Role of Drug Anesthesia and Cancer

Drug Research ◽  
2017 ◽  
Vol 68 (03) ◽  
pp. 125-131 ◽  
Author(s):  
Mahmoud Moradkhani ◽  
Arash Karimi

AbstractMortality and morbidity rate among cancer patients is at an alarming rate and its ratio of incidence is increasing as a result of its effects of metastasis and recurrence in its patients. Anesthetists are faced with the challenges daily of handling and treating cancer patients, for surgical resection to removal of the primary tumor. Retrospective analyses and studies have proposed a link between anesthetic technique and cancer outcomes. In this mini-review, we will give a summary of some of the available effects of anesthetic and analgesic techniques on cancer metastasis as derived from experimental cell culture and live animal data and also from clinical studies.

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 4985
Author(s):  
Saima Usman ◽  
Naushin H. Waseem ◽  
Thuan Khanh Ngoc Nguyen ◽  
Sahar Mohsin ◽  
Ahmad Jamal ◽  
...  

Epithelial-mesenchymal transition (EMT) is a reversible plethora of molecular events where epithelial cells gain the phenotype of mesenchymal cells to invade the surrounding tissues. EMT is a physiological event during embryogenesis (type I) but also happens during fibrosis (type II) and cancer metastasis (type III). It is a multifaceted phenomenon governed by the activation of genes associated with cell migration, extracellular matrix degradation, DNA repair, and angiogenesis. The cancer cells employ EMT to acquire the ability to migrate, resist therapeutic agents and escape immunity. One of the key biomarkers of EMT is vimentin, a type III intermediate filament that is normally expressed in mesenchymal cells but is upregulated during cancer metastasis. This review highlights the pivotal role of vimentin in the key events during EMT and explains its role as a downstream as well as an upstream regulator in this highly complex process. This review also highlights the areas that require further research in exploring the role of vimentin in EMT. As a cytoskeletal protein, vimentin filaments support mechanical integrity of the migratory machinery, generation of directional force, focal adhesion modulation and extracellular attachment. As a viscoelastic scaffold, it gives stress-bearing ability and flexible support to the cell and its organelles. However, during EMT it modulates genes for EMT inducers such as Snail, Slug, Twist and ZEB1/2, as well as the key epigenetic factors. In addition, it suppresses cellular differentiation and upregulates their pluripotent potential by inducing genes associated with self-renewability, thus increasing the stemness of cancer stem cells, facilitating the tumour spread and making them more resistant to treatments. Several missense and frameshift mutations reported in vimentin in human cancers may also contribute towards the metastatic spread. Therefore, we propose that vimentin should be a therapeutic target using molecular technologies that will curb cancer growth and spread with reduced mortality and morbidity.


2021 ◽  
Vol 10 (3) ◽  
pp. 5-14
Author(s):  
N.  V. Dengina ◽  
T. V. Mitin ◽  
I.  V. Tsimafeyeu ◽  
S.  V. Usychkin

Current approaches to the treatment of patients with metastatic malignant tumors have changed significantly over the past decade. Instead of a purely palliative systemic or just supportive therapy, a large proportion of patients receive an aggressive local treatment directed not only to the primary tumor, but also to metastatic foci, and a number of studies demonstrate the advantage of such approach. This review provides information on the role of radiation therapy as a local method of treatment of cancer patients with oligometastases.


2021 ◽  
Vol 11 ◽  
Author(s):  
Soudeh Ghafouri-Fard ◽  
Amin Agabalazadeh ◽  
Atefe Abak ◽  
Hamed Shoorei ◽  
Mohammad Mehdi Hassanzadeh Taheri ◽  
...  

Tumors of the nervous system can be originated from several locations. They mostly have high mortality and morbidity rate. The emergence of resistance to chemotherapeutic agents is a hurdle in the treatment of patients. Long non-coding RNAs (lncRNAs) have been shown to influence the response of glioblastoma/glioma and neuroblastoma to chemotherapeutic agents. MALAT1, NEAT1, and H19 are among lncRNAs that affect the response of glioma/glioblastoma to chemotherapy. As well as that, NORAD, SNHG7, and SNHG16 have been shown to be involved in conferring this phenotype in neuroblastoma. Prior identification of expression amounts of certain lncRNAs would help in the better design of therapeutic regimens. In the current manuscript, we summarize the impact of lncRNAs on chemoresistance in glioma/glioblastoma and neuroblastoma.


2017 ◽  
pp. 53-58
Author(s):  
Y. A. Shelygin ◽  
S. I. Achkasov ◽  
O. I. Sushkov ◽  
A. A. Ponomarenko

AIM. To assess early results and survival in patients with CRS and IIC strategy. METHOD. 56 CRC with PC patients underwent CRS+IIC. pT4 stage occurred in 38 (67,5 %) pts. N+ status was detected in 39 (69 %) cases. In 44 (79 %) pts. carcinomatosiswas synchronous. PCI was rangedfrom 1 to 21 (Me=3). RESULTS. Mortality and morbidity rate in postoperative 30 days was 0 % and 14 %, respectively. The median disease-free survival (DFS) was 21 months. Multivariate analysis revealed that PCI (p=0,0007) and the presence of extraperitoneal metastases (p=0,0097) were independent negative predictors of DFS. The empirical analysis showed that level of PCI more than 8 was the predictor of negative prognosis (p=0,044). CONCLUSION. It has been shown that poor prognosis factors were PCI more than 8, and the presence of distant extraperitoneal metastases of CRC.


2018 ◽  
Vol 84 (5) ◽  
pp. 703-711
Author(s):  
Eung Chang Lee ◽  
Sung-Sik Han ◽  
Seung Duk Lee ◽  
Sang-Jae Park

Hepatopancreatoduodenectomy (HPD) is usually indicated for the resection of locally advanced bile duct (BD) cancer or gallbladder (GB) cancer. Previous studies have demonstrated a favorable survival rate in BD cancer patients after HPD if R0 resection is achieved. By contrast, the benefit of HPD for GB cancer remains controversial. This study aimed to analyze the outcomes of GB and BD cancer after HPD. Between January 2004 and December 2013, a total of 22 patients underwent HPD for BD (n = 14) or GB cancer (n = 8). We analyzed the survival, mortality, morbidity, and prognostic factors. After HPD, the mortality rate was 4.5 per cent and the morbidity rate was 68.2 per cent. Pancreatic fistula occurred in 50.0 per cent of the patients (grade A, 40.9%; grade B, 9.1%). Liver failure did not occur. The 1-, 3-, and 5-year survival rates for BD cancer patients were 57.1, 17.9, and 17.9 per cent and those for GB cancer patients were 62.5, 25.0, and 25.0 per cent, respectively ( P = 0.768). In BD cancer, significant prognostic factors were tumor size, portal vein invasion, multiple lymph node metastases, and operation time. Furthermore, BD cancer patients with three or more of risk factors showed poorer survival than those with fewer than three risk factors. HPD for GB and BD cancer can be performed with acceptable mortality and morbidity rates. GB cancer patients who underwent HPD showed comparable survival rates compared with BD cancer patients. Long-term survival can be achieved in selected patients with BD cancer.


Author(s):  
Jun Wen ◽  
Xuejie Min ◽  
Mengqin Shen ◽  
Qian Hua ◽  
Yuan Han ◽  
...  

Abstract Background Colon cancer is the second leading cancer worldwide. Recurrent disease and chemotherapeutic drug resistance are very common in the advanced stage of colon cancer. ATP-citrate lyase (ACLY), the first-step rate-controlling enzyme in lipid synthesis, is elevated in colon cancer. However, it remains unclear about the exact role of ACLY in the development of colon cancer metastasis. Methods To evaluate the role of ACLY in colon cancer metastasis, we performed cell migration and invasion assays in two ACLY-deficient colon cancer cell lines. Colon cancer mouse model is used to examine ACLY’s effects on colon metastasis potentials in vivo. We analyzed the correlation between ACLY and CTNNB1 protein in 78 colon cancer patients by Pearson correlation. To finally explore the relationship of ACLY and CTNNB1, we used western blots, migration and invasion assays to confirm that ACLY may regulate metastasis by CTNNB1. Results Our data showed that the abilities of cell migration and invasion were attenuated in ACLY-deficient HCT116 and RKO cell lines. Furthermore, we describe the mechanism of ACLY in promoting colon cancer metastasis in vitro and in vivo. ACLY could stabilize CTNNB1 (beta-catenin 1) protein by interacting, and the complex might promote CTNNB1 translocation through cytoplasm to nucleus, subsequently promote the CTNNB1 transcriptional activity and migration and invasion abilities of colon cancer cells. Immunohistochemical analysis of 78 colon cancer patients showed that the high expression levels of ACLY and CTNNB1 protein was positively correlated with metastasis of colon cancer. Conclusions These results shed new light on the molecular mechanism underlying colon cancer metastasis, which might help in improving therapeutic efficacy.


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