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  • 1
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    Online Resource
    Desmoplasia and its relevance to colorectal tumour invasion
    Wiley ; 1993
    In:  International Journal of Cancer Vol. 53, No. 1 ( 1993-01-02), p. 62-69
    Details
    In: International Journal of Cancer, Wiley, Vol. 53, No. 1 ( 1993-01-02), p. 62-69
    Abstract: Some invasive tumours characteristically have an abundant stroma rich in collagen, the production of which is termed the desmoplastic response. It has been suggested that this response may have a protective effect, and act to limit the process of tumour invasion. To investigate this possibility, we have examined various colorectal tumours for inter‐ and intra‐tumoural variations in the desmoplastic response. As markers of this response, the distributions of collagen‐I protein and myofibroblasts have been demonstrated by immunocytochemistry, while collagen‐I messenger RNA has been demonstrated by in situ hybridization (ISH). Evidence of a desmoplastic response was obvious in carcinomas, but not in non‐invasive adenomas. In carcinomas, we found that the response was marked in the tumour centre, where morphological features of active invasion have been reported to be absent. By contrast, we found little evidence of a desmoplastic response at the invasive edge of these carcinomas, where features suggestive of active invasion are prominent: in this location, collagen‐I immunostaining was limited and myofibroblasts were sparsely distributed or absent. While our ISH results suggested active collagen‐I synthesis in the tumour centre, there was little evidence of collagen‐I synthesis in host tissues ahead of the invasion front. On the basis of these and other reported findings, we suggest that, while the desmoplastic response may reduce the invasive activity of neoplastic cells in the tumour centre, it fails to prevent the spread of colorectal cancer because of its deficiency at the invasive edge.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v53:1
    DOI: 10.1002/ijc.2910530113
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 1993
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 2
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    Basement membrane collagen‐IV synthesis in colorectal tumours
    Wiley ; 1992
    In:  International Journal of Cancer Vol. 51, No. 4 ( 1992-06-19), p. 530-536
    Details
    In: International Journal of Cancer, Wiley, Vol. 51, No. 4 ( 1992-06-19), p. 530-536
    Abstract: Many studies suggest that increased proteolysis accounts for the epithelial basement membrane (EBM) breaks commonly seen in carcinomas. As failure to produce or maintain EBM may also be important, we chose to investigate synthesis of basement membrane collagen‐IV in human colorectal carcinomas. First, to determine the cellular origin of EBM collagen‐IV, speciesspecific antibodies were used to analyse caecal xenografts of 4 different human colorectalcarcinomaderived cell lines. The results of this study suggest an exclusively stromal cell origin for EBM collagen‐IV. Next, the distribution of periglandular myofibroblasts in carcinomas was examined, since in normal mucosa their location and ultrastructural features suggest that they play a role in EBM maintenance. They were generally abundant in normal mucosa and adenomas, but sparsely distributed in carcinomas, particularly at the invasive periphery where EBM collagen‐IV immunostaining is most deficient. Finally, the in situ hybridization technique was used to define cell populations synthesizing collagen‐IV. In normal mucosa, no collagen‐IV mRNA was detected in any component, while in carcinomas, the mRNA was clearly detectable in vascular endothelial cells but not in any other cell type. Increased vascular collagen‐IV production in carcinomas may be at least partly due to tumourinduced angiogenesis, since new bloodvessel formation requires the synthesis of new vascular basement membranes. © 1992 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v51:4
    DOI: 10.1002/ijc.2910510405
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 1992
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 3
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    Morphometric evidence that epithelial basement membrane breaks are a feature of both squamous and basal cell carcinomas of the skin
    Wiley ; 1996
    In:  International Journal of Cancer Vol. 66, No. 1 ( 1996-03-28), p. 24-28
    Details
    In: International Journal of Cancer, Wiley, Vol. 66, No. 1 ( 1996-03-28), p. 24-28
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Journal
    URL: Article
    DOI: 10.1002/(SICI)1097-0215(19960328)66:1〈〉1.0.CO;2-L
    DOI: 10.1002/(ISSN)1097-0215
    DOI: 10.1002/(SICI)1097-0215(19960328)66:1〈24::AID-IJC5〉3.0.CO;2-0
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 1996
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 4
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    Relationships between epithelial basement membrane staining patterns in primary colorectal carcinomas and the extent of tumour spread
    Wiley ; 1991
    In:  International Journal of Cancer Vol. 48, No. 6 ( 1991-07-30), p. 855-860
    Details
    In: International Journal of Cancer, Wiley, Vol. 48, No. 6 ( 1991-07-30), p. 855-860
    Abstract: In colorectal cancer an association has been found between lack of epithelial basement membrane (EBM) immunostaining in the tumour centre and more extensive malignant spread. Interestingly, ultrastructural investigations suggest that EBM loss at the tumour periphery may be part of an invasive mechanism. To further assess the significance of EBM deficiencies in different tumour areas, we carried out a detailed study of the basement membrane laminin immunostaining patterns in 130 cases of colorectal carcinoma. We find that discontinuous EBM staining in the tumour centre is associated with poor tumour differentiation (p 〈 0.005). presence of lymph‐node metastases (p 〈 0.02), and more advanced Dukes stage (p 〈 0.02). The latter association is strengthened by excluding cases in which numerous polymorphonuclear leukocytes (PMNs) are present adjacent to EBM breaks, suggesting that these inflammatory cells are a confounding factor. Discontinuous EBM staining is more frequently observed in tumour deep to muscularis propria than in submucosal tumour (p 〈 0.02). indicating intra‐tumoral variation. At the tumour periphery, extensive EBM discontinuity shows no association with lymph‐node involvement, but is linked with deeper local invasion (p 〈 0.05). While EBM staining patterns around central and peripheral tumour glands are related (p 〈 0.001). staining around peripheral glands is almost invariably more discontinuous. However, EBM lack at the tumour periphery is not as absolute as previously suggested, since in 18% of tumours fewer than 25% of peripheral tumour glands show EBM breaks. This appears consistent with the hypothesis that invasive changes at the tumour periphery are temporary and reversible.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v48:6
    DOI: 10.1002/ijc.2910480611
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 1991
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 5
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    Distribution of collagenase and tissue inhibitor of metalloproteinases (TIMP) in colorectal tumours
    Wiley ; 1991
    In:  International Journal of Cancer Vol. 49, No. 5 ( 1991-11-11), p. 666-672
    Details
    In: International Journal of Cancer, Wiley, Vol. 49, No. 5 ( 1991-11-11), p. 666-672
    Abstract: Increased collagenase activity in colorectal carcinomas has recently been shown to be associated with increased malignant potential. To determine the tissue distribution of collagenase and its specific inhibitor, tissue inhibitor of metalloproteinases (TIMP), we carried out an immunohistochemical study on colorectal carcinomas (n = 20), adenomas (n = 7) and normal mucosa (n = 6). We found increased staining for collagenase in the connective tissue stroma of carcinomas, as compared with adenomas and normal mucosa. Little evidence of epithelial cell staining for collagenase was seen in any tissue. In carcinomas, both stromal fibroblasts and collagen fibres stained strongly and stromal staining was strongest close to neoplastic glands. Vascular staining was more prominent in neoplastic than normal tissues, perhaps reflecting the increased proteolytic activity during tumour angiogenesis. The pattern of TIMP immunostaining was similar to that of collagenase, although basement membrane staining for TIMP was generally more intense. Another difference was that, unlike TIMP, staining for collagenase was often increased at the invasive edge of carcinomas, perhaps reflecting increased collagenase activity at this location.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v49:5
    DOI: 10.1002/ijc.2910490507
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 1991
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 6
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    The biological, clinical and prognostic implications of p53 transcriptional pathways in breast cancers
    Wiley ; 2010
    In:  The Journal of Pathology Vol. 220, No. 4 ( 2010-03), p. 419-434
    Details
    In: The Journal of Pathology, Wiley, Vol. 220, No. 4 ( 2010-03), p. 419-434
    Abstract: We hypothesized that the functional status of p53 transcriptional pathways, rather than p53 protein expression alone, could accurately discriminate between low‐ and high‐risk breast carcinoma (BC) and inform about individuals' tumour biological behaviour. To test this, we studied a well‐characterized series of 990 BCs with long‐term follow‐up, immunohistochemically profiled for p53, its main regulators and downstream genes. Results were validated in an independent series of patients ( n = 245) uniformly treated with adjuvant anthracycline‐based chemotherapy. Eleven p53 transcriptional phenotypes were identified with just two main clinical outcomes. (a) Low risk/good prognosis group (active/partially inactive p53 pathways), defined as p53 ± /MDM4 + /MDM2 ± /Bcl2 ± /p21 ± , p53 − /MDM4 − /MDM2 + /Bcl2 + /p21 ± and p53 ± /MDM4 − /MMD2 − /Bcl2 + /p21 ± . These tumours had favourable clinicopathological characteristics, including ER + and long survival after systemic adjuvant‐therapy (AT). (b) High risk/poor prognosis group (completely inactive p53 pathways), defined as p53 ± /MDM4 − MDM2 − /Bcl2 − /p21 − , p53 − /MDM4 − MDM2 + /Bcl2 − /p21 − and p53 ± /MDM4 − /MDM2 − /Bcl2 − /p21 + . These tumours were characterized by aggressive clinicopathological characteristics and showed shortened survival when treated with AT. Completely inactive p53 pathways but intact p21 axis p53 ± /MDM4 − /MDM2 − /Bcl2 − /p21 + had the worst prognosis, particularly patients who received AT. Multivariate Cox regression models, including validated prognostic factors for both test and validation series, revealed that the functional status of p53 transcriptional pathways was an independent prognosticator for BC‐specific survival (HR 2.64 and 4.5, p 〈 0.001, respectively) and disease‐free survival (HR 1.93 and 2.5, p 〈 0.001, respectively). In conclusion, p53 functional status determined by assessment of p53 regulatory and downstream targets provides independent prognostic value and may help determine more adequate therapeutic regimens for specific subgroups of breast cancer patients. Copyright © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Type of Medium: Online Resource
    ISSN: 0022-3417 , 1096-9896
    URL: Issue
    URL: Article
    DOI: 10.1002/path.v220:4
    DOI: 10.1002/path.2663
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2010
    detail.hit.zdb_id: 3119-7
    detail.hit.zdb_id: 1475280-3
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  • 7
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    Proposal for a modified grading system based on mitotic index and Bcl2 provides objective determination of clinical outcome for patients with breast cancer
    Wiley ; 2010
    In:  The Journal of Pathology Vol. 222, No. 4 ( 2010-12), p. 388-399
    Details
    In: The Journal of Pathology, Wiley, Vol. 222, No. 4 ( 2010-12), p. 388-399
    Abstract: We hypothesized that the interaction between mitotic index (M) and Bcl2 could accurately discriminate between low‐ and high‐grade breast cancer (BC) and provide a more objective measure of clinical outcome than histological grade, especially for patients with intermediate histological grade (G2), small size or oestrogen receptor (ER)‐negative cancers. A well‐characterized series of 1650 BCs with long‐term follow‐up was subjected to immunohistochemical analysis for Bcl2. Mitotic index (M) was assessed according to Nottingham Grading System (NGS) guidelines: M1: 〈 10 mitoses; M2: 10–18 mitoses; M3: 〉 18 mitoses. Results were validated in an independent series of patients ( n = 245) uniformly treated with adjuvant anthracycline‐based chemotherapy. Subsequently, BCs were classified according to the combined M/Bcl2 profile and compared with NGS. Multivariate Cox regression models using validated prognostic factors demonstrated that the subgroups defined by M/Bcl2 profile remained significantly associated with patients' outcome but also performed better than lymph node status and tumour size. Incorporation of the M/Bcl2 profile into the Nottingham Prognostic Index (NPI) reclassified twice as many patients into the excellent prognosis group, potentially improving decision‐making and sparing patients unneeded systemic adjuvant therapy. Patients with M2–3/Bcl2− and M3/Bcl2+ (high risk) had a two‐ to three‐fold increased risk of recurrence when treated with either adjuvant hormone therapy or anthracycline‐based chemotherapy compared with those with M1/Bcl2 ± and M2/Bcl2+ (low risk) [HR = 3.4 (2.8–5.6); p 〈 0.0001 and HR = 2.3 (1.2–4.3); p = 0.0009]. In conclusion, a grading system defined by mitotic counting and Bcl2 expression accurately reclassified patients with NGS‐G2, small tumour size or ER‐negative cancers into two groups: low risk (NGS‐G1‐like) versus high risk (NGS‐G3‐like) of BC mortality and recurrence, improving prognosis and therapeutic planning. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Type of Medium: Online Resource
    ISSN: 0022-3417 , 1096-9896
    URL: Issue
    URL: Article
    DOI: 10.1002/path.v222:4
    DOI: 10.1002/path.2775
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2010
    detail.hit.zdb_id: 3119-7
    detail.hit.zdb_id: 1475280-3
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  • 8
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    Understanding the HER family in breast cancer: interaction with ligands, dimerization and treatments
    Wiley ; 2010
    In:  Histopathology Vol. 56, No. 5 ( 2010-04), p. 560-572
    Details
    In: Histopathology, Wiley, Vol. 56, No. 5 ( 2010-04), p. 560-572
    Abstract: Barros F F T, Powe D G, Ellis I O & Green A R
(2010) Histopathology 56 , 560–572 Understanding the HER family in breast cancer: interaction with ligands, dimerization and treatments Breast carcinoma is the most frequent type of cancer affecting women. Among the recently described molecular and phenotypic classes of breast cancer, human epidermal growth factor receptor 2 (HER2)‐positive tumours are associated with a poor prognosis. HER2 plays an important role in cancer progression being targeted to provide predictive and prognostic information. Moreover, HER2 is related to cancer resistance against a variety of therapies; however, trastuzumab (herceptin) has proved successful in treatment of this subgroup. Nevertheless, resistance to this drug may be acquired by patients after a period of treatment, which indicates that other molecular mechanisms might influence success of this therapy. Dimerization between members of the HER family may contribute to resistance against treatments due to different combinations that trigger different downstream pathways. This is promoted by ligands, which are expressed as transmembrane precursor protein molecules and have a conserved epidermal growth factor‐like domain. Through resistance to trastuzumab, other drugs are being developed to interact in different domains of HER2 protein. It might be a good strategy to apply new drugs simultaneously to trastuzumab due to act in different domains of HER2. The study of interaction between receptors/ligands will characterize specifically their signalling pathway and understand which strategy to acquire.
    Type of Medium: Online Resource
    ISSN: 0309-0167 , 1365-2559
    URL: Issue
    URL: Article
    DOI: 10.1111/his.2010.56.issue-5
    DOI: 10.1111/j.1365-2559.2010.03494.x
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2010
    detail.hit.zdb_id: 2006447-0
    detail.hit.zdb_id: 131914-0
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  • 9
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    Histological grading of breast cancer on needle core biopsy: the role of immunohistochemical assessment of proliferation
    Wiley ; 2010
    In:  Histopathology Vol. 57, No. 2 ( 2010-08), p. 212-219
    Details
    In: Histopathology, Wiley, Vol. 57, No. 2 ( 2010-08), p. 212-219
    Abstract: Kwok T C, Rakha E A, Lee A H S, Grainge M, Green A R, Ellis I O & Powe D G
(2010) Histopathology 57 , 212–219 Histological grading of breast cancer on needle core biopsy: the role of immunohistochemical assessment of proliferation Aims:  Histological grade assessed on needle core biopsy (NCB) moderately concurs with the grade in the surgical excision specimen (SES) (κ‐values between 0.35 and 0.65). A major cause of the discrepancy is underestimation of mitoses in the NCB specimen. The aim was to determine the best method of assessing proliferation on NCB. Methods and results:  Proliferative activity of 101 invasive carcinomas of the breast on NCB and SES was assessed using mitotic counts on routine haematoxylin and eosin (H & E) sections and immunohistochemical markers Mib‐1 and phosphorylated histone H3 (PPH3). H & E mitotic count in SES was considered as the gold standard. H & E mitotic count was found to be underestimated on NCB when compared with that in SES ( P   〈  0.001), but no significant difference was detected between NCB and SES regarding Mib‐1 ( P  = 0.13) or PPH3 ( P  = 0.073). Using receiver–operating characteristic curve, Mib‐1 on NCB was found to agree with the gold standard significantly better than routine H & E on NCB. Conclusions:  Immunohistochemical markers in NCB showed better concordance with H & E mitotic count in SES (gold standard) than routine H & E mitotic count in NCB. Further refinement of cut‐offs and scoring methods is needed.
    Type of Medium: Online Resource
    ISSN: 0309-0167 , 1365-2559
    URL: Issue
    URL: Article
    DOI: 10.1111/his.2010.57.issue-2
    DOI: 10.1111/j.1365-2559.2010.03620.x
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2010
    detail.hit.zdb_id: 2006447-0
    detail.hit.zdb_id: 131914-0
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  • 10
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    Online Resource
    Biologic and Clinical Characteristics of Breast Cancer With Single Hormone Receptor–Positive Phenotype
    American Society of Clinical Oncology (ASCO) ; 2007
    In:  Journal of Clinical Oncology Vol. 25, No. 30 ( 2007-10-20), p. 4772-4778
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 25, No. 30 ( 2007-10-20), p. 4772-4778
    Abstract: Response to endocrine therapy in breast cancer correlates with estrogen receptor (ER) and progesterone receptor (PgR) status. It is usually easier to decide treatment strategies in cases of double-positive/-negative phenotypes than in single-positive tumors. Patients and Methods We have examined a large and well-characterized series of primary invasive breast carcinoma (1,944 cases) with long-term clinical follow-up and hormone therapy data. Patients were stratified according to ER and PgR expression and the study was focused on the single-positive groups (ER–/PgR+ and ER+/PgR–), to assess their main features and evaluate any prognostic and predictive difference between them and compare them with the double-positive/-negative tumors. Results ER+/PgR–tumors were found more frequently in elderly, postmenopausal women. The majority were grade 2 ductal/no specific type carcinomas. There was no difference between the two groups with regard to lymph node stage. Survival analyses showed no difference between the two groups in terms of disease-free interval and overall survival. However, when compared with the double-negative phenotype, ER+/PgR–showed an association with better outcome but no such survival advantage was detected in case of ER–/PgR+ tumors. In the group of patients with ER+ tumors who received adjuvant hormonal therapy, absence of PgR (ER+/PgR–) was an independent predictor of development of recurrence and shorter survival and, hence, poorer response to hormonal therapy. Conclusion ER+/PgR–and ER–/PgR+ tumors are biologically and clinically distinct groups of breast cancer that may require different treatment strategies with ER–/PgR+ exhibiting more aggressive behavioral characteristics.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2007.12.2747
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2007
    detail.hit.zdb_id: 2005181-5
    detail.hit.zdb_id: 604914-X
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