Microvessel Density and Distribution in Ductal Carcinoma In Situ of the Breast

Guidi, Anthony J.; Fischer, Lars; Harris, Jay R.; Schnitt, Stuart J.

doi:10.1093/jnci/86.8.614

Cited by 264 publications

(166 citation statements)

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“…There was also a significant negative correlation between vascular density and both the cross-sectional areas of the ducts involved and the extent of the necrosis of the tumour they contained. The last finding is in apparent conflict with the study of Guidi et al (1994), who found that comedo-type lesions were more likely to be associated with higher microvessel density. In their study, however, vessels up to 500 mm from the involved structures were included and only those from the five most vascular fields were recorded.…”

Section: Mvd (Vessels MMcontrasting

confidence: 60%

“…We therefore felt that it was reasonable to hypothesize that changes in periductal vascularity may precede the development of invasive carcinoma in DCIS. Two patterns of angiogenesis have been described in DCIS: a diffuse stromal vascularity (pattern I) and a vascular rim around the involved ducts (pattern II) (Guidi et al, 1994). Subsequently, it was proposed that pattern II resulted from angiogenic factors secreted by tumour cells and pattern I from recruitment of accessory cells, which release angiogenic factors (Engels et al, 1997a).…”

Section: Discussionmentioning

confidence: 99%

“…There have been many studies of the process of angiogenesis in breast carcinoma but most have focused on invasive disease. In DCIS and other precursor lesions (Guidi et al, 1994;Engels et al, 1997a,b;Lee et al, 1997;Lee et al, 1999;Sales et al, 1999;Valtola et al, 1999), two patterns of vascularity have been described: diffuse stromal vascularity and a vascular rim around the involved ducts. Pre-malignant lesions of the breast can induce angiogenesis in animal experimental systems and in the human breast (Gimbrone and Gullino, 1976;Brem et al, 1977;Heffelfinger et al, 1996;Lichtenbeld et al, 1998), it thus seems possible that the pattern or extent of vascularisation around DCIS may be an important factor in determining the transformation from in situ to invasive carcinoma.…”

mentioning

confidence: 99%

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Vascular density and phenotype around ductal carcinoma in situ (DCIS) of the breast

et al. 2002

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Up to 50% of recurrences of ductal carcinoma in situ of the breast are associated with invasive carcinoma but no pathological or molecular features have yet been found to predict for the development of invasive disease. For a tumour to invade, it requires the formation of new blood vessels. Previous studies have described a vascular rim around ducts involved by ductal carcinoma in situ, raising the possibility that the characteristics of periductal vascularisation may be important in determining transformation from in situ to invasive disease. Periductal vascular density and phenotype were determined using morphometry and a panel of anti-endothelial antibodies (von Willebrand factor, CD31, CD141 and CD34) and related to the presence of invasive carcinoma and other histological features. Compared to normal lobules, pure ductal carcinoma in situ exhibited a greater density of CD34 + and CD31 + vessels but a decrease in those that were immunopositive for vWF, indicating a difference in phenotype and in density. Ductal carcinoma in situ associated with invasive carcinoma showed a profile of vascular immunostaining similar to that of pure ductal carcinoma in situ but there were significantly greater numbers of CD34 + and CD141 + vessels and fewer staining for vWF. There was a significant negative correlation between vascular density and both the cross-sectional areas of the ducts involved and the extent of the necrosis of the tumour they contained. A correlation between vascular density and nuclear grade was also noted, being highest in the intermediate grade. The greater density of CD34 + and CD141 + vessels around ductal carcinoma in situ associated with invasive carcinoma could reflect a greater predisposition to invade but a direct effect of co-existent invasive carcinoma cannot entirely be ruled out in the present study. The relationship between vascular density, grade, duct size and nuclear grade suggests that periductal angiogenesis increases with tumour growth rate but is unable to keep pace with the most rapidly growing lesions.

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Section: Mvd (Vessels MMcontrasting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Vascular density and phenotype around ductal carcinoma in situ (DCIS) of the breast

et al. 2002

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“…The amount of vessels in the stroma between normal breast ducts was used as a reference in each case. We also noted if there was a dense rim of microvessels adjacent to the basement membrane of DCIS ducts (cuffing phenomenon) as earlier described by Guidi and by Engels (Guidi et al, 1994;Engels et al, 1997). The cuffing phenomenon was scored as present (defined as microvessels completely surrounding one involved duct or surrounding at least 50% of 2 or more involved ducts) or absent.…”

Section: Methodsmentioning

confidence: 97%

Tumour markers in breast carcinoma correlate with grade rather than with invasiveness

Wärnberg

Nordgren

Bergkvist³

et al. 2001

Br J Cancer

105

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Summary Ductal breast carcinoma in situ (DCIS) is regarded as a precursor to invasive breast cancer. The progression from in situ to invasive cancer is however little understood. We compared some tumour markers in invasive and in situ breast carcinomas trying to find steps in this progression. We designed a semi-experimental setting and compared histopathological grading and tumour marker expression in pure DCIS (n = 194), small invasive lesions (n = 127) and lesions with both an invasive and in situ component (n = 305). Grading was done according to the Elston-Ellis and EORTC classification systems, respectively. Immunohistochemical staining was conducted for p53, c-erbB-2, Ki-67, ER, PR, bcl-2 and angiogenesis. All markers correlated with grade rather than with invasiveness. No marker was clearly associated with the progression from in situ to invasiveness. The expression of tumour markers was almost identical in the 2 components of mixed lesions. DCIS as a group showed a more 'malignant picture' than invasive cancer according to the markers, probably, due to a higher proportion of poorly differentiated lesions. The step between in situ and invasive cancer seems to occur independently of tumour grade. The results suggest that well-differentiated DCIS progress to well-differentiated invasive cancer and poorly differentiated DCIS progress to poorly differentiated invasive cancer.

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“…A key role for VEGF in tumour biology is supported by observations of production by numerous tumour cell lines (Senger et al, 1983(Senger et al, , 1986 and immunohistochemical demonstration in human carcinomas of several tissues, including breast Anan et al, 1996), lung (Mattern et al, 1996), liver , gastrointestinal tract (Brown et al, 1993b;Takahashi et al, 1995;Maeda et al, 1996), bladder (Brown et al, 1993a, O'Brien et al, 1995, kidney (Brown et al, 1993a;Sato et al, 1994;Takahashi et al, 1994) and ovary (Boocock et al, 1995; Abu-Jawdeh et al, (Toi et al, 1993;Guidi et al, 1994;Toi et al, 1994;Takahashi et al, 1995) and between VEGF expression and prognosis in breast, gastric and bladder cancer (O'Brien et al, 1995). Use of neutralizing antibodies to VEGF or transfection with antisense VEGF cDNA have been shown to result in inhibition of growth of tumour cell lines in nude mice and inhibition of metastatic spread (Asano et al, 1995;Warren et al, 1995;Claffey et al, 1996;Saleh et al, 1996).…”

mentioning

confidence: 87%

Release of the angiogenic cytokine vascular endothelial growth factor (VEGF) from platelets: significance for VEGF measurements and cancer biology

Banks

Forbes²,

Kinsey³

et al. 1998

Br J Cancer

555

373

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Vascular endothelial growth factor (VEGF) is a potent angiogenic factor with a key role in several pathological processes, including tumour vascularization. Our preliminary observations indicated higher VEGF concentrations in serum samples than in matched plasma samples. We have now demonstrated that this difference is due to the presence of VEGF within platelets and its release upon their activation during coagulation. In eight healthy volunteers, serum VEGF concentrations ranged from 76 to 854 pg ml(-1) and were significantly higher (P < 0.01) than the matched citrated plasma VEGF concentrations, which ranged from < 9 to 42 pg ml(-1). Using platelet-rich plasma, mean (s.d.) platelet VEGF contents of 0.56 (0.36) pg of VEGF 10(-6) platelets were found. Immunocytochemistry demonstrated the cytoplasmic presence of VEGF within megakaryocytes and other cell types within the bone marrow. From examination of the effects of blood sample processing on circulating VEGF concentrations, it is apparent that for accurate measurements, citrated plasma processed within 1 h of venepuncture should be used. Serum is completely unsuitable. The presence of VEGF within platelets has implications for processes involving platelet and endothelial cell interactions. e.g. wound healing, and in tumour metastasis, when platelets adhering to circulating tumour cells may release VEGF at points of adhesion to endothelium, leading to hyperpermeability and extravasation of cells. Images Figure 4 Figure 3

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Microvessel Density and Distribution in Ductal Carcinoma In Situ of the Breast

Cited by 264 publications

References 0 publications

Vascular density and phenotype around ductal carcinoma in situ (DCIS) of the breast

Vascular density and phenotype around ductal carcinoma in situ (DCIS) of the breast

Tumour markers in breast carcinoma correlate with grade rather than with invasiveness

Release of the angiogenic cytokine vascular endothelial growth factor (VEGF) from platelets: significance for VEGF measurements and cancer biology

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