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Relationship between pattern of intracranial artery abnormalities on transcranial doppler and Oxfordshire Community Stroke Project clinical classification of ischemic stroke.

BACKGROUND AND PURPOSE: The Oxfordshire Community Stroke Project (OCSP) devised a simple classification for acute stroke based on clinical features only, which is of value in predicting prognosis. We investigated whether the pattern of intracranial vascular abnormalities is related to the clinical syndrome. METHODS: Patients with acute ischemic stroke were classified by a stroke physician as having total or partial anterior circulation infarct (TACI or PACI, respectively), lacunar infarct (LACI), or posterior circulation infarct (POCI). Color-coded power transcranial Doppler was done whenever possible. Intracranial arterial velocities were compared in the 4 subtypes of ischemic stroke after adjustment for age and time to transcranial Doppler. RESULTS: Middle cerebral artery velocity was abnormal (hyperemia, reduced velocity, occlusion, or focal stenosis) in 38 of 69 TACIs (55%), 50 of 171 PACIs (29%), and 20 of 236 LACIs or POCIs (8%) (P<0.001). Velocity in the A1 segment of the anterior cerebral artery was reversed in 12 of 69 TACIs (17%), 20 of 171 PACIs (12%), and 8 of 236 LACIs or POCIs (3%) (P<0.001). Basilar artery velocity was abnormal in 8 of 121 POCIs (7%) compared with 5 of 355 (1%) of the other subtypes (P=0.005). Vertebral artery velocity was abnormal (reduced velocity, occlusion, stenosis) in 20 of 121 POCIs (17%) compared with 20 of 355 others (6%) (P=0.01). CONCLUSIONS: Intracranial arterial abnormalities were related to OCSP clinical subtype. Therefore, it is possible to stratify patients according to OCSP classification in trials of new treatments in which treatment effectiveness may depend on the underlying pattern of arterial pathology and before any arterial imaging is available.

Aged↗

Therapeutic applications of angiotensin II receptor antagonists.

The renin-angiotensin system (RAS) represents today one of the most strategic targets of the therapy of cardiovascular diseases. During the last 30 years a number of more or less successful approaches to inhibit the activity of the RAS have been attempted. In particular, the use of ACE-inhibitiors has led to significant improvments in the outcom/treatment of hypertension, congestive heart failure, ischemic heart disease and nephropathies. On the other hand, Ace-inhibitors are not specifically targeted to RAS since they interfere with an enzyme with multiple different substrates. Furthermore, the inhibition of ACE does not prevent the formation of angiotensin II through alternative pathways, and thus the inhibition of RAS is often incomplete, especially under pathologic conditions stimulating RAS. For these reasons, the recent discovery of angiotensin II receptors antagonists, which selectively inhibit the action of angiotensin II at the level of the AT1 subtype receptor, is particularly attracting. This article reviews the background, the rationale and some of the clinical findings and potential applications with this new class of compounds.

Angiotensin Receptor Antagonists↗

Detection of Epstein-Barr virus sequences in Hodgkin's disease by the polymerase chain reaction.

The authors examined paraffin-embedded lymph node biopsies from 65 cases of Hodgkin's disease for the presence of Epstein-Barr virus (EBV) DNA, using the highly sensitive polymerase chain reaction technique. Overall 40% of the cases were positive for EBV DNA; there were no statistically significant differences in the frequency of EBV positivity among the different subtypes of Hodgkin's disease. These results are in agreement with those of previous studies that employed less sensitive detection techniques and suggest that EBV either is present in pathologic tissues only in some phases of the evolution of Hodgkin's disease or is a pathogenetic factor involved in only a portion of cases.

Biopsy↗

[Clinical and pathological studies on incidental renal cell carcinoma].

During the five-year period from 1985 to 1989, a total of 69 patients with renal cell carcinoma received treatment at Daisan Hospital of Jikei University School of Medicine. Among these patients, there were 23 patients (33.3%) with incidental renal cell carcinoma. These 23 cases were studied clinically and pathologically in comparison with 46 symptomatic cases. The tumor was detected by ultrasonography (US) or computed tomography (CT) conducted for the diagnosis of other diseases in 16 cases and by US included in the battery of physical examinations in the remaining 7 cases. As compared to symptomatic cases, less hematological abnormalities were found in these cases, since ESR was accelerated in only 2 cases and anemia and elevation in alpha 2-globulin level were found in none of the cases. As for diagnostic imaging, CT could detect the tumor in all of 23 cases and US in 20 out of 21 cases. Intravenous pyelography gave normal pyelograms in 4 cases. Normovascular findings were obtained by renal angiography in 2 cases. The mean largest diameter of tumors of these 23 cases was 3.9 cm, being smaller than the corresponding mean diameter of 7.7 cm for symptomatic cases. In 8 out of 23 cases tumors were small renal cell carcinoma of 2.5 cm or less in diameter. Pathologically, incidental renal cell carcinoma was characterized by small size, expansive growth pattern (INF alpha in 18 cases and INF beta in 5 cases) and prevalence of clear cell subtype (clear cell subtype in 18 cases, granular cell subtype in 2 cases and mixed cell subtype in 3 cases).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Cytokeratins in different types of human lung cancer as monitored by chain-specific monoclonal antibodies.

The expression of cytokeratins (CKs) in human lung cancer was studied using chain-specific monoclonal antibodies to CKs 4, 7, 8, 10, 13, 18, and 19. When applied to adenocarcinomas (ACs) of the lung, high levels of CKs 7, 8, 18, and 19 were detected in all tumors, while CK 4 was found in high concentrations in some ACs. CK 10 and 13 were completely absent, or only present in low numbers of cells. Small cell lung cancers (SCLCs) and lung carcinoids contained CK 18 and sometimes 8 and 19, but no CK 7 in most cases. Three out of four tumors, histologically classified as SCLC, and expressing CK 7 in a variable number of cells were found by electron microscopic studies to contain regions with AC and/or squamous cell carcinoma (SQC) differentiation. The monoclonal antibody specific for CK 7 can therefore possibly help to distinguish AC differentiation within SCLC. CKs 10 and 13 were completely absent in SCLCs and lung carcinoids, while few CK 4-positive cells were found in some SCLCs and in one lung carcinoid. Within SQCs the monoclonal antibodies revealed a pronounced heterogeneity in CK expression. CKs 4, 7, 8, 10, 13, 18, and 19 could be detected, although not evenly distributed among all tumor cells. Highly differentiated SQCs expressed high levels of the CKs specific for squamoid differentiation, i.e., CKs 4, 10, and 13 in variable numbers of cells. With decreasing histologically detectable SQC differentiation these markers were gradually lost, while the number of cells containing CKs 7, 8, 18, and 19 increased. Application of this panel of monoclonal antibodies can therefore distinguish not only the main subtypes of lung cancer, but can also indicate the degree of differentiation and the degree of heterogeneity. These findings can be used as a diagnostic aid in lung tumor pathology, which may have an impact on treatment and prognosis.

Antibodies, Monoclonal↗

[The brain dopaminergic systems: receptor heterogeneity, functional role and pharmacological regulation].

Recent advances in molecular neurobiology led to a new understanding on mammalian brain dopaminergic system which play a major role in the regulation of motor, cognitive, emotional, neuroendocrine function as well as in the pathogenesis of several pathological conditions, including neurodegenerative diseases, affective disorders, schizophrenia, drug addiction etc. Functional, biochemical and pharmacological heterogeneity of dopamine receptors, which were divided into D1-like (D1 and D5 subtypes) and D2-like (D2, D3 and D4) families of receptors has been postulated. The article reviews the recent advances including author's own results concerning the structure and function of main dopaminergic brain system, i.e. nigrostriatal and mesolimbic. The problem of autoreceptor regulation of dopaminergic neurotransmission, particularly, the processes of dopamine synthesis, release and metabolism has been specially discussed. An involvement of D2 and D3 dopamine autoreceptors in the control of these processes and differences in the mode of action of typical and atypical neuroleptics demonstrating various affinities to D2 and D3 dopamine receptors are analysed in detail. Dopamine and its metabolites have been determined on freely moving rats using brain microdialysis and high performance liquid chromatography. It is hypothesized that dopamine D3 autoreceptor is preferentially involved in the regulation of dopamine release while D2 one is responsible for the control of dopamine synthesis and metabolism in rat basal ganglia in vivo.

Amino Acid Sequence↗

[Brain dopamine receptors: structure, functional role, and modulation by psychotropic substances].

Recent advances in molecular neurobiology led to a new understanding on mammalian brain dopaminergic system which plays a major role in the regulation of motor, cognitive, emotional, neuroendocrine functions as well as in the pathogenesis of several pathological conditions, including neurodegenerative diseases, affective disorders, schizophrenia, drug addiction etc. Functional, biochemical and pharmacological heterogeneity of dopamine receptors, which were divided into D1-like (D1 and D5 subtypes) and D2-like (D2, D3 and D4) families of receptors has been postulated. The article reviews the recent advances including author's own results concerning the structure and function of main dopaminergic brain system, i.e. nigrostriatal and mesolimbic. The problem of autoreceptor regulation of dopaminergic neurotransmission, particularly, the processes of dopamine synthesis, release and metabolism has been specially discussed. An involvement of D2 and D3 dopamine autoreceptors in the control of these processes and differences in the mode of action of typical and atypical neuroleptics demonstrating various affinities to D2 and D3 dopamine receptors are analysed in detail. Dopamine and its metabolites have been determined on freely moving rats using brain microdialysis and high performance liquid chromatography. It is hypothesized that dopamine D3 autoreceptor is preferentially involved in the regulation of dopamine release while D2 one is responsible for the control of dopamine synthesis and metabolism in rat basal ganglia in vivo.

Animals↗

[Functional role and pharmacological regulation of the dopaminergic system of the brain].

The dopaminergic systems of the brain are thought to play a major role in the regulation of motor, cognitive, neuroendocrine functions and in the pathogenesis of several pathological conditions, including neurodegenerative diseases, affective disorders, schizophrenia, drug addiction, etc. Functional, biochemical, and pharmacological heterogeneity of dopamine receptors, which were divided into D1-like (D1 and D5 subtypes) and D2-like (D2, D3, and D4) families of receptors, has been postulated. The paper concerns the recent advances in the study of the structure and function of two main dopaminergic brain systems, i.e. nigrostriatal and mesolimbic. The problem of autoreceptor regulation of dopaminergic neurotransmission, particularly the processes of dopamine synthesis, release, and metabolism is discussed. The involvement of D2 and D3 dopamine autoreceptors in the control of these processes and differences in the mode of action of typical neuroleptics are analyzed. It is hypothesized that dopamine D3 autoreceptor is preferentially involved in the regulation of dopamine release while D2 one is responsible for the control of dopamine synthesis and metabolism in rat basal ganglia in vivo.

Animals↗

Interobserver agreement and reproducibility in classification of invasive breast carcinoma: an NCI breast cancer family registry study.

The United States National Cancer Institute Breast/Ovarian Cancer Family Registry is the largest international Registry of this type; over 37 724 individuals have been enrolled to date. One activity of this Registry is the semicentralized pathologic review of tumors from all probands. Given the semicentralized nature of the review, this study was undertaken to determine the reproducibility, source(s) of classification discrepancies and stratagems to circumvent discrepancies for histologic subtyping and grading of invasive breast cancer among the reviewing pathologists. A total of 13 pathologists reviewed 35 invasive breast cancers and classified them by primary and secondary histologic type, Nottingham grade and score. Lymph-vascular space invasion, circumscribed margins, syncytial growth and lymphocytic infiltrate were also evaluated. A training session using a separate set of slides was conducted prior to the study. General agreement, in terms of category-specific kappa's and percent agreement, and accuracy of classification relative to a reference standard were determined. Classification of histologic subtype was most consistent (and accurate) for mucinous carcinoma (kappa=1.0), followed by tubular (kappa=0.8) and lobular subtypes (kappa=0.8). Classification of medullary subtype was moderate (kappa=0.4), but additional evaluation of degree of lymphocytic infiltrate, syncytial growth and circumscribed margins identified most cases. Category-specific kappa's were moderate to good for Nottingham grade (kappa=0.5-0.7), with the greatest agreement obtained in categorizing grade I (kappa=0.7), and grade III tumors (kappa=0.7). A flexible classification strategy that employs individual and combined criteria provides good interobserver agreement for invasive breast cancers with uniform, unambiguous histology and compensates for classification discrepancies in the more histologically ambiguous or heterogeneous cancers.

Breast↗

Methylation of the NMDA receptor agonist L-trans-2,3-pyrrolidine-dicarboxylate: enhanced excitotoxic potency and selectivity.

This study investigated the excitotoxic properties of a novel series of NMDA analogues in which a methyl group was introduced to the 5-position of the pyrrolidine ring of L-trans-2,3-PDC, a previously identified NMDA receptor agonist. While all of these compounds induced NMDA-receptor-mediated injury, methylation increased in vivo excitotoxic potency 1000-fold. Injections (1 mu 1) in rat dorsal hippocampus of cis- and trans-5-methyl-L-trans-2,3-PDC (0.1 nmol) induced 50-70% neuronal damage to areas CA1 and CA4, comparable to that induced by 100 nmol of L-trans-2,3-PDC. Further, cis- and trans-methylated analogues induced distinct patterns of hippocampal pathology consistent with differential excitotoxic vulnerability of neurons expressing NMDA receptors. Neuronal damage produced by the 5-methyl-L-trans-2,3-PDCs could be blocked by coadministration of MK-801 (3 mg/kg ip), but not NBQX (25 nmol). Biochemical and physiological assays confirmed the action of the analogues as NMDA agonists, but did not provide an explanation for differences in excitotoxic potency between the methylated and nonmethylated 2,3-PDCs. or example, the activity of the compounds as inhibitors of 3H-glutamate binding (IC50 values: 0.4, 1.4, and 1.2 microM for cis-5-methyl-,trans-5-methyl-, and L-trans-2,3-PDC, respectively), agonists at NR1A/NR2B receptors (EC50 values: 5, 49, and 16 microM for cis-5-methyl-,trans-5-methyl-, and L-trans-2,3-PDC, respectively), and in vitro excitotoxins in cortical cultures varied only two- to fivefold as a consequence of methylation. Potential roles of NMDA receptor subtypes and transport in these effects are discussed. As potent and selective NMDA excitotoxins, cis- and trans-5-methyl-L-trans-2,3-PDC will be of value studying excitotoxic mechanisms, MDA-receptor-mediated pathology, and NMDA receptor heterogeneity.

Animals↗

[A case of systemic sclerosis with crescentic glomerulonephritis associated with perinuclear-antineutrophil cytoplasmic antibody (p-ANCA)].

A 50-year-old female with systemic sclerosis (SSc) developed rapidly progressive renal insufficiency. Laboratory findings showed rapid elevation of serum creatinine level (3.8 mg/dl) and a high titer of perinuclear-antineutrophil cytoplasmic antibody (p-ANCA) (504 EU/ml). Renal pathology revealed crescentic glomerulonephritis (CrGN) without mucoid intimal proliferation of the interlobal arteries and fibrinoid necrosis of the afferent arterioles, Immunofluorescent micrography showed focal segmental granular deposition of IgG and C 3 in the mesangium and along the capillary loop and was in agreement with pauci-immune type. Recently, a subtype of renal involvement in SSc that is associated exclusively with normotensive renal failure and recognizable by p-ANCA is suggested. On the other hand, SSc with p-ANCA-positive glomerulonephritis as this case can be considered to be overlap syndrome of SSc and microscopic polyangitis nodosa (microscopic PN) because in microscopic PN, p-ANCA is detected at the range of 50% to 80% and renal pathology reveals necrotizing glomerulonephritis. In this point, we may describe this case as a suggestive one about p-ANCA-positive glomerulonephritis.

Antibodies, Antineutrophil Cytoplasmic↗

Mucinous carcinoma of the breast: a pathologic study of 82 cases.

A series of 82 consecutive cases of mucinous carcinomas of the female breast was investigated for their clinical, morphological, and histochemical features and for the influence of some tumor characteristics on its prognosis. Two groups, a "pure" subtype (n = 58) and a "mixed" subtype (n = 24), were considered, according to the absence or the presence of concomitant areas with typical infiltrating ductal carcinoma. Eighty patients were followed with an average of 7.4 years. The actuarial survival was 58.5% at 10 years. The group of pure mucinous carcinomas showed a statistically significant better prognosis (P = 0.0007) than that of the group of mixed tumors, as well as a lower percentage of axillary nodal metastasis. Tumor dimension of both pure and mixed mucinous carcinomas influenced the prognosis, since patients with T1 tumors had longer survival than those with T2 tumors (P = 0.05) and the latter showed less mortality than T3 tumor cases (P = 0.036). Node-negative patients also had a more favorable outcome with lower mortality than node positive patients (P = 0.007). None of the T1 pure mucinous carcinomas had axillary metastasis, which may have implications for the surgical protocols. The evaluation of quantitative and qualitative content in mucosubstances did not correlate with the prognosis. However, sulfomucins were demonstrated in 30.5% of cases; this fact points to add breast carcinoma to the group of neoplasms that may present as a metastatic sulfomucin-producing adenocarcinoma.

Actuarial Analysis↗

[WHO classification of Hodgkin's lymphoma and its molecular pathological relevance].

The current WHO classification of Hodgkin's lymphoma (HL) generally distinguishes the relatively rare variant (approximately 5% of all cases of HL) of nodular lymphocyte predominant type from a second group, which comprises classical HL and is separated into four subtypes: lymphocyte rich type, nodular sclerosis type, mixed cellularity type and lymphocyte depleted type. The classical lymphocyte rich subtype is a new entity and based on the typical morphology, can be recognized by definition only by the immunohistochemical characteristics of the Hodgkin and Reed/Sternberg cells (HRS) (CD30+, CD15+, CD20-). Molecular single cell studies are consistent with the dichotomy of HL in nodular lymphocyte predominant and classical types and stress the exceptional position of the former, which shows similarities with non-Hodgkin's lymphomas in several aspects. On the molecular biology level the tumor cells of all kinds of HL turn out to be clonal B cells derived from germinal center cells. However, tumor cells of nodular lymphocyte predominant HL differ from those of classical HL by the pattern of somatic mutations. Considering the inability of HRS cells of classical HL to express a B cell receptor, they should perish under normal conditions. However, they escape from apoptosis by mechanisms so far only partially understood, such as genomic mutations of the l-kappa B gene and the fas receptor gene or probably by down-regulation of B cell markers. In rare cases, HRS cells of HL can also be derived from T cells, as could be demonstrated by single cell analysis. Also, it could be shown by single cell PCR that HL and non-Hodgkin's lymphoma of both B and T cell types can arise from a common precursor. These results suggest that future classifications of HL will not only take into account the morphological and phenotypical profile, but also mechanisms of transformation yet to be discovered.

Biomarkers, Tumor↗

Chromophobe renal cell carcinoma: comprehensive analysis of 104 cases from multicenter European database.

OBJECTIVES: To analyze the clinical behavior of chromophobe renal cell carcinoma (CRCC), we retrospectively evaluated the data from six European centers. In 1985, CRCC was identified as a new RCC histologic subtype. Because of its low frequency, only few large CRCC series are available. METHODS: We created a renal cancer database including 3228 patients who underwent surgery between 1986 and 2002 in six European centers. The relevant clinical and pathologic data were extracted from the clinical charts at each institution and collected into a unique database. RESULTS: Of the 3228 patients, 104 (3.2%) affected by CRCC were identified. The mean age at diagnosis was 57.6 years (range 22 to 83). Of the 104 patients, 51 (49%) were men and 53 (51%) were women. The mean tumor size was 6.4 +/- 3.6 cm. An incidental diagnosis accounted for 61.5% of the cases. Radical nephrectomy was performed in 88 patients (85%). After a median follow-up of 38 months (mean 44, range 1 to 153), no local recurrence was observed. The 5-year overall survival rate for CRCC was 81%. Of the 104 patients, 5 (4.8%) and 9 (8.6%) died of unrelated causes and renal cancer, respectively. CONCLUSIONS: Our series confirmed a favorable outcome for the CRCC subtype with little local aggressiveness and a low propensity for progression and death from cancer.

Adult↗

Cardioprotection specific for the G protein Gi2 in chronic adrenergic signaling through beta 2-adrenoceptors.

Two subtypes of beta-adrenoceptors, beta 1 and beta 2, mediate cardiac catecholamine effects. These two types differ qualitatively, e.g., regarding G protein coupling and calcium channel stimulation. Transgenic mice overexpressing human beta 2-adrenoceptors survive high-expression levels, unlike mice overexpressing beta 1-adrenoceptors. We examined the role of inhibitory Gi proteins, known to be activated by beta 2- but not beta 1-adrenoceptors, on the chronic effects of human beta 2-adrenoreceptor overexpression in transgenic mice. These mice were crossbred with mice where G alpha i2, a functionally important cardiac Gi alpha-subunit, was inactivated by targeted gene deletion. Survival of beta 2-adrenoreceptor transgenic mice was reduced by heterozygous inactivation of G alpha i2. Homozygous knockout/beta 2-adrenoreceptor transgenic mice died within 4 days after birth. Heterozygous knockout/beta 2-adrenoreceptor transgenic mice developed more pronounced cardiac hypertrophy and earlier heart failure compared with beta 2-adrenoreceptor transgenic mice. Single calcium-channel activity was strongly suppressed in heterozygous knockout/beta 2-adrenoreceptor transgenic mice. In cardiomyocytes from these mice, pertussis toxin treatment in vitro fully restored channel activity and enhanced channel activity in cells from homozygous G alpha i2 knockout animals. Cardiac G alpha i3 protein was increased in all G alpha i2 knockout mouse strains. Our results demonstrate that G alpha i2 takes an essential protective part in chronic signaling of overexpressed beta 2-adrenoceptors, leading to prolonged survival and delayed cardiac pathology. However, reduction of calcium-channel activity by beta 2-adrenoreceptor overexpression is due to a different pertussis-toxin-sensitive pathway, most likely by G alpha i3. This result indicates that subtype-specific signaling of beta 2-adrenoreceptor functionally bifurcates at the level of Gi, leading to different effects depending on the G alpha isoform.

Animals↗

Uroplakin-III to distinguish primary vulvar Paget disease from Paget disease secondary to urothelial carcinoma.

Paget disease of the vulva can be mimicked by several disease entities histopathologically, but most of these entities can be clinically distinguished from vulvar Paget disease. However, vulvar Paget disease is in itself a heterogeneous group of epithelial neoplasms that can be similar both clinically and histopathologically. The subtypes of vulvar Paget disease include primary Paget disease arising from a pluripotent stem cell within the epithelium of the vulva, and secondary Paget disease of the vulva. Secondary vulvar Paget disease results from spread of an internal malignancy, most commonly from an anorectal adenocarcinoma or urothelial carcinoma of the bladder or urethra, to the vulvar epithelium. We have recently proposed that these lesions be classified as primary (of cutaneous origin) or secondary (of extracutaneous origin). These subtypes can present similarly as eczematoid skin lesions and may appear similar on routine hematoxylin and eosin-stained slides. Immunohistochemical studies can help differentiate between them. Our current study includes 17 patients with a pathologic diagnosis of vulvar Paget disease. We performed a panel of immunohistochemical stains, including cytokeratin (CK) 7 and 20, carcinoembryonic antigen (CEA), gross cystic disease fluid protein-15 (GCDFP-15), and uroplakin-III (UP-III). Of these 17 patients, 14 (80%) had primary intraepithelial cutaneous Paget disease, 13 without invasion and 1 with associated invasion. Three patients had urothelial carcinoma with spread to the vulva, manifesting as secondary vulvar Paget disease. Immunohistochemically, primary vulvar Paget disease is immunoreactive for CK 7 and GCDFP-15, but uncommonly for CK 20. Vulvar Paget disease secondary to anorectal carcinoma demonstrates CK 20 immunoreactivity but is usually nonreactive for CK 7 and consistently nonimmunoreactive for GCDFP-15. Vulvar Paget disease secondary to urothelial carcinoma is immunoreactive for CK 7 and CK 20 but nonimmunoreactive for GCDFP-15. In addition, we propose the use of a new, commercially available antibody, UP-III, which is specific for urothelium and, in our experience, is immunoreactive in secondary vulvar Paget disease of urothelial origin. The distinction between these 3 types of Paget and Paget-like lesions is essential in that the specific diagnosis has a significant influence on current treatment. The difference in surgical approach to the subtypes of vulvar Paget disease justifies classifying them into distinct lesions, which may be aided by the use of immunohistochemistry, including UP-III.

Biomarkers, Tumor↗

[High-resolution CT of epidermoid carcinoma in peripheral lung fields: radiologic-pathologic correlation].

We correlated high-resolution CT (HR-CT) images of 30 surgically resected epidermoid carcinomas in peripheral lung fields with pathologic findings. We classified peripheral epidermoid carcinomas into three types based on HR-CT findings. All tumors showed a notch along their margin. Type 1 shows scanty speculations without the convergence of surrounding lung structures. Type 2, which has two subtypes, shows a spiculated border with the convergence of peripheral lung structures. Type 2a has fine irregularities in its border, while type 2b has few fine irregularities. The convergence of peripheral lung structures seen in type 2 carcinoma is caused by the presence of scar tissue within tumors. Speculations corresponded to tumor extension or lymphocytic infiltration, sometimes along pulmonary vessels or interlobular septa, and fine irregularities seen in type 2a corresponded to summation of fibrous thickening of alveolar septa. Nine tumors showed varying-sized cavities, which were caused by the circulatory disturbance and/or central necrosis seen in tumor nests. In conclusion, HR-CT images were well correlated with pathologic findings of the resected specimens; however, some type 2a tumors may mimic adenocarcinoma on HR-CT findings.

Adult↗

A proposal for the histopathological diagnosis of ductal carcinoma in situ of the breast.

BACKGROUND: As the incidence of ductal carcinoma in situ (DCIS) is increasing, it is necessary to make a guideline for the pathological examination and diagnosis of DCIS, by creating criteria based on clinical and biological aspects of the disease. METHOD: We collected biopsy specimens originally diagnosed as benign lesions, from patients who subsequently developed invasive carcinoma in the ipsilateral breast. The histology of the biopsy specimens was re-evaluated principally according to the 1995 Philadelphia Consensus on DCIS. Histopathological agreement on each biopsy specimen was made by the JBCS Study Group members under a multiviewer microscope. In the course of making conclusive agreements among the pathologists, we developed a consensus for the histopathological diagnosis of DCIS, especially non-comedo types. RESULTS: DCIS is defined as a carcinoma of ductal epithelial origin, without any evidence of stromal invasion. It is necessary to note the methods of pathologic examination required to diagnose DCIS. Stromal invasion is an important prognostic factor, and should be diagnosed with caution. Classification of proliferative ductal lesions as benign or malignant (DCIS), the subtype of DCIS (nuclear grade, architecture, and necrosis), and the histological grading of DCIS are proposed and recommended. CONCLUSION: Although we have made a new proposal according to current concepts, there are still several unresolved problems. Thus further examination and modification will be necessary in the future.

Breast Neoplasms↗