Role of arterial occlusion in pulmonary scar cancers

Kolín, A; T, Koutoulakis

doi:10.1016/s0046-8177(88)80147-3

Cited by 40 publications

(11 citation statements)

References 16 publications

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“…28 The identification of vascular space invasion has been shown to increase when greater numbers of tumor blocks are submitted. 87 Tumor grade has the same issues as vascular space invasion in regard to the literature and inclusion of patients with different stages and tumor types. Most analysis data of an almost 2-fold larger odds ratio for lymphatic vascular space invasion compared with highest nuclear grade when tumor size and central fibrosis were treated as categoric variables.…”

Section: Discussionmentioning

confidence: 99%

Prognostic Factors in T1 NO MO Adenocarcinomas and Bronchioloalveolar Carcinomas of the Lung

Goldstein¹,

Mani²,

Chmielewski

et al. 1999

Am J Clin Pathol

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A b s t r a c tAdenocarcinoma of the lung constituted 9% of all lung carcinomas in men 30 years ago.1 During the last several decades, its incidence has been increasing. [2][3][4][5][6][7][8] It is the most common cell type in females and in nonsmoking patients, and it is the most common tumor subtype in some regions of the world. 9-14 The incidence of bronchioloalveolar carcinoma (BAC) is also increasing. 15-17Many studies have evaluated pathologic prognostic features of adenocarcinomas, including cell types, architectural patterns, and stage. The majority these studies have not specifically examined Tl NO MO adenocarcinomas. Some studies used the previous definition of a stage I carcinoma and included patients with Nl metastases, other studies grouped adenocarcinomas with non-small cell carcinomas, and many have grouped Tl with T2 carcinomas.18~38 This has left a dearth of attention directed toward identifying prognostic factors for patients with Tl NO MO adenocarcinomas and BACs that undergo curative surgical excision. Prognostic features for this group of patients are important because the 5-year disease-free survival of patients with Tl NO MO adenocarcinoma is 66% to 85%. 39^6 Separation of adenocarcinomas from other pulmonary carcinomas and examining the subset of patients with Tl disease is essential to understand the metastatic potential and prognostic strength of pathologic factors of the different tumors included under the rubric of stage I adenocarcinoma and BAC. 43 In addition, the prognostic significance of distinguishing between BAC and conventional adenocarcinoma and the threshold for amount of central fibrosis allowable within the BAC category for prognostication has not been defined fully. Finally, the identification of prognostic variables within this group of patients is important for future adjuvant therapy studies to identify the subset of patients that are at higher risk of having an adverse carcinoma-related outcome.We retrospectively studied 218 cases of completely resected, surgically staged, Tl NO adenocarcinomas and

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Section: Discussionmentioning

confidence: 99%

Prognostic Factors in T1 NO MO Adenocarcinomas and Bronchioloalveolar Carcinomas of the Lung

Goldstein¹,

Mani²,

Chmielewski

et al. 1999

Am J Clin Pathol

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“…These char acteristics may well mimic those in gastric cancer, in which cancer cells in the scirrhous portion within gastric cancer tissues showed much stronger immunoreactivity for PSTI than those in the nonscirrhous portion [7], To date, several hypotheses for the mecha nism of scar formation in lung cancer, in par ticular in pulmonary adenocarcinoma, have been proposed. It is commonly accepted that scar formation or cicatrix may occur in the development of the tumor [ 14]; this is consid ered to be caused by infarction due to arterial thrombosis [20,21], collapse of alveoli due to airway occlusion, and chronic inflammatory lung diseases [ 15,20,22], In contrast, a recent report noted that scar formation may be due to the active desmoplastic reaction of cancer cells themselves to the stromal cells [23][24][25], Growth factor-like substances derived from cancer cells have been observed to exert an effect on extracellular matrix in cancer tis sues, and thus, interaction between cancer cells and stromal cells is now regarded as a paracrine system.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical Analysis of Pancreatic Secretory Trypsin Inhibitor Expression in Pulmonary Adenocarcinoma: Its Possible Participation in Scar Formation of the Tumor Tissues

Higashiyama

Doi²,

Kodama³

et al. 1992

Tumor Biol

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The expression of pancreatic secretory trypsin inhibitor (PSTI) was examined immunohistochemically in pulmonary adenocarcinoma. Of 86 carcinomas examined, 65 (76%) showed immunoreactivity for PSTI. Cases with the papillary subtype and those with early stage disease contained PSTI in cancer cells more frequently and were more strongly positive. There was a slight tendency to strong expression of PSTI in cases with the histologically well-differentiated type, tumor size of approximately 30 mm maximum diameter, and marked scar formation. Furthermore, 37 cases, which were the majority of the PSTI-positives, appeared to contain PSTI predominantly in cancer cells within the central or subpleural scar tissue and/or its surrounding tissue. Thus, pulmonary adenocarcinoma may commonly express PSTI and, considering previous reports that PSTI acts as a growth factor-like substance on fibroblasts in vitro in addition to the present findings of its immunohistochemical distribution in the tumor tissues, it is suggested that PSTI expressed in cancer cells of some pulmonary adenocarcinomas may possibly participate in tumor scar formation.

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“…It has been reported by the writers and others (Kolin and Koutoulakis, 1988;Kolin, 1995;Pezzella et al, 1996Pezzella et al, , 1997Pezzella et al, , 2000Offersen et al, 2001) that both lung primaries and secondaries can be divided into two groups, one of which shows no histological evidence of neoangiogenesis. A pattern of non-angiogenic growth has also been described in glioblastoma multiforme (Wesseling et al, 1994).…”

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confidence: 95%

Vascular phenotype in angiogenic and non-angiogenic lung non-small cell carcinomas

Trivella²,

et al. 2002

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We have previously described a group of non-small cell lung carcinomas without morphological evidence of neo-angiogenesis. In these tumours neoplastic cells fill up the alveoli and the only vessels present appear to belong to the trapped alveolar septa. In the present study we have characterised the phenotype of the vessels present in these non-angiogenic tumours, in normal lung and in angiogenic non-small cell lung carcinomas. The vessels, identified by the expression of CD31, were scored as mature when expressing the epitope LH39 in the basal membrane and as newly formed when expressing aVb3 on the endothelial cells and/or lacking LH39 expression. In the nine putative non-angiogenic cases examined, the vascular phenotype of all the vessels was the same as that of alveolar vessels in normal lung: LH39 positive and aVb3 variable or negative. Instead in 104 angiogenic tumours examined, only a minority of vessels (mean 13.1%; range 0-60%) expressed LH39, while aVb3 (in 45 cases) was strongly expressed on many vessels (mean 55.5%; range 5-90%). We conclude that in putative non-angiogenic tumours the vascular phenotype is that of normal vessels and there is no neo-angiogenesis. This type of cancer may be resistant to some anti-angiogenic therapy and different strategies need to be developed.

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Role of arterial occlusion in pulmonary scar cancers

Cited by 40 publications

References 16 publications

Prognostic Factors in T1 NO MO Adenocarcinomas and Bronchioloalveolar Carcinomas of the Lung

Prognostic Factors in T1 NO MO Adenocarcinomas and Bronchioloalveolar Carcinomas of the Lung

Immunohistochemical Analysis of Pancreatic Secretory Trypsin Inhibitor Expression in Pulmonary Adenocarcinoma: Its Possible Participation in Scar Formation of the Tumor Tissues

Vascular phenotype in angiogenic and non-angiogenic lung non-small cell carcinomas

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