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  • 1
    Electronic Resource
    Electronic Resource
    Immunglobulin origin of localized nodular pulmonary amyloidosis (1972)
    Springer
    Research in experimental medicine 159 (1972), S. 75-86 
    Details
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01856034
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  • 2
    Electronic Resource
    Electronic Resource
    Diagnostic criteria and cancer risk of proliferative breast lesions (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 53 (1993), S. 59-64 
    Details
    ISSN: 0730-2312
    Keywords: Atypical hyperplasia ; breast cancer ; cancer risk ; hyperplasia ; family history ; premalignancy ; proliferative disease ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Breast cancer risk assessment in women following a benign breast biopsy is a promising area with regard to intermediate endpoint determination, and has been particularly fostered by the consensus agreement concerning the risk attributed to specific diagnoses [1]. Several recent studies have largely verified this approach [2-4], and a recent report demonstrates general agreement among most expert pathologists regarding diagnostic criteria for these lesions [5]. However, in a limited number of cases, determining exact levels of risk for individual patients has been problematic as a result of a failure by pathologists to achieve consensus on diagnostic criteria for these same lesions. This situation has arisen primarily because it is much more tenable to disagree over subjective diagnostic criteria, than it is to argue with robustly supported epidemiological data. Without agreement on reproducible diagnostic criteria, widely promulgated consensus risk estimates for these specific histologic entities are no longer applicable. In addition, those individuals who choose different diagnostic criteria for proliferative breast lesions fail to realize that the terminology, epidemiological risk estimates, and diagnostic criteria used by Dupont and Page are inexorably linked. Since the publication of the consensus statement [1], those using the terms “atypical ductal hyperplasia” and “atypical lobular hyperplasia” have by default accepted the diagnostic criteria of Dupont and Page. Therefore, surgical pathologists who desire to make use of the consensus risk estimates must familiarize themselves with diagnostic criteria for the various histologic entities that comprise proliferative disease of the breast as defined by Dupont and Page [6]. This presentation will concentrate on the importance of a combined histologic and cytologic approach to diagnose proliferative breast lesions, and will specifically focus on usual hyperplasia, atypical ductal hyperplasia, atypical lobular hyperplasia, and both ductal and lobular carcinoma in situ.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240531111
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Indicators of increased breast cancer risk in humans (1992)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 50 (1992), S. 175-182 
    Details
    ISSN: 0730-2312
    Keywords: atypical hyperplasia ; breast cancer ; cancer risk ; family history ; hyperplasia ; premalignancy ; proliferative disease ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Specific atypical histological patterns of epithelial hyperplasia (AH) indicate a medically relevant risk of breast cancer development in 5-10% of women with otherwise benign biopsies. This risk is about four times that of similar womer, i.e., of the same age and at risk for the same length of time. These relative risks are not stable with time and fall 10-15 years after detection. Absolute risk for invasive breast cancer after AH is about 10% in 10-15 years after biopsy and is most certain for perimenopausal women. Proliferative disease without atypia predicts only a slight elevation of risk with a relative risk (RR) of 1.5 to 2 times that to the general population.There is such a strong interaction between family history and AH that it is relevant to consider women with atypical hyperplasia who have a positive family history (FH) of breast cancer separately from those who do not. The absolute risk of breast cancer development in women with AH without a FH was 8% in 10 years (RR about 4), whereas those with a positive family history experienced a risk of about 20% at 15 years (RR of about10). This interaction of AH and FH has also been observed in other recent studies.Low replacement doses of conjugated estrogen after menopause do not further elevate risk beyond that identified by hostology. In our cohort of over 10,000 women who underwent benign breast biopsy in Nashville, TN, we found no association between proliferative breast disease without atypia and a first-degree FH of breast cancer; the prevalence of these lesions was 27% and 29% in women with and without such a history, respectively. Women with this family hostory did, however, have a higher prevalence of AH than did women without this history (4.8% versus 3.9%, respectively; p = 0.02). It would appear that these histologic lesions are not due to an estrogen effect, but are an unrelated phenomenon, and that FH of breast cancer is not related to the proliferative lesions associated with only slightly increased risk of breast cancer.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240501130
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    Paper (German National Licenses)
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