cyclo-oxygenase (COX)-2 inhibitor with significantly less toxicity. The study was conducted to determine whether celecoxib is effective and safe in prevention of oral cancer. The antiangiogenic activity of celecoxib was studied to explore the potential mechanism involved. Study Design Randomized animal study. Methods The study consisted of two phases. In the phase 1, 10 mice were used to determine the efficacy and safety of celecoxib with intradermal inoculation with oral carcinoma cells. The 10 mice were equally divided into two groups 5 mice (30 inoculated sites) in each group to receive 1,500 parts per million (ppm) celecoxib mixed in with the diet or to eat a normal diet, respectively, for 21 days. In phase 2, 10 more mice were inoculated to determine the effect of celecoxib on angiogenesis. Five mice received 3,000 ppm celecoxib in the diet, with the other five mice as control animals. The antiangiogenic activity was evaluated by comparing the density of newly growing microvessels after the inoculation. Results The results indicated that celecoxib significantly delayed cell growth and reduced tumor volume. There was statistical significance in the quantity of new vasculature in the tumor sites between the two groups. No toxic effect was found by means of measurement of body weight loss and microscopic dissection of organs. Conclusions The study provided the first evidence to show the chemopreventive efficacy of celecoxib on oral cancer in a nude mouse model. Clinical trials are warranted to determine the efficacy in humans. [source]


Inhibitory effect of esculin on oxidative DNA damage and carcinogenesis induced by N-nitrosobis(2-oxopropyl)amine in hamster pancreas

BIOFACTORS, Issue 1-4 2004
Takao Kaneko
Abstract The effects of esculin, a natural coumarin compound, on the formation of 8-ox O2,,-deoxyguanosine (8-oxodG) and carcinogenesis induced by a chemical carcinogen, N-nitrosobis(2-oxopropyl)amine (BOP), were examined in the pancreas of female Syrian golden hamsters. Animals were given a diet containing esculin for 7 days, and killed 4h after BOP treatment, and the contents of 8-oxodG were measured in the nuclear DNA of the pancreas. Esculin suppressed significantly the increase in the 8-oxodG content of hamster pancreas induced by BOP. Furthermore, the effect of esculin on the rapid production model experiment for pancreatic carcinogenesis using BOP was investigated. Esculin was given ad libitum as a 0.05% aqueous solution during either the initiation or promotion phases. The incidence of invasive tumors in animals given esculin during the initiation phase was significantly lower than in the control group, while the incidence in animals given esculin during the promotion phase showed no significant change. These results suggest that the intake of esculin has an inhibitory effect on BOP-induced oxidative DNA damage and carcinogenesis in hamster pancreas. [source]


Screening mammography performance and cancer detection among black women and white women in community practice

CANCER, Issue 1 2004
Karminder S. Gill M.S.P.H.
Abstract BACKGROUND Despite improvement in mammography screening attendance, black women continue to have poorer prognosis at diagnosis than white woman. Data from the Carolina Mammography Registry were used to evaluate whether there may be differences in mammography performance or detected cancers when comparing black women with white women who are screened by mammography. METHODS Prospectively collected data from community-based mammography facilities on 468,484 screening mammograms (79,397 in black women and 389,087 in white women) were included for study. Mammograms were linked to a pathology data base for identification of cancers. Sensitivity, specificity, positive predictive value, and cancer detection rates were compared between black women and white women. Logistic regression methods were used to control for covariates associated with performance characteristics. Differences in cancer characteristics were compared between black women and white women using chi-square statistics. RESULTS Screening mammography performance results for black women compared with white women were as follows: sensitivity, odds ratio (OR) = 1.07 (95% confidence interval [95% CI], 0.83,1.39); specificity, OR = 1.02 (95% CI, 0.98,1.06); and positive predictive value, OR = 1.07 (95% CI, 0.94,1.23). Among women with no previous screening, black women had a larger proportion of invasive tumors that measured , 2 cm (38% vs. 26%; P = 0.04). The cancer detection rate was highest among black women who reported symptoms at screening (13.9 per 1000 black women vs. 7.9 per 1000 white women). Invasive cancers in black women were poorer grade (P = 0.001), and more often had negative estrogen receptor status and progesterone receptor status (P < 0.001). CONCLUSIONS Overall, screening mammography performed equally well in black women and white women controlling for age, breast density, and time since previous mammogram. Black women who reported symptoms had larger and higher grade tumors compared with white women. Educational efforts need to be strengthened to encourage black women to react sooner to symptoms, so that the tumors detected will be smaller and black women will have a better prognosis when they appear for mammography. Cancer 2004;100:139,48. © 2003 American Cancer Society. [source]


The relevance of occult axillary micrometastasis in ductal carcinoma in situ,

CANCER, Issue 10 2003
A clinicopathologic study with long-term follow-up
Abstract BACKGROUND Ductal carcinoma in situ (DCIS) represents 20% of newly diagnosed breast carcinoma cases. Historically, the incidence of axillary metastasis in DCIS has been small (1,2%) and its significance has been debated. It is widely known that serial sections of lymph nodes coupled with keratin immunohistochemistry (IHC) increases identification of micrometastasis. The advent of sentinel lymph node evaluation underscores the need to reevaluate the significance of occult micrometastases in DCIS. METHODS Patients with DCIS and negative axillary lymph nodes from 1974 to 1992 were selected from the Saint Barnabas Medical Center Tumor Registry. All diagnoses were confirmed, and paraffin blocks were retrieved after acceptance into the study. Seven serial sections were obtained from each block and evaluated with two cytokeratin IHC stains. Clinical follow-up ranged from 10 to 28 years. RESULTS One hundred two patients were included in the study. Micrometastases were identified in 13 patients (13%), mostly on 1 level and composed of microscopic clusters in the subcapsular sinus. Seven of these lymph node,positive patients (58%) had high-grade comedo DCIS, 4 (33%) had intermediate grades of various types of DCIS, and one had a low-grade micropapillary DCIS. The overall disease recurrence rate was 12%, but micrometasis was not detected in any of the patients who developed disease recurrence. CONCLUSIONS Serial IHC evaluation of lymph nodes dramatically increased the identification of occult micrometastasis. However, IHC detected micrometastasis has no apparent clinical significance in DCIS, based on the current long-term clinicopathologic study. Therefore, the authors questioned the significance of occult micrometastasis, identified by IHC, in DCIS of any type and extent. Further evaluation and follow-up of lymph node micrometastases in patients with invasive tumors of various sizes are needed. The current findings would not support altering the stage of patients with DCIS and micrometastasis detected by IHC only. Cancer 2003. © 2003 American Cancer Society. [source]


Increased expression of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 is correlated with poor prognostic variables in patients with thymic epithelial tumors

CANCER, Issue 9 2003
Ken-ichi Sogawa M.D., Ph.D.
Abstract BACKGROUND A distinction between noninvasive, invasive, and metastatic thymoma on the basis of the cytologic features is difficult. The current study investigated whether the expression of MMP and TIMP was correlated with tumor invasiveness and prognosis in patients with thymoma. METHODS Tumor tissue samples were obtained from 42 patients with thymic epithelial tumors between 1974 and 2001 at Tokushima University Hospital. Three-micrometer-thick, formalin-fixed, paraffin-embedded tissue sections were immunostained using specific antibodies against MMP-2, MMP-9, TIMP-1, and TIMP-2. RESULTS MMP-2 expression was detected in 30 tumors (71%), and TIMP-2 expression was detected in 31 tumors (74%). MMP-9 expression was detected in 22 of 36 tumors (61%), and TIMP-1 expression was detected in only 7 tumors (19%). MMP-2 and TIMP-2 expression levels were very low (10% and 0%, respectively) in noninvasive tumors but were very high (91% and 97%, respectively) in invasive tumors. In thymic epithelial tumors, the more progressive the clinical stage of tumor, the higher the strongly positive rate of MMP-2 and TIMP-2 expression. There was no correlation between positivity for MMP-9 and stage. Twenty-five percent of Type AB thymomas and 50% of Type B1 thymomas expressed MMP-2 and TIMP-2. Most of Type A, Type B2, Type B3, and Type C thymomas expressed MMP-2 and TIMP-2. There were significant differences in disease-free survival at 5 years between patients without and with MMP-2 expression (91% vs. 55%, respectively) and patients without and with TIMP-2 expression (100% vs. 53%, respectively). CONCLUSIONS MMP-2 and TIMP-2 are key enzymes for invasiveness of thymic epithelial tumors. The expression of these proteins can predict a poor outcome in patients with thymoma. Cancer 2003. © 2003 American Cancer Society. [source]


A review of p53 expression and mutation in human benign, low malignant potential, and invasive epithelial ovarian tumors

CANCER, Issue 2 2003
Leanne M. Kmet M.Sc.
Abstract BACKGROUND In the current study, the authors present pooled data from studies that investigated p53 protein expression and/or mutation in human epithelial ovarian tumors. METHODS The English literature in the MEDLINE, PubMed, and Ingenta databases was searched to the end of the year 2000 to identify relevant studies. Data were pooled across eligible studies, and the prevalence of p53 expression and mutation among benign, low malignant potential (LMP), and invasive tumors was determined. Prevalence estimates by tumor histology, International Federation of Gynecology and Obstetrics (FIGO) stage, and grade also were calculated. RESULTS The pooled prevalence estimate for p53 overexpression among epithelial ovarian carcinomas was 51% (95% confidence intervals [95% CI], 50,53%) compared with 17% (95% CI, 15,20%) among LMP tumors and 7% (95% CI, 5,10%) among benign tumors. p53 mutation prevalence estimates were 45% (95% CI, 42,47%), 5% (95% CI, 2,9%), and 1% (95% CI, 0,5%), respectively, for invasive, LMP, and benign tumors. The prevalence of these p53 abnormalities was found to be associated positively with increasing tumor grade and stage. Differences based on histologic subtype also were found. CONCLUSIONS Although these pooled estimates might appear to offer support for various hypotheses regarding the role of p53 in ovarian carcinoma, the limitations inherent in these data hamper the interpretation of the significance of any of the findings. Future studies will require innovative methods to address the limitations of many previous investigations and more comprehensive investigation into defective tumor suppression mechanisms. Cancer 2003;97:389,404. © 2003 American Cancer Society. DOI 10.1002/cncr.11064 [source]


The pattern of breast cancer screening utilization and its consequences

CANCER, Issue 1 2002
James Michaelson Ph.D.
Abstract BACKGROUND The objective of this study was to describe the pattern of screening utilization and its consequences in terms of tumor size and time of tumor appearance of invasive breast carcinoma among a population of women who were examined at a large service screening/diagnostic program over the last decade. METHODS Utilization of mammography was assessed from a population of 59,899 women who received 196,891 mammograms at the Massachusetts General Hospital Breast Imaging Division from January 1, 1990 to March 1, 1999, among which 604 invasive breast tumors were found. Two hundred six invasive, clinically detected tumors also were seen during this period among women who had no record of a previous mammogram. Additional information was available on screening of women from March 1, 1999 to June 1, 2001. RESULTS Fifty percent of the women who used screening did not begin until the age of 50 years, although 25% of the invasive breast tumors were found in women age < 50 years. Relatively few of the women who used screening returned promptly for their annual examinations; by 1.5 years, only 50% had returned. Approximately 25% of the invasive breast tumors were found in women for whom there was no record of a previous screening mammogram, and these tumors were larger (median, 15 mm) than the screen-detected tumors (median, 10 mm). Approximately 30% of the 604 invasive breast tumors in the screening population were found on nonmammographic grounds, and they also were larger (median, 15 mm) than the screen-detected tumors (median, 10 mm). However, only 3% of these 604 tumors were found by nonmammographic criteria within 6 months of the previous negative examination, and only 12% were found within 1 year. By back calculating the likely size of each of these tumors at the time of the negative mammogram, it could be seen that most tumors probably emerged as larger, palpable masses not because they were missed at the previous negative mammogram, because most were too small then to have been detected, but because too much time had been allowed to pass. CONCLUSIONS Far too many women did not comply with the American Cancer Society recommendation of prompt annual screening from the age of 40 years. Consequently, almost 50% of the invasive tumors emerged as larger and, thus, potentially more lethal, palpable masses. Cancer 2002;94:37,43. © 2002 American Cancer Society. [source]


OCIA domain containing 2 is highly expressed in adenocarcinoma mixed subtype with bronchioloalveolar carcinoma component and is associated with better prognosis

CANCER SCIENCE, Issue 1 2007
Tadashi Ishiyama
Although lung adenocarcinoma is a major cause of cancer death worldwide, details of its molecular carcinogenesis and stepwise progression are still unclear. To characterize the sequential progression from bronchioloalveolar adenocarcinoma of the lung (BAC, in situ carcinoma) to adenocarcinoma mixed subtype with BAC component, polymerase chain reaction-based cDNA suppression subtractive hybridization (SSH) was carried out using two representative cases of BAC (non-invasive tumors) and adenocarcinoma mixed subtype with BAC (invasive tumors). Through differential screening, virtual reverse northern hybridization and quantitative real-time reverse-transcription,polymerase chain reaction (qRT-PCR) we selected five genes (TncRNA, OCIAD2, ANXA2, TMED4 and LGALS4) that were expressed at significantly higher levels in invasive adenocarcinoma mixed subtype with BAC than in BAC. After in situ hybridization and qRT-PCR analyses, we confirmed that only the OCIAD2 gene showed significantly higher expression in the tumor cells of invasive adenocarcinoma mixed subtype with BAC than in BAC (P = 0.026). We then carried out in situ hybridization of OCIAD2 in 56 adenocarcinoma mixed subtype with BAC component and assessed the correlation between OCIAD2 expression and clinicopathological features. In contrast to our expectation, the patients with OCIAD2 expression showed a better clinical outcome than those without OCIAD2 expression, and OCIAD2 expression showed an inverse correlation with lymphatic invasion, blood vessel invasion and lymph node metastasis. These results suggest that OCIAD2 begins to express at the progression from in situ to invasive carcinoma, and is associated with the favorable prognosis of adenocarcinoma mixed subtype with BAC component. (Cancer Sci 2007; 98: 50,57) [source]


Cytogenetic profile of locally invasive posterior uveal melanoma

ACTA OPHTHALMOLOGICA, Issue 2009
R PARROZZANI
Purpose To analyze cytogenetic profile of locally invasive posterior uveal melanoma (UM). Methods Twenty consecutive cases of large posterior UM with histopathologically confirmed extrascleral extension were included in this non-comparative cases series. Fine needle aspiration biopsy (FNAB) of the intraocular tumor portion was performed using 25-gauge trans-scleral approach, immediately after enucleation of the globe. FNAB of the extrascleral tumor portion was also performed when it was > 1mm in thickness. Sampled material underwent fluorescence in situ hybridization (FISH). Follow-up was longer than 12 months. Results Six tumors (30%) had both intraocular and extraocular tumor samplings, whereas 14 tumors (70%) showed extrascleral extension less than 1 mm in thickness. Monosomy 3 was found in 5 tumors (25%), whereas disomy 3 in 15 tumors (75%). Cytogenetic profile of the intraocular tumor portion appears to be maintained in the extrascleral extension in all cases (100%). Five patients (25%) developed metastatic disease during follow-up (all had monosomy 3 tumors). Conclusion Extrascleral extension appears more frequent in disomy 3 tumors. Cytogenetic profile of locally invasive posterior UM is maintained in the extrascleral tumor portion and must be considered the most important prognostic factor in locally invasive tumors. [source]