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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Inc
    The @breast journal 10 (2004), S. 0 
    ISSN: 1524-4741
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract:  Although the relationship of various breast lesions and cancer risk is complex, and is compounded by the uniqueness of each patient, numerous clinical investigations have validated the implications of specific lesions and future risk. While variations in lesion cytology, histology, and molecular biology present a challenge to the clinician in determining disease risk and formulating a management strategy for individual patients, research has yielded several guidelines. These include patient variables, such as age and menopausal status, as well as information concerning the lesion itself. Ductal carcinoma in situ (DCIS) has emerged as the central lesion against which others must be compared. Accurate diagnosis of DCIS is integral in determining the risk of local or regional future malignancy.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Histopathology 6 (1982), S. 0 
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The elucidation of molecular alterations that occur during human breast cancer progression may contribute to the development of preventative strategies. Using in situ hybridizations on a cohort of 94 biopsy lesions, quantitatively increased cyclin D mRNA expression levels were observed in only ...
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  • 4
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] We have characterized expression of the familial breast and ovarian cancer gene, BRCA1, in cases of non–hereditary (sporadic) breast cancer and analyzed the effect of antisense inhibition of BRCA1 on the proliferative rate of mammary epithelial cells. BRCA1 mRNA levels are markedly decreased ...
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    World journal of surgery 18 (1994), S. 32-38 
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Il existe chez 5 à 10 % des femmes qui ont apparemment des résultats normaux de biopsies mammaires, des aspects histologiques et cytologiques d'hyperplasie épithéliale atypique (HEA) du sein qui semblent prédire un certain risque de développer un cancer du sein. Ce risque a été estimé à 4–5 fois celui que présentent les femmes du même âge avec les mêmes autres facteurs de risque, mais qui n'ont pas de telles anomalies histo-cytologiques. Ce risque n'est cependant pas constant et semble diminuer avec le temps, rejoignant le même risques qu'ont d'autres femmes aux mêmes âges 10 à 15 ans après la première détection de ces anomalies. Le risque de voir se développer une prolifération sans atypie cellulaire, même extensive ou complexe, n'est que deux fois celui de la population en générale. L'HEA se voit souvent dans la fratrie des familles a cancer du sein, du moins chez les cousines au premier degré. Ce risque, deux fois celui de l'HEA, se situe à 20% environ 10–15 ans après la biopsie, en particulier chez les femmes de la cinquième (40–49) ou au début de la sixième (50) décennie. Ces considérations ont moins d'importance après l'âge de 60 ans. Un traitement par des oestrogènes à de faibles doses après la ménopause ne semble pas augmenter ce risque. Seuls les cancers intracanalaires in situ non comédocarcinomateux peuvent être considérés comme des lésions précancéreuses et ne nécessitent pas de traitement étendu, que nécessitent, par contre, les lésions du type comédocarcinome, même in situ. Des lésions non comédocarcinomateuses peuvent parfois devenir des cancers invasifs en 6 à 10 ans. Il faut les
    Abstract: Resumen Patrones histológicos y citológicos combinados de hiperplasia epitelial atípica (HA) en la glándula mamaria son indicativos de un riesgo de desarrollar cáncer del orden de 5 a 10% en las mujeres con lesiones por lo demás benignas. El riesgo es 4–5 veces mayor que el de mujeres de poblaciones similares que no poseen tales lesiones. Tales riesgos relativos no son estables, y disminuyen 10–15 años luego de la detección, para aproximarse a los riesgos de mujeres de edades comparables. La enfermedad proliferativa sin atipia, no importa qué tan extensa o compleja sea, predice un ligero riesgo mayor, el cual se acerca al doble del de la población de referencia. Hay una fuerte interacción de la HA con la historia familiar de cáncer mamario en por lo menos los familiaries de primer grado. Tal riesgo dobla al riesgo de HA sola, la dobla y se aproxima al 20% a los 10–15 años después de la biopsia, en particular en mujeres en las edades de los 40 y los primero 50 años, pero tales consideraciones son de menor importancia clínica en mujeres de 60 años. Los estrógenos conjugados en dosis bajas, administrados después de la menopausia, no parecieron incrementar el riesgo por encima del que fue identificado mediante patrones histológicos. Sólo el carcinoma in situ de tipo no comedo puede ser considerado como lesión precursora pero que no da lugar al tratamiento más extenso que se recomienda para el tipo más avanzado de comedo carcinoma ductal in situ. Pequeños carcinomas ductales in situ de tipo no comedo pueden resultar en carcinoma invasivo en un periodo de 6 a 10 años. Estos pueden ser tratados con resección local amplia sìn ìrradiación, pudiendose esperar que probablemente no se presentara recurrencia hasta en 8–10 años de seguimiento. Los carcinomas ductales in situ pueden ser lesiones muy extensas, y esta conducta conservadora debe ser reservada para las lesiones menores.
    Notes: Abstract Specific, combined histologic and cytologic patterns of atypical epithelial hyperplasia (AH) in the breast indicate a medically relevant risk of breast cancer development in 5% to 10% of women with otherwise benign biopsies. This risk is four to five times that of similar women without such lesions, that is, women of the same age and at risk for the same period of time. These relative risks are not stable and fall 10 to 15 years after detection, more closely approximating the risks of women of comparable age. Proliferative disease without atypia, no matter how extensive or complex, predicts only a slight elevation of risk, which approaches double that of the reference population. There is a strong interaction of AH with family history of breast cancer in at least a first degree relative. This risk doubles the risk of AH alone and is approximately 20% at 10 to 15 years after biopsy, particularly for women in their forties and early fifties. These considerations are of less clinical importance in women over age 60. Low replacement doses of conjugated estrogen after the menopause do not further elevate risk beyond that identified by histologic patterns. Noncomedo ductal carcinoma in situ may be considered a true precursor lesions; however, it differs significantly in many ways from the more advanced lesion recognized as the comedo type of ductal carcinoma in situ. Small examples of noncomedo ductal carcinoma in situ can eventuate in invasive carcinoma after 6 to 10 years. They may be treated by wide local excision without radiation, with no recurrence up to 8 to 10 years in all likelihood. Ductal carcinoma in situ lesions can be extensive within the breast, and this conservative posture should be reserved for smaller lesions.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 159 (1972), S. 75-86 
    ISSN: 1433-8580
    Keywords: Amyloid fibril protein ; Immunoglobulin light chain ; Localized amyloidosis ; Lung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The major protein of an amyloid fibril concentrate from a patient with localized nodular pulmonary amyloidosis has been purified by sequential gel filtration on Sepharose 4 B and Sephadex G-100 columns using 5 M guanidine-HCl in 1 N acetic acid. The molecular weight of 15250, unreactive amino-terminal amino acid, peptide map pattern, and immunochemical cross-reactivity with some, but not all, lambda Bence Jones proteins identifies this amyloid fibril protein as being derived primarily from the aminoterminal segment of a homogeneous lambda light polypeptide chain of an immunoglobulin protein. Although the immunoglobulin origin of amyloid fibrils has been demonstrated in several pathologic settings, this is the first example of their immunoglobulin origin in a case of amyloidosis with restricted tissue involvement.
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  • 7
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Jensen et al. reply—Since our report appeared suggesting that BRCA1 is secreted and exhibits properties of a granin1 questions have been raised about the specificity of BRCA1 antibodies, the subcellular localization of BRCA1, the significance of the granin site in BRCA1 and the plausibility ...
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  • 8
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Germline mutations in BRCA1 are responsible for most cases of inherited breast and ovarian cancer. However, the function of the BRCA1 protein has remained elusive. We now show that BRCA1 encodes a 190-kD protein with sequence homology and biochemical analogy to the granin protein family. ...
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  • 9
    ISSN: 1432-1335
    Keywords: Cancer therapy ; Inflammation ; Endothelial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract GBS toxin is a polysaccharide exotoxin produced by group BStreptococcus. This organism causes sepsis and respiratory distress in human neonates (so-called early onset disease). This disease is marked by a strong inflammatory response only in the lung, with pulmonary sequestration of granulocytes and extensive capillary endothelial damage, and occurs only during the first few days after birth. We have found that a similar inflammatory response can be induced by i.v. infusion of picomole quantities of GBS toxin in the developing vasculature of transplanted tumors in mice and can significantly retard the tumor growth. When optimum treatment with GBS toxin was started shortly after tumor implantation, a majority of tumors in the mice regressed and the mice remained tumor-free for over 5 months. Some tumors regressed in mice receiving short-term treatment with GBS toxin, but recurred after the treatment was stopped. Median survival times were extended by all regimens and all doses of GBS toxin tested. No evidence of toxicity to the vasculature of other tissues was observed. GBS toxin is being tested for cancer therapy in humans.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1335
    Keywords: Endothelial cells ; Inflammation ; Cancer therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A group B streptococcus (GBS) isolated from human neonates diagnosed with sepsis and respiratory distress (“early-onset disease”) produces a polysaccharide exotoxin (GBS toxin) that, when infused in sheep, causes lung pathophysiology similar to that seen in humans. Histological studies have demonstrated that GBS toxin induces a strong inflammatory response in the lung, with pulmonary sequestration of granulocytes and extensive capillary endothelial damage. The susceptibility of humans to GBS toxin is age-dependent and limited to about 4 days after birth. It is rarely evident thereafter. This suggests that the binding of GBS toxin to the target endothelium occurs via specific components in the developing lung endothelial cells of the newborn that are later lost. We report here that GBS toxin can also bind to developing endothelium associated with neoplasia and induce an inflammatory response. GBS toxin was shown by immunohistochemistry to bind to capillary endothelium of human large-cell carcinomas. In nude mice bearing human tumor xenografts, intravenously administered GBS toxin caused tumor necrosis and hemorrhagic lesions, and substantially inhibited the rate of growth of the tumors. In BALB/c mice bearing Madison lung tumors, GBS toxin induced an inflammatory response resulting in marked changes in tumor morphology, including vasodilation, endothelial and tumor cell necrosis, invasion of lymphocytes and macrophages, and capillary thrombosis. In these tumor models, no evidence of toxicity to the vasculature of other tissues was observed. The reported pathophysiology of GBS in human neonates, the lack of disease in non-neonates colonized with GBS, and these results suggest that GBS toxin may have potential as a well tolerated agent in cancer therapy of some human tumors.
    Type of Medium: Electronic Resource
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