The effect of surgical wounding on tumour development

1999 ◽  
Vol 25 (3) ◽  
pp. 231-243 ◽  
Author(s):  
S.O.P. Hofer ◽  
G. Molema ◽  
R.A.E.C. Hermens ◽  
H.J. Wanebo ◽  
J.S. Reichner ◽  
...  
Keyword(s):  
Tumour Development

Severe Head Injury linked to Subsequent Development of Malignant Brain Tumour within a Short Period- A Case Report

2018 ◽  
Vol 3 (2) ◽  
Keyword(s):  
Head Injury ◽  
Brain Tumour ◽  
Severe Head Injury ◽  
Case Reports ◽  
Subsequent Development ◽  
Malignant Brain Tumour ◽  
Tumour Development ◽  
Short Period ◽  
The Brain

There have been a few case reports of head injury leading to brain tumour development in the same region as the brain injury. Here we report a case where the patient suffered a severe head injury with contusion. He recovered clinically with conservative management. Follow up Computed Tomography scan of the brain a month later showed complete resolution of the lesion. He subsequently developed malignant brain tumour in the same region as the original contusion within a very short period of 15 months. Head injury patients need close follow up especially when severe. The link between severity of head injury and malignant brain tumour development needs further evaluation. Role of anti-inflammatory agents for prevention of post traumatic brain tumours needs further exploration.

P15 Gastrointestinal tumour development in irradiated neonatal and adult ApcMin/+ CHB6 F1 mice.

2001 ◽  
Vol 199 (1-2) ◽  
pp. 225-225
Author(s):  
M. ELLENDER ◽  
M. BARR ◽  
O. HOUGHTON ◽  
J. D. HARRISON ◽  
K. E. CARR
Keyword(s):  
Tumour Development

scholarly journals Fusion of immortalized myoblasts induces genomic instability that drives tumour development and progression

2019 ◽  
Vol 30 ◽  
pp. v703-v704
Author(s):  
C. Merle ◽  
J. Baud ◽  
N. Thebaud ◽  
T. Lesluyes ◽  
G. Pérot ◽  
...  
Keyword(s):  
Genomic Instability ◽  
Tumour Development

scholarly journals ROS and TGFβ: from pancreatic tumour growth to metastasis

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Chao-Hui Chang ◽  
Siim Pauklin
Keyword(s):  
Tumour Growth ◽  
Cancer Metastasis ◽  
Transforming Growth Factor ◽  
Cancer Therapeutics ◽  
Transforming Growth Factor Β ◽  
Ductal Adenocarcinoma ◽  
Cellular Processes ◽  
Tumour Development ◽  
Pancreatic Tumour ◽  
Tgfβ Signalling

AbstractTransforming growth factor β (TGFβ) signalling pathway switches between anti-tumorigenic function at early stages of cancer formation and pro-tumorigenic effects at later stages promoting cancer metastasis. A similar contrasting role has been uncovered for reactive oxygen species (ROS) in pancreatic tumorigenesis. Down-regulation of ROS favours premalignant tumour development, while increasing ROS level in pancreatic ductal adenocarcinoma (PDAC) enhances metastasis. Given the functional resemblance, we propose that ROS-mediated processes converge with the spatial and temporal activation of TGFβ signalling and thereby differentially impact early tumour growth versus metastatic dissemination. TGFβ signalling and ROS could extensively orchestrate cellular processes and this concerted function can be utilized by cancer cells to facilitate their malignancy. In this article, we revisit the interplay of canonical and non-canonical TGFβ signalling with ROS throughout pancreatic tumorigenesis and metastasis. We also discuss recent insight that helps to understand their conflicting effects on different stages of tumour development. These considerations open new strategies in cancer therapeutics.

scholarly journals Attenuated TGFB signalling in macrophages decreases susceptibility to DMBA-induced mammary cancer in mice

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Xuan Sun ◽  
Sarah M. Bernhardt ◽  
Danielle J. Glynn ◽  
Leigh J. Hodson ◽  
Lucy Woolford ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Mammary Cancer ◽  
Breast Tissue ◽  
Mammary Gland Development ◽  
Transforming Growth Factor ◽  
Cancer Susceptibility ◽  
Dominant Negative ◽  
Target Cells ◽  
Tumour Development ◽  
Gland Development

AbstractBackgroundTransforming growth factor beta1 (TGFB1) is a multi-functional cytokine that regulates mammary gland development and cancer progression through endocrine, paracrine and autocrine mechanisms. TGFB1 also plays roles in tumour development and progression, and its increased expression is associated with an increased breast cancer risk. Macrophages are key target cells for TGFB1 action, also playing crucial roles in tumourigenesis. However, the precise role of TGFB-regulated macrophages in the mammary gland is unclear. This study investigated the effect of attenuated TGFB signalling in macrophages on mammary gland development and mammary cancer susceptibility in mice.MethodsA transgenic mouse model was generated, wherein a dominant negative TGFB receptor is activated in macrophages, in turn attenuating the TGFB signalling pathway specifically in the macrophage population. The mammary glands were assessed for morphological changes through wholemount and H&E analysis, and the abundance and phenotype of macrophages were analysed through immunohistochemistry. Another cohort of mice received carcinogen 7,12-dimethylbenz(a)anthracene (DMBA), and tumour development was monitored weekly. Human non-neoplastic breast tissue was also immunohistochemically assessed for latent TGFB1 and macrophage marker CD68.ResultsAttenuation of TGFB signalling resulted in an increase in the percentage of alveolar epithelium in the mammary gland at dioestrus and an increase in macrophage abundance. The phenotype of macrophages was also altered, with inflammatory macrophage markers iNOS and CCR7 increased by 110% and 40%, respectively. A significant decrease in DMBA-induced mammary tumour incidence and prolonged tumour-free survival in mice with attenuated TGFB signalling were observed. In human non-neoplastic breast tissue, there was a significant inverse relationship between latent TGFB1 protein and CD68-positive macrophages.ConclusionsTGFB acts on macrophage populations in the mammary gland to reduce their abundance and dampen the inflammatory phenotype. TGFB signalling in macrophages increases mammary cancer susceptibility potentially through suppression of immune surveillance activities of macrophages.

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