Tumor growth characteristics of the Walker 256 AR tumor, a regressive variant of the rat Walker 256 A tumor

Guimarães, Fernando; Schanoski, Alessandra Soares; Cavalcanti, Tereza Cristina Samico; Juliano, Priscila Bianchi; Viera-Matos, Ana Neuza; Rettori, O

doi:10.1590/s1516-89132010000500014

Cited by 5 publications

(7 citation statements)

References 22 publications

(30 reference statements)

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“…Similar to the well-known human scenario of breast cancer regression (Lewison, 1976 ; Hutter, 1982 ; Burnside et al, 2006 ; Barry, 2009 ; Onuigbo, 2012 ), Walker 256 breast cancer cells may also potentially transform into a regressive variant in vivo (Guimarães et al, 2010 ) resulting in complete regression if the study is prolonged (Jensen and Muntzing, 1970 ; Cavalcanti et al, 2003 ; Schanoski et al, 2004 ). The mechanisms underlying spontaneous regression are not entirely clear but may involve development of an adaptive immune response (Pardoll and Topalian, 1998 ; Rees and Mian, 1999 ), differential propagation of tumor sub clones in their microenvironment (Khong and Restifo, 2002 ) and consequent elimination by immune cells, antibodies, cytokines, and chemokines (Dunn et al, 2002 , 2006 ; Bui and Schreiber, 2007 ; Jaganjac et al, 2008 ).…”

Section: Regression Of Tumor and Resolution Of Painmentioning

confidence: 91%

“…Physical activity of the animals, exercise (Hoffman et al, 1962 ; Deminice et al, 2016b ), dietary factors (Bekesi and Winzler, 1970 ; Kwong et al, 1984 ; Luty et al, 2016 ), or hormonal levels (Khegai, 2013 ; Khegay and Ivanova, 2015 ) may influence the regression of these cells or inhibit the activities driven by these cells (Campos-Ferraz et al, 2016 ; Cruz et al, 2016 ; Deminice et al, 2016a ; Fracaro et al, 2016 ; Toneto et al, 2016 ). In most studies, tumor regression is generally overlooked as the tumor-bearing rats are sacrificed before regression is evident (Guimarães et al, 2010 ). Thus, the verification of tibial tumor burden post-mortem is very important.…”

Section: Regression Of Tumor and Resolution Of Painmentioning

confidence: 99%

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The Walker 256 Breast Cancer Cell- Induced Bone Pain Model in Rats

et al. 2016

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The majority of patients with terminal breast cancer show signs of bone metastasis, the most common cause of pain in cancer. Clinically available drug treatment options for the relief of cancer-associated bone pain are limited due to either inadequate pain relief and/or dose-limiting side-effects. One of the major hurdles in understanding the mechanism by which breast cancer causes pain after metastasis to the bones is the lack of suitable preclinical models. Until the late twentieth century, all animal models of cancer induced bone pain involved systemic injection of cancer cells into animals, which caused severe deterioration of animal health due to widespread metastasis. In this mini-review we have discussed details of a recently developed and highly efficient preclinical model of breast cancer induced bone pain: Walker 256 cancer cell- induced bone pain in rats. The model involves direct localized injection of cancer cells into a single tibia in rats, which avoids widespread metastasis of cancer cells and hence animals maintain good health throughout the experimental period. This model closely mimics the human pathophysiology of breast cancer induced bone pain and has great potential to aid in the process of drug discovery for treating this intractable pain condition.

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Section: Regression Of Tumor and Resolution Of Painmentioning

confidence: 91%

Section: Regression Of Tumor and Resolution Of Painmentioning

confidence: 99%

The Walker 256 Breast Cancer Cell- Induced Bone Pain Model in Rats

et al. 2016

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“…Similar to the well-known human scenario of breast cancer regression (Barry, 2009, Hutter, 1982, Lewison, 1976, Onuigbo, 2012, Burnside et al, 2006, Walker 256 breast cancer cells may also potentially transform into a regressive variant in vivo (Guimarães et al, 2010) resulting in complete regression if the study is prolonged (Cavalcanti et al, 2003, Schanoski et al, 2004, Jensen and Muntzing, 1970. The mechanisms underlying spontaneous regression are not entirely clear but may involve development of an adaptive immune response (Pardoll andTopalian, 1998, Rees andMian, 1999), differential propagation of tumor sub-clones in their microenvironment (Khong and Restifo, 2002) and consequent elimination by immune cells, antibodies, cytokines and chemokines (Dunn et al, 2002, Dunn et al, 2006, Bui and Schreiber, 2007, Jaganjac et al, 2008.…”

Section: Regression Of Tumor and Resolution Of Painmentioning

confidence: 90%

“…Physical activity of the animals, exercise (Hoffman et al, 1962, Deminice et al, 2016b, dietary factors (Kwong et al, 1984, Bekesi and Winzler, 1970, Luty et al, 2016, DeWys et al, 1970 or hormonal levels (Khegay andIvanova, 2015, Khegai, 2013) may influence the regression of these cells or inhibit the activities driven by these cells (Cruz et al, 2016, Deminice et al, 2016a, Fracaro et al, 2016, Campos-Ferraz et al, 2016, Toneto et al, 2016. In most studies, tumor regression is generally overlooked as the tumor-bearing rats are sacrificed before regression is evident (Guimarães et al, 2010). Thus, the verification of tibial tumor burden post-mortem is very important.…”

Section: Regression Of Tumor and Resolution Of Painmentioning

confidence: 99%

“…The phenomenon of breast cancer regression is well-known in humans (Lewison, 1976, Hutter, 1982, Burnside et al, 2006, Barry, 2009, Onuigbo, 2012. Similarly, W256 breast cancer cells also have the potential to transform into a variant known for its regression in vivo (Guimarães et al, 2010), causing cancer regression with the prolonged duration of the study (Jensen and Muntzing, 1970, Cavalcanti et al, 2003, Schanoski et al, 2004.…”

Section: Trabecular Number (Tbn)mentioning

confidence: 99%

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Establishment, optimization and characterization of a rat model of breast cancer induced bone pain

Shenoy¹

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providing me necessary infrastructure, funds and all the guidance and support required throughout my PhD candidature. I will always remain very thankful to Dr Vetter who chose me as a PhD student and provided me with a life-changing opportunity of studying in Australia. My PhD project work was conducted in Professor Smith's laboratory at Centre for Integrated Preclinical Drug Development (CIPDD/TetraQ) (Centre for Clinical Research, Faculty of Medicine). I have seen Professor Smith as a strict mentor, yet certainly one of the kindest, most compassionate and revered persons I have ever met. These years of my professional associations with Professor Smith have left deep positive imprints on me, and I will cherish them for the rest of my life. Without Professor Smith's solid support throughout my candidature, I would have never seen this day of my life. Words will never be enough to express my feelings, but all I can very genuinenly say is that I have experienced the Almighty God in Professor Smith. I am grateful to Dr Kuo for his persistent support in my candidature.

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L‐glutathione 1% promotes neuroprotection of nitrergic neurons and reduces the oxidative stress in the jejunum of rats with Walker‐256‐bearing tumor

de Oliveira,

Perles,

de Souza

et al. 2023

Neurogastroenterology Motil

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AimsOur main goals were to investigate the effects of L‐glutathione (1%) treatment in Walker‐256 tumor‐bearing rats by analyzing immunoreactive neurons (IR), responsive to the nNOS enzyme and 3‐Nitrotyrosine, in their jejunum myenteric plexus. Moreover, the oxidative state and inflammatory process in these animals were investigated.MethodsFour experimental groups were utilized: control (C), control treated with L‐glutathione (CGT), Walker‐256 tumor‐bearing rats (TW), and Walker‐256 tumor‐bearing rats treated with L‐glutathione (TWGT). After 14 days of tumor inoculation, the jejunum was collected for immunohistochemical techniques and assessment of oxidative status. Plasma was collected to evaluate oxidative status and measure cytokines.ResultsThe TW group exhibited a decrease of reduced glutathione in their jejunum, which was prevented in the L‐glutathione treated TWGT group. TW animals presented pronounced oxidative stress by increasing levels of lipoperoxidation in their jejunum and malondialdehyde in their plasma; however, the L‐glutathione treatment in TWGT group was not able to avoid it. The total antioxidant capacity was altered in groups TW and TWGT, yet the last one had a better index in their plasma. The IL‐10, and TNF‐α levels increased in TWGT animals. The nNOS‐IR neuron density decreased in the jejunum myenteric plexus of the TW group, which was avoided in the TWGT group. The nNOS +3‐Nitrotyrosine neurons quantification did not show significative alterations.ConclusionThe treatment with L‐glutathione (1%) imposed an important defense to some parameters of oxidative stress induced by TW‐256, leading to neuroprotection to the loss in the nNOS‐IR neuron density.

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Tumor growth characteristics of the Walker 256 AR tumor, a regressive variant of the rat Walker 256 A tumor

Abstract: ABSTRACT

Cited by 5 publications

References 22 publications

The Walker 256 Breast Cancer Cell- Induced Bone Pain Model in Rats

The Walker 256 Breast Cancer Cell- Induced Bone Pain Model in Rats

Establishment, optimization and characterization of a rat model of breast cancer induced bone pain

L‐glutathione 1% promotes neuroprotection of nitrergic neurons and reduces the oxidative stress in the jejunum of rats with Walker‐256‐bearing tumor

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