scholarly journals Canine mammary cancer

2020 ◽  
Vol 51 (4) ◽  
pp. 425-439
Author(s):  
Alejandro Clavijo-Maldonado ◽  
Enio Ferreira ◽  
Carlos Vargas-Hernández ◽  
Fredy A. Rivera-Páez

Canine mammary cancer (CMC) is one of the most common neoplasms in intact females in comparison to other species. Several risk factors have been identified, including breed, genetic predisposition, age, reproductive history, hormonal influence, diet, and body condition, in addition to previous lesions to the mammary gland, such as mammary atypical hyperplasia. An understanding of the genetic markers for the disease and a clinical approach are important for establishing a specific therapy that can allow adequate patient survivorship. Overexpression of the HER-2 gene in canines and humans is associated with a poor clinical prognosis, mainly short survivorship, although the clinical relationship is not clear. The incidence of HER-2 in female dogs can range from 29.7% to 38%. However, overexpression of HER-2 is not necessarily associated with malignancy processes of the mammary tissue, although it participates in cellular proliferation. Finally, canines remain one of the most important models for comparative oncology with humans due to the great similarity in the spontaneous presentation and development of cancer, and in the high homology in the amino acid sequence.

2011 ◽  
Author(s):  
Marlene Weichselbaumer ◽  
Josef Singer ◽  
Erika Jensen-Jarolim ◽  
Thomas Stockner ◽  
Diana Mechtcheriakova ◽  
...  

Author(s):  
Sanaz Rismanchi ◽  
Pejman Mortazavi ◽  
Samad Muhammadnejad

Background: In the last two decades, canine mammary cancer has played an essential role in human breast cancer research. There are various similarities between biological and clinical features of canine breast cancer and female breast cancer in many cases. Clinical studies and evaluation of prognostic factors in canine mammary cancer can increase reliability in generalizing results to human cancers. This study was performed in the direction of comparative oncology. Methods: We collected clinicopathological data of an invasive type of canine mammary carcinoma from clinical records and pathology reports. Age, tumor laterality, tumor size, lymph node status, and tumor grade were recorded, and the relationships between the parameters were evaluated using linear regression analysis. Results: Ninety-seven patients were included in the study, and the mean age was 10.06 ± 2.73 years. The left mammary gland was involved in 51% of cases, and pT2 was the most common tumor size. Lymph nodes were involved in 27% of patients, and 43% of tumors were grade I. Statistical analysis showed no relationship between tumor size and laterality with other clinicopathological features. However, there was a statistically significant relationship between tumor size and tumor grade, and lymph node status. As the tumor size increased, tumor grade and the risk of lymph node involvement raised. Conclusion: Similar results of this study to breast cancer in women show that canine mammary carcinoma is a suitable model in comparative oncology research. Dogs live shorter than humans so that researchers can get the results of treatment and perform survival rate assessments faster in clinical trials. By considering ethical principles, dogs with breast cancer may replace phases I and II of human clinical trials in some cancer types soon.


2020 ◽  
Vol 26 (15) ◽  
pp. 1729-1741 ◽  
Author(s):  
Seyed H. Shahcheraghi ◽  
Venant Tchokonte-Nana ◽  
Marzieh Lotfi ◽  
Malihe Lotfi ◽  
Ahmad Ghorbani ◽  
...  

: Glioblastoma (GBM) is the most common and malignant astrocytic glioma, accounting for about 90% of all brain tumors with poor prognosis. Despite recent advances in understanding molecular mechanisms of oncogenesis and the improved neuroimaging technologies, surgery, and adjuvant treatments, the clinical prognosis of patients with GBM remains persistently unfavorable. The signaling pathways and the regulation of growth factors of glioblastoma cells are very abnormal. The various signaling pathways have been suggested to be involved in cellular proliferation, invasion, and glioma metastasis. The Wnt signaling pathway with its pleiotropic functions in neurogenesis and stem cell proliferation is implicated in various human cancers, including glioma. In addition, the PI3K/Akt/mTOR pathway is closely related to growth, metabolism, survival, angiogenesis, autophagy, and chemotherapy resistance of GBM. Understanding the mechanisms of GBM’s invasion, represented by invasion and migration, is an important tool in designing effective therapeutic interventions. This review will investigate two main signaling pathways in GBM: PI3K/Akt/mTOR and Wnt/beta-catenin signaling pathways.


2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Jing Li ◽  
Ruiqin Wu ◽  
Mingo M. H. Yung ◽  
Jing Sun ◽  
Zhuqing Li ◽  
...  

AbstractThe JAK2/STAT pathway is hyperactivated in many cancers, and such hyperactivation is associated with a poor clinical prognosis and drug resistance. The mechanism regulating JAK2 activity is complex. Although translocation of JAK2 between nucleus and cytoplasm is an important regulatory mechanism, how JAK2 translocation is regulated and what is the physiological function of this translocation remain largely unknown. Here, we found that protease SENP1 directly interacts with and deSUMOylates JAK2, and the deSUMOylation of JAK2 leads to its accumulation at cytoplasm, where JAK2 is activated. Significantly, this novel SENP1/JAK2 axis is activated in platinum-resistant ovarian cancer in a manner dependent on a transcription factor RUNX2 and activated RUNX2/SENP1/JAK2 is critical for platinum-resistance in ovarian cancer. To explore the application of anti-SENP1/JAK2 for treatment of platinum-resistant ovarian cancer, we found SENP1 deficiency or treatment by SENP1 inhibitor Momordin Ic significantly overcomes platinum-resistance of ovarian cancer. Thus, this study not only identifies a novel mechanism regulating JAK2 activity, but also provides with a potential approach to treat platinum-resistant ovarian cancer by targeting SENP1/JAK2 pathway.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sibel Durlanik ◽  
Katrin Fundel-Clemens ◽  
Coralie Viollet ◽  
Heinrich J. Huber ◽  
Martin Lenter ◽  
...  

AbstractMore than 70% of colorectal, prostate, ovarian, pancreatic and breast cancer specimens show expression of CD276 (B7–H3), a potential immune checkpoint family member. Several studies have shown that high CD276 expression in cancer cells correlates with a poor clinical prognosis. This has been associated with the presence of lower tumor infiltrating leukocytes. Among those, tumor-associated macrophages can comprise up to 50% of the tumor mass and are thought to support tumor growth through various mechanisms. However, a lack of information on CD276 function and interaction partner(s) impedes rigorous evaluation of CD276 as a therapeutic target in oncology. Therefore, we aimed to understand the relevance of CD276 in tumor-macrophage interaction by employing a 3D spheroid coculture system with human cells. Our data show a role for tumor-expressed CD276 on the macrophage recruitment into the tumor spheroid, and also in regulation of the extracellular matrix modulator PAI-1. Furthermore, our experiments focusing on macrophage-expressed CD276 suggest that the antibody-dependent CD276 engagement triggers predominantly inhibitory signaling networks in human macrophages.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Sebastian R. Nielsen ◽  
Jan E. Strøbech ◽  
Edward R. Horton ◽  
Rene Jackstadt ◽  
Anu Laitala ◽  
...  

AbstractPancreatic ductal adenocarcinoma (PDAC) patients have a 5-year survival rate of only 8% largely due to late diagnosis and insufficient therapeutic options. Neutrophils are among the most abundant immune cell type within the PDAC tumor microenvironment (TME), and are associated with a poor clinical prognosis. However, despite recent advances in understanding neutrophil biology in cancer, therapies targeting tumor-associated neutrophils are lacking. Here, we demonstrate, using pre-clinical mouse models of PDAC, that lorlatinib attenuates PDAC progression by suppressing neutrophil development and mobilization, and by modulating tumor-promoting neutrophil functions within the TME. When combined, lorlatinib also improves the response to anti-PD-1 blockade resulting in more activated CD8 + T cells in PDAC tumors. In summary, this study identifies an effect of lorlatinib in modulating tumor-associated neutrophils, and demonstrates the potential of lorlatinib to treat PDAC.


Oncogene ◽  
2021 ◽  
Author(s):  
Sheng-Kai Liang ◽  
Chia-Chan Hsu ◽  
Hsiang-Lin Song ◽  
Yu-Chi Huang ◽  
Chun-Wei Kuo ◽  
...  

1999 ◽  
Vol 81 (3) ◽  
pp. 409-415 ◽  
Author(s):  
N Veldhoen ◽  
J Watterson ◽  
M Brash ◽  
J Milner

2018 ◽  
Vol 14 (1) ◽  
Author(s):  
Xóchitl Zambrano-Estrada ◽  
Brianda Landaverde-Quiroz ◽  
Andrés A. Dueñas-Bocanegra ◽  
Marco A. De Paz-Campos ◽  
Gerardo Hernández-Alberto ◽  
...  

2021 ◽  
Vol 141 (5) ◽  
pp. S62
Author(s):  
E. Pedersen ◽  
P. Harms ◽  
L. Zhao ◽  
A. Andea ◽  
M. Chan ◽  
...  

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