Home About us Contact | |||
Situ Carcinoma (situ + carcinoma)
Selected AbstractsPathogenesis of breast carcinomaINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 1 2004Ian S. Fentiman Summary Breast cancer usually develops after a series of epithelial changes in the terminal ductolobular unit. There are multiple benign causes of breast lumps, the majority of which are not associated with an increased risk of breast cancer. Histological changes of pre-malignancy such as atypical hyperplasia and in situ carcinoma can be identified, and these are indications for either close surveillance or further surgery. At the time of diagnosis, breast cancers can be staged both clinically and pathologically, and this facilitates international comparisons of results of treatment. [source] Very early cytological and DNA-cytometric diagnosis of in situ carcinoma in an immunosuppressed liver transplant recipientJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 8 2006Prof. Dr. A. Burkhardt No abstract is available for this article. [source] Effective management of smoking in an oral dysplasia clinic in LondonORAL DISEASES, Issue 1 2006TWJ Poate Background:, Precancerous lesions precede the development of oral cancer; of several clinical types the most common is leukoplakia. The risk factors include tobacco and excess alcohol use and diets low in antioxidants. Studies concerning the management of risk factors related to oral precancer are meager. Objectives:, We investigated the effectiveness of smoking cessation at a dysplasia clinic among patients followed up for at least for 12 months. Methods:, Data from case notes relating to180 patients with white and red patches of oral mucosa (excluding other benign disorders confirmed by biopsy findings) attending a dysplasia clinic at a teaching hospital in London and seen by one consultant between 1993 and 2003 were transcribed. Effect of referring to a smoker's clinic to receive specialist help was evaluated against brief advice given at the dysplasia clinic ± medications. Results:, The mean age at the first visit was 48.5 years (±12.5), 65% were male, and 88% were white European. One hundred and sixty-two patients (90%) had used tobacco and 83% were current smokers. Of the smokers 95% had smoked over 10 years, the majority smoking over 10 cigarettes per day. Nine were alcohol misusers including two binge drinkers. One hundred and forty-six were diagnosed with oral leukoplakia, 16 with non-homogeneous types (speckled or nodular). Three patients were diagnosed with an erythroplakia. Nineteen per cent exhibited the presence of dysplasia and one subject had in situ carcinoma. Five patients in the sample quit smoking prior to arrival in the dysplasia clinic. Twenty-seven cases (20%) with oral leukoplakia quit smoking while registered as a patient at the dysplasia clinic: 17 of 100 subjects quit with brief advice ± medications and 10 of 30 following referral to the smoker's clinic. The difference between the two groups was significant for point prevalence abstinence at the last visit to the clinic (minimum 12 months follow up). Out of a total of 180 precancer cases managed in the dysplasia clinic (mean follow up 4.2 years) three patients subsequently developed invasive carcinoma during follow up. Conclusions:, Smoking cessation needs to be an integral component of management of cases attending a dysplasia clinic and referring to smoker's clinics could help to improve the effectiveness of managing patients with oral precancer to quit smoking. [source] BI-RADS MRI Enhancement Characteristics of Ductal Carcinoma In SituTHE BREAST JOURNAL, Issue 6 2007Eric L. Rosen MD Abstract:, To identify the Breast Imaging Reporting and Data System magnetic resonance imaging (MRI) enhancement characteristics of ductal carcinoma in situ (DCIS). A retrospective review of consecutive patients who underwent breast MRI for newly diagnosed breast carcinoma prior to surgery was conducted. This yielded 381 lesions in 361 patients with pathologic confirmation of either DCIS alone, invasive carcinoma alone, or mixed invasive and in-situ disease. Presence or absence of a MRI lesion at the site of the documented carcinoma was recorded, and for all identified MRI lesions the Breast Imaging Reporting and Data System morphology patterns were recorded. MRI features of the different malignancy types were compared utilizing Fisher's exact tests; 64/381 (16.8%) lesions had DCIS, 101/381 (26.5%) had invasive carcinoma, and 216/381 (56.7%) had mixed invasive/in situ carcinoma. A MRI lesion corresponding to the known cancer was identified in 55/64 (85.9%) cases of DCIS, 98/101 (97.0%) cases of invasive carcinoma, and 212/216 (98.1%) cases of mixed invasive and in-situ carcinoma. For pure DCIS lesions, 38/64 (59.4%) exhibited nonmass-like enhancement (NMLE), 9/64 (14.1%) were masses, and 8/64 (12.5%) were a focus. For pure invasive carcinomas 79/101(78.2%) were masses, 16/101 (15.8%) were NMLE, and 3/101 (3.0%) were a focus. For mixed lesions 163/216 (75.5%) were masses, 44/216 (20.4%) demonstrated NMLE, and 5/216 (2.3%) were a focus. The most common NMLE patterns of pure DCIS were segmental distribution and clumped internal enhancement. Although there is overlap in the MRI morphology and enhancement pattern of in situ and invasive breast carcinoma, DCIS more frequently manifests as NMLE than does invasive carcinoma. [source] Triad of Columnar Cell Alteration, Lobular Carcinoma in Situ, and Tubular Carcinoma of the BreastTHE BREAST JOURNAL, Issue 2 2005Sunati Sahoo MD Abstract: Columnar cell alteration in the breast encompasses a spectrum of pathologic changes ranging from simple columnar cell change to more complex columnar cell hyperplasia with and without atypia to in situ carcinoma, often with a micropapillary architecture. For reasons that remain unclear, the columnar cell lesions are associated with tubular carcinomas and lobular carcinoma in situ. Therefore it is important to be familiar with the spectrum of changes and the associated lesions, especially in breast core biopsies for further management., [source] Co-localization of multiple ErbB receptors in stratified epithelium of oral squamous cell carcinomaTHE JOURNAL OF PATHOLOGY, Issue 3 2001Roberto Bei Abstract The expression of all four ErbB receptors was compared by immunohistochemistry, using receptor-specific polyclonal antisera, in 32 invasive, 11 in situ carcinomas, six benign lesions, and 22 samples of histologically normal mucosa adjacent to specimens of carcinoma originating from oral cavity epithelium. Among invasive and in situ carcinoma, EGFR expression was the most prevalent (in 29/32 and 8/11 cases, respectively) followed by ErbB2 (17/32 and 2/11) and ErbB4 (9/32 and 1/10), while ErbB3 was only detected in invasive tumours (12/32). Specific patterns included invasive tumours with expression of EGFR (8/32) or ErbB4 (1/32) alone, as well as different receptor combinations (EGFR+ErbB2, EGFR+ErbB4, EGFR+ErbB2+ErbB3, EGFR+ErbB2+ErbB4, and all four receptors). Simultaneous expression of three or four ErbB receptors correlated with tumour invasion (p=2.2×10,4) and localized in the intermediate epithelial cell layer of well and moderately differentiated tumours. No other significant correlation with clinico-pathological features was noticed. Some benign lesions and histologically normal mucosa adjacent to carcinomas showed weak immunostaining of EGFR (10/28), ErbB2 (4/28) or ErbB4 (3/28). By comparison, overexpression, as indicated by increased staining intensity, was observed in invasive tumours for EGFR (18/32), ErbB2 (8/32), ErbB4 (3/32), and ErbB3 (3/32). Statistical evaluation demonstrated a significant association of EGFR or ErbB2 overexpression with invasive carcinoma when compared with benign lesions and apparently normal epithelium (p=5.2×10,7 and p=5×10,3, respectively). Tumour-specific overexpression of ErbB receptors and their co-expression, most frequently involving EGFR and ErbB2, in the same cell layer of neoplastic epithelium, implicate receptor heterodimers in the pathogenesis of oral squamous carcinoma. Copyright © 2001 John Wiley & Sons, Ltd. [source] A population-based study of skin cancer incidence and prevalence in renal transplant recipientsBRITISH JOURNAL OF DERMATOLOGY, Issue 3 2006F.J. Moloney Summary Background, Cancers occurring following solid organ transplantation are a rapidly growing public health concern. Defining the extent of the problem has been limited by surveillance systems with incomplete registration of cases and the paucity of reliable national incidence data. Objectives, To determine the incidence of all cancers following renal transplantation and to make a detailed examination of trends and patterns associated with postrenal transplant skin cancers. Methods, Integration of data from the national renal transplant database and the national cancer registry in Ireland enabled accurate determination of the number of renal transplant recipients (RTRs) with skin cancers and other malignancies in the time period 1 January 1994 to 31 December 2001. Results, We demonstrated a biphasic increase in skin cancer incidence following renal transplantation, determined by the age at transplantation. There was a steady increase in risk for older RTRs (age 50+ years) from year 2 post-transplant, whereas the increased risk in younger RTRs (age <,50 years) occurred later but much more significantly, reaching 200 times the risk for an age-matched nontransplanted population by year 6 post-transplant. The number of nonmelanoma skin cancers (NMSCs) registered in RTRs accounted for 1% of all NMSCs registered nationally over the study period. The standardized incidence rates for invasive NMSC (33-fold increase) and in situ carcinoma of the skin (65-fold increase) were significantly increased (P < 0·05). The risk for invasive squamous cell carcinoma (SCC) was increased 82-fold compared with the nontransplanted population. Male RTRs were at particular risk of invasive SCC at sun-exposed sites such as the scalp and the external ear. Risk of malignant melanoma and Kaposi sarcoma were also increased relative to the nontransplanted population. Conclusions, This comprehensive national study illustrates how rates of skin cancer in Irish RTRs have influenced the national incidence of skin cancer. The high incidence of SCC, basal cell carcinoma and Bowen's disease in the early post-transplant period for older patients and the cumulative risk in younger patients with increased duration of transplantation highlight the importance of implementing early and continued cancer surveillance regimens post-transplant. [source] OCIA domain containing 2 is highly expressed in adenocarcinoma mixed subtype with bronchioloalveolar carcinoma component and is associated with better prognosisCANCER SCIENCE, Issue 1 2007Tadashi 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] Topical treatment of intraepithelial penile carcinoma with imiquimodCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 2003G. Micali Summary Intraepithelial penile carcinoma (IPC) is an in situ carcinoma of the penis, which can be difficult to diagnose. Current treatments include excisional surgery, Mohs' micrographic surgery, cryotherapy, carbon dioxide laser therapy and topical 5-fluorouracil. We report two cases of men with 12,18 month histories of IPC (Bowen's disease, squamous cell carcinoma in situ) that were previously unsuccessfully treated with antifungals and antibiotics. Treatment with imiquimod 5% cream for 8,10 weeks was effective in both cases with no clinical evidence of relapse at 4 and 6 months. Both patients experienced adverse effects, resulting in temporary discontinuation of treatment. [source] Experimental esophageal carcinogenesis: technical standardization and resultsDISEASES OF THE ESOPHAGUS, Issue 4 2002J. A. Sallet SUMMARY., The aim of this research was to determine the occurrence of epidermoid carcinoma of the esophagus induced by diethylnitrosamine (DEN) in Wistar rats. DEN was administered (250,300 g) in drinking water (10 mg/kg body weight) to four groups of rats for 72 h/week, for a duration of 90, 120, 150, or 200 days (groups T90, T120, T150, and T200). Ten animals whose drinking water did not contain DEN constituted the control group. All rats were sacrificed and their esophaguses studied macro- and microscopically. The control group did not exhibit either carcinomas or preneoplasic lesions. The T120 and T200 groups presented, respectively, 47 and 58 in situ carcinomas; 1 and 20 submucosal carcinomas (P < 0.05); 4 and 17 microinvasive carcinomas (P < 0.05); 4 and 11 advanced carcinomas (P < 0.05); and 1 and 1 cases of benign hyperplasia. Pulmonary and liver carcinomas were also found in the T200 group. The majority of advanced macroscopic lesions in the T200 group were polypoid, exophytic, and not microscopically invasive in the esophageal wall. This research confirms the effectiveness of the DEN in bringing about carcinogenesis in the Wistar rat esophagus and also shows that the lesions are dosage dependent. [source] Topical 3.0% diclofenac in 2.5% hyaluronic acid gel induces regression of cancerous transformation in actinic keratosesJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 3 2010T Dirschka Abstract Background, Actinic keratoses (AKs) are frequently diagnosed in dermatological patients. As they represent in situ carcinomas, effective treatment is required. Objectives, We investigated the effect of topical 3.0% diclofenac in 2.5% hyaluronic acid gel on AK. Methods, Sixty-five patients with AKs were clinically evaluated before and after 3 months' treatment with topical 3.0% diclofenac in 2.5% hyaluronic gel. Biopsy specimens were taken and stained with haematoxylin-eosin and immunohistological markers. Specimens were evaluated for histological type of AKs using the AK classification scheme suggested by Röwert-Huber et al. [(early) in situ squamous cell carcinoma type AK Grade I,III], number of mitoses per high-power field and expression of immunohistological markers. Results, Complete clinical resolution was observed in 11 patients (16.9%). A significant (P < 0.001) downgrading of AK grade was observed. Complete histological resolution was achieved in 15 patients (23.1%). The number of mitoses per high-power field was reduced significantly (P < 0.001). The expression of anti-p53-antibody decreased significantly (P = 0.009), as did the expression of anti-MiB-1 antibody (P = 0.021). Conclusions, 3.0% diclofenac in 2.5% hyaluronic acid gel causes regression of signs of cancerous transformation after 3 months' therapy. [source] Co-localization of multiple ErbB receptors in stratified epithelium of oral squamous cell carcinomaTHE JOURNAL OF PATHOLOGY, Issue 3 2001Roberto Bei Abstract The expression of all four ErbB receptors was compared by immunohistochemistry, using receptor-specific polyclonal antisera, in 32 invasive, 11 in situ carcinomas, six benign lesions, and 22 samples of histologically normal mucosa adjacent to specimens of carcinoma originating from oral cavity epithelium. Among invasive and in situ carcinoma, EGFR expression was the most prevalent (in 29/32 and 8/11 cases, respectively) followed by ErbB2 (17/32 and 2/11) and ErbB4 (9/32 and 1/10), while ErbB3 was only detected in invasive tumours (12/32). Specific patterns included invasive tumours with expression of EGFR (8/32) or ErbB4 (1/32) alone, as well as different receptor combinations (EGFR+ErbB2, EGFR+ErbB4, EGFR+ErbB2+ErbB3, EGFR+ErbB2+ErbB4, and all four receptors). Simultaneous expression of three or four ErbB receptors correlated with tumour invasion (p=2.2×10,4) and localized in the intermediate epithelial cell layer of well and moderately differentiated tumours. No other significant correlation with clinico-pathological features was noticed. Some benign lesions and histologically normal mucosa adjacent to carcinomas showed weak immunostaining of EGFR (10/28), ErbB2 (4/28) or ErbB4 (3/28). By comparison, overexpression, as indicated by increased staining intensity, was observed in invasive tumours for EGFR (18/32), ErbB2 (8/32), ErbB4 (3/32), and ErbB3 (3/32). Statistical evaluation demonstrated a significant association of EGFR or ErbB2 overexpression with invasive carcinoma when compared with benign lesions and apparently normal epithelium (p=5.2×10,7 and p=5×10,3, respectively). Tumour-specific overexpression of ErbB receptors and their co-expression, most frequently involving EGFR and ErbB2, in the same cell layer of neoplastic epithelium, implicate receptor heterodimers in the pathogenesis of oral squamous carcinoma. Copyright © 2001 John Wiley & Sons, Ltd. [source] Treatment of Laryngeal Carcinomas by Laser Endoscopic Microsurgery ,THE LARYNGOSCOPE, Issue 6 2000Pierre R. Moreau MD Abstract Objectives To determine if laser endoscopic microsurgery is a reliable and appropriate approach in the treatment of laryngeal cancers. Study Design Retrospective study of 160 patients treated from 1988 to 1996 at Liège. Analysis of indication, technique, and oncologic results. Methods Glottic tumors were treated with either type I, type II, or type III cordectomy, with or without conservation of an inferior muscular band, and extended if necessary to all or part of the contralateral cord. For supraglottic cancers, an excision limited to a part of the vestibule, a trans-preepiglottic resection, or a radical supraglottic resection was carried out. Results Our corrected actuarial survival at 5 years was 97% for the 98 infiltrative glottic tumors and 100% for the 18 infiltrative supraglottic and 27 in situ carcinomas. No local recurrences were noted, in either the group of 118 infiltrating cancers (in whom two precancerous lesions were treated with a further laser excision), or in the 27 in situ carcinomas. Local control was thus 100%. One patient died of his cancer, with lung metastases after neck recurrence. Conclusions Like Steiner and Rudert, this series demonstrates the oncologic validity of this surgical approach to the treatment of unadvanced glottic tumors. Unlike these authors' study, however, strict case selection, as in cases with significant involvement of the anterior commissure, has allowed us to avoid local recurrences and consequently to avoid salvage total laryngectomies. Our experience with supraglottic cancers is too small to confirm the oncologic validity of this type of surgery but seems promising. [source] |