Laparotomy and laparoscopy differentially accelerate experimental flank tumour growth

Costa, M. L. Da; Redmond, H. P.; Finnegan, N.; Flynn, Michael G.; Bouchier‐Hayes, David

doi:10.1046/j.1365-2168.1998.00853.x

Cited by 106 publications

(78 citation statements)

References 32 publications

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“…In addition, removal of the primary tumour, a source of the endogenous angiogenesis inhibitor, angiostatin, may remove a 'brake' on metastatic growth (O'Reilly et al, 1997). Previously, we have shown that the surgical insult accelerates the growth of the primary tumour and increases pulmonary metastases (Da Costa et al, 1998;Pidgeon et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…In most cancer patients, metastases are already present at time of diagnosis (Fidler and Ellis, 1994) and while surgery remains the mainstay of treatment for primary tumours it may paradoxically enhance growth of residual or metastatic disease (Da Costa et al, 1998;Pidgeon et al, 1999;Demichelli et al, 2001). This may occur as a consequence of an alteration in the balance between pro-and antiangiogenic factors as part of the healing process and removal of the tumour can of itself stimulate tumour growth by removing the source of angiostatin (O'Reilly et al, 1997).…”

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confidence: 99%

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Antimetastatic activity of a cyclooxygenase-2 inhibitor

et al. 2004

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Cyclooxygenase-2 (COX-2) expression is increased in breast cancer and surgery has been shown to increase the growth of metastatic tumours. We investigated the effect of selective COX-2 inhibition on the growth of metastases in either an experimental metastasis model or following excision of a murine primary breast tumour. 50 000 4T1 mammary carcinoma cells were injected into the mammary fat pad of female BALB/c mice. When the mean TD reached 870.4 mm, tumours were excised and the mice were randomised into two groups (n ¼ 12 per group) to receive daily intraperitoneal injections of the selective COX-2 inhibitor, SC-236 or drug vehicle for 14 days. Alternatively, experimental metastases were established by tail-vein injection of 50 000 4T1 cells. Mice received either the selective COX-2 inhibitor, SC-236 or drug vehicle for 14 days (n ¼ 12 per group). SC-236 treatment significantly reduced tumour burden, the number and size of spontaneous metastases following primary tumour excision. SC-236 treatment also reduced tumour burden, the number and size of experimental metastases. Immunohistochemical staining demonstrated that COX-2 inhibition reduced microvessel density and increased apoptosis within both spontaneous and experimental metastases. These data clearly demonstrate that the selective COX-2 inhibitor, SC-236, has potent antimetastatic activity against both spontaneous metastases arising following primary tumour excision and experimental metastases.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Antimetastatic activity of a cyclooxygenase-2 inhibitor

et al. 2004

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“…Extensive clinical and experimental evidence indicates that tumor removal adversely alters the growth kinetics of residual neoplasia (11)(12)(13)(14)(15)(16)(17)(18). Tumor cell proliferation is increased in local tumor recurrences following curative-intent excisional surgery (3,7).…”

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confidence: 99%

Phosphoinositide 3-Kinase Accelerates Postoperative Tumor Growth by Inhibiting Apoptosis and Enhancing Resistance to Chemotherapy-induced Apoptosis

Coffey¹,

Wang²,

Smith³

et al. 2005

Journal of Biological Chemistry

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Tumor removal remains the principal treatment modality in the management of solid tumors. The process of tumor removal may potentiate the resurgent growth of residual neoplastic tissue. Herein, we describe a novel murine model in which flank tumor cytoreduction is followed by accelerated local tumor recurrence. This model held for primary and recurrent tumors generated using a panel of human and murine (LS174T, DU145, SW480, SW640, and 3LL) cell lines and replicated accelerated tumor growth following excisional surgery. In investigating this further, epithelial cells were purified from LS174T primary and corresponding recurrent tumors for comparison. Baseline as well as tumor necrosis factor apoptosis-inducing ligand (TRAIL)-induced apoptosis were significantly reduced in recurrent tumor epithelia. Primary and recurrent tumor gene expression profiles were then compared. This identified an increase and reduction in the expression of p110␥ and p85␣ class Ia phosphoinositide 3-kinase (PI3K) subunits in recurrent tumor epithelia. These changes were further confirmed at the protein level. The targeting of PI3K ex vivo, using LY294002, restored sensitivity to TRAIL in recurrent tumor epithelia. In vivo, adjuvant LY294002 prolonged survival and significantly attenuated recurrent tumor growth by greatly enhancing apoptosis levels. Hence, PI3K plays a role in generating the antiapoptotic and chemoresistant phenotype associated with accelerated local tumor recurrence.

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“…Hence, any disruption of immune function as a result of surgery can also lead to potentiating tumour growth. Interestingly, this immuno-suppression is greater dependent on the extent of surgery (Da Costa, 1998;. The immunosuppressive effects of surgery can last anywhere from between 4 to 14 days depending on the size of surgical trauma induced but peaks day three post-operatively in most cases.…”

Section: Mechanisms Of Surgery Induced Tumourigenesismentioning

confidence: 99%