766 Specialist oncology activity devoted to lung cancer patients compared with breast and colorectal cancer patients

Lung Cancer ◽  
1997 ◽  
Vol 18 ◽  
pp. 196
Author(s):  
N.P. O'Rourke ◽  
J. Graham ◽  
R.D. Jones
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zhou Jie ◽  
Zeng Zhiying ◽  
Li Li

AbstractUsing the method of meta-analysis to systematically evaluate the consistency of treatment schemes between Watson for Oncology (WFO) and Multidisciplinary Team (MDT), and to provide references for the practical application of artificial intelligence clinical decision-support system in cancer treatment. We systematically searched articles about the clinical applications of Watson for Oncology in the databases and conducted meta-analysis using RevMan 5.3 software. A total of 9 studies were identified, including 2463 patients. When the MDT is consistent with WFO at the ‘Recommended’ or the ‘For consideration’ level, the overall concordance rate is 81.52%. Among them, breast cancer was the highest and gastric cancer was the lowest. The concordance rate in stage I–III cancer is higher than that in stage IV, but the result of lung cancer is opposite (P < 0.05).Similar results were obtained when MDT was only consistent with WFO at the "recommended" level. Moreover, the consistency of estrogen and progesterone receptor negative breast cancer patients, colorectal cancer patients under 70 years old or ECOG 0, and small cell lung cancer patients is higher than that of estrogen and progesterone positive breast cancer patients, colorectal cancer patients over 70 years old or ECOG 1–2, and non-small cell lung cancer patients, with statistical significance (P < 0.05). Treatment recommendations made by WFO and MDT were highly concordant for cancer cases examined, but this system still needs further improvement. Owing to relatively small sample size of the included studies, more well-designed, and large sample size studies are still needed.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4696-4696
Author(s):  
Scott Davi d Ramsey ◽  
Jeannine S McCune ◽  
David K Blough ◽  
Lauren C Clarke ◽  
Cara L McDermott ◽  
...  

Abstract Chemotherapy regimens, patient factors, and the use of colony stimulating factor (CSF) influence cancer patients’ risk for febrile neutropenia (FN) when they receive myelosuppressive chemotherapy. The incidence of FN and patient factors influencing that risk are relatively unknown in community settings. Using claims from Medicare, Medicaid and two private health insurance plan enrollees linked to the Puget Sound SEER registry, we examined the incidence of FN among breast, lung and colorectal cancer patients diagnosed 2002–05 who received adjuvant chemotherapy. We used logistic regression models to determine factors influencing the risk for FN within the first chemotherapy cycle, controlling for cancer stage, age, sex, race, comorbidities, chemotherapy-regimen related FN risk (as designated by the National Comprehensive Cancer Network), CSF use, health insurance type, and surgery or radiation ≤30 days from administration of first chemotherapy. Over the time horizon, 1096 breast, 1142 lung, and 755 colorectal cancer patients received chemotherapy. The incidence of any FN in the first chemotherapy cycle was (counts per 100 recipients by high, intermediate, and low-risk myelosuppressive chemotherapy according to NCCN categories respectively) 7.36, 10.0, 4.70 for breast cancer, 17.12, 14.15, 12.22 for lung cancer, and 25.0, 8.96, 6.37 for colorectal cancer. Significant predictors (p&lt;0.05) of any FN were: breast cancer—radiation ≤ 30 days from first chemotherapy administration (OR 2.90, 95% CI 1.21–6.94), other non-black race vs. white race (OR 2.82, 95% CI 1.29–6.17), or Medicaid insurance (OR 2.31, 95% CI 1.10–4.89); lung cancer—radiation ≤ 30 days from first chemotherapy administration (OR 1.63, 95% CI 1.01–2.61), surgery ≤ 30 days from first chemotherapy administration (OR 2.08, 95% CI 1.02–4.25), Medicaid insurance (OR 2.29, 95% CI 1.08–4.84), or a Charlson comorbidity score ≥ 2 (OR 2.56, 95% CI 1.11–5.91); colorectal cancer—female gender (OR 1.86, 95% CI 1.02–3.41) or high myelosuppressive risk chemotherapy regimen (OR 7.66, 95% CI 2.95–19.89). In this analysis, predictors of FN varied between cancers. Limitations of this analysis include lack of information about chemotherapy and CSF doses, as this is not captured in the SEER registry or claims data. These results indicate that several factors may interact to influence a patient’s likelihood of developing FN in the first cycle of adjuvant chemotherapy.


2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 18037-18037
Author(s):  
P. Yang ◽  
S. Mandrekar ◽  
S. Hillman ◽  
K. Allen ◽  
J. Jett ◽  
...  

18037 Background: Platinum compounds are major chemotherapeutic agents in lung cancer and are metabolized by the glutathione pathway enzymes. We reported that genotypes of glutathione-related enzymes, especially GCLC, may be host factors in predicting survival of patients with stage IIIB/IV non-small cell lung cancer who were stable or responding from prior platinum-based chemotherapy (Yang et al., ASCO 2006). NCCTG investigators previously correlated allelic variants in 5-FU metabolizing genes with QOL in colorectal cancer patients (Sloan et al., ASCO 2004). We sought to evaluate the role of glutathione pathway genotypes on QOL. Methods: DNA samples were analyzed using 6 polymorphic DNA markers in the glutathione metabolic pathway. The contrasting genotypes in the analysis were GSTM1 and GSTT1 (null vs. present), GSTP1-I105V (AA vs. GA/GG), GSTP1-A114V (CC vs. CT/TT), GPX1 (CC vs. TT/TC), and GCLC (homozygous repeat 77 vs. heterozygous 7*). Forty-six patients completed the FACT-L and the UNISCALE QOL questionnaires at baseline and week-8, and we have results for all 6 genotypes. A clinically significant decline (CSD) in QOL was defined as a 10% decrease from baseline to week-8. A multivariate logistic regression model was used to evaluate the association of all 6 genotypes with a CSD in QOL. Results: Patients carrying the GPX1-CC genotype had a CSD in the UNISCALE (Odds Ratio (OR): 10.0; p=0.02), total FACT-L score (OR: 7.9; p=0.03), the FACT-L physical well being construct (OR: 13.7; p=0.02), and the FACT-L functional well being construct (OR: 5.3; p=0.05). Other constructs, i.e., emotional, social and family, and additional concerns were not significantly associated with the genotypes. Conclusions: Genotypes of glutathione-related enzymes, especially GPX1 may be inherited factors in predicting patients’ QOL after platinum-based chemotherapy. Further investigation to define and measure the direct or indirect effects of these genes on QOL is critical, particularly, via drug responses, toxicities, and disease recurrence. (This work was partly supported by NIH grants CA77118, CA80127, and CA84354.) No significant financial relationships to disclose.


Author(s):  
Pham Thi Bich ◽  
Nguyen Thi Van ◽  
Ta Van To ◽  
Trinh Hong Thai

Some mutations of mt-DNA which encode tRNA (mt-tRNA) were previously reported  to be associated with clinical manifestations of neuromuscular disorders syndrome. In addition, alterations of the mitochondrial genome have been suggested to contribute to mitochondrial dysfunction and tumorigenesis. Alterations in some mt-tRNA genes have also been identified in breast cancer, lung cancer and colorectal cancer. However, so far, we have not found any report on mt-tRNA gene alteration in the Vietnamese colorectal cancer patients. So that, in this study, we analyzed the alterations of some mt-tRNA genes in a group of  Vietnamese colorectal cancer patients and predicted influence of the alterations to secondary structure of tRNA based on bioinformatic tools. PCR-RFLP and DNA sequencing methods were used to screening alterations, secondary structure of tRNA was predicted in silico by using a tool of the  Vienna RNA Websuite. Results: both A12309G and A12310G of tRNALeu were identified together in two out of 98 patients, and both T12150G and C12154G of tRNAHis were indentified in one  out of 19 patients. All of these alterations were heteroplasmic and have not been reported in cancer patients. In particular, the C12154G  alteration in the DHR loop led to change of secondary structure of  tRNAHis and may affect to function of this tRNA molecule. Keywords mt-tRNA, Vietnamese colorectal cancer, PCR-RFLP, DNA sequencing References [1] http://globocan.iarc.fr/Pages/online.aspx (30/11/2017).[2] M. Brandon, P. Baldi, D.C Wallace, Mitochodrial mutations in cancer, Oncogen 25(34) (2006) 4647.[3] G. Li, YX. Duan, XB. Zhang, F Wu, Mitochondrial RNA mutations may be infrequent in hepatocellular carcinoma patients, Genet Mol Res15(2) (2016) doi: 10.4238/gmr.15027665.[4] F. Mohammed, AR. Rezaee, E. Mosaieby, M. Houshmand, Mitochondrial A12308G alteration in RNA Leu (CUN)) in colorectal cancer samples, Diagn Pathol (2015) doi: 10.1186/s13000-015-0337-6.[5] S. Datta, M. Majumder, NK. Biswas, N. Sikdar, B. Roy, Increased risk of oral cancer in relation to common Indian mitochondrial polymorphisms and Autosomal GSTP1 locus, Cancer, 110 (2007) 1999.[6] L .Wang , ZJ. Chen , YK. Zhang , HB. Le, The role of mitochondrial RNA mutations in lung cancer, Int J Clin Exp Med 8(8) (2015) 13341.[7] AR. Gruber, R. Lorenz, SH. Bernhart, R. Neubock, IL Hofacker The Vienna ARN Websuite, Nucleic Acids Res 36 (2008) 70.[8] https://blast.ncbi.nlm.nih.gov/Blast.cgi (11/2017).[9] Y. Goto, I Nonaka, S Horai, A mutation in the RNALeu (UUR) gene associated with the MELAS subgroup of mitochondrial encephalomyopathies, Nature 348(6302 (1990) 651[10] http://www.mitomap.org/MITOMAP (11/2017).[11] A. Lorenc, J. Bryk Golik P, Homoplasmic MELAS A3243G mtDNA mutation in a colon cancer sample, Mitochondrion 3(2) (2003) 119.[12] EL. Blakely, J.W Yarham , C.L. Alston , K Craig , J. Poulton , C. Brierley , SM. Park , A. Dean , JH. Xuereb , KN. Anderson , A. Compston , C. Allen , S. Sharif , P. Enevoldson , M. Wilson , SR. Hammans , DM. Turnbull , R. McFarland , RW.Taylor , Pathogenic mitochondrial tRNA point mutations: nine novel mutations affirm their importance as a cause of mitochondrial disease, Hum Mutat 34(9) (2013) 1260.[13] S. DiMauro, Mitochondrial ADN medicine, Biosci Rep 27(3) (2007) 5.[14] DC. Wallace, D. Chalkia, Mitochondrial ADN genetics and the heteroplasmy conundrum in evolution and disease”, Cold Spring Harb Perspect Biol 5(11) (2013), doi:10.1101/cshperspect. a021220  


2014 ◽  
Vol 32 (15_suppl) ◽  
pp. e18537-e18537
Author(s):  
Aritoshi Hattori ◽  
Kenji Suzuki ◽  
Keiju Aokage ◽  
Takahiro Mimae ◽  
Kanji Nagai ◽  
...  

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