Pathologica pulmonis cancer quaestio
Perhaps it is because of the direct feeling of the respiratory system. As the haze continues, we feel more and more people suffering from lung cancer around us. Indeed, lung cancer is the fastest growing malignant tumor in the world. The incidence and mortality of pulmonis cancer, are the first among men, and the incidence and mortality of women are the second. Every year on November 17th is the “International Lung Cancer Day”, and 2015 is the “First Year of Precision Medicine”. We hope that on this special day, we will pass on more lung cancer knowledge to people with lung cancer patients around us: lung cancer is not Incurable disease, scientific prevention and treatment of lung cancer, starting from understanding lung cancer.
Causas de pulmone cancer
The main causes of lung cancer include smoking, environmental pollution, occupational exposure, chronic lung disease, and genetic susceptibility. Among them, smoking is the first high-risk factor for the incidence of lung cancer. More than 80% of lung cancers are considered to be caused by smoking, and smokers are more than 10 times more likely to develop lung cancer than non-smokers. Women who do not smoke will have a 30% increased risk of lung cancer because their husband smokes. In particular, the “three 20” population, that is, people who have smoked for more than 20 years, people who have started smoking before the age of 20, and people who smoke more than 20 cigarettes a day are all high-risk groups for lung cancer. Because of very high number of smoker’s in India, incidence of lung cancer here is very high.
Environmental factores quasi fumantis occupational nuditate, et environmental pollutio et non aliud 'Sclerotium cepivorumFludioxonil' pro geneticae et alia backgrounds, exempli gratia, aliqui conveniant in "tres XX" condiciones, sed non pulmone cancer erit, cum aliorum Carmina pulmonis cancer. Genere discrimen vocetur "suscipiendi imperator".
Pathologica pulmonis cancer susceptibilitatem
Significat quod ex potentia suscipiendi geneticae ex geneticae factores, vel ex defectu virtutis certum, quod habet naturam entis prone ut quidam morbo. Sicut supra dictum est, in diversis hominibus eiusdem fumigant quantum, et qui non develop aliqui develop cancer pulmonis cancer pulmonis. Et hoc determinari potest a geneticae passiones. Geneticae et alia est magna passiones pulmonis cancer pulmonis cancer investigationis agro. Maxime cum pulmone cancer sunt ad geneticae factores nisi recta quaedam familiaria pulmonis cancer, per investigationis et analysis modos pestis-wide consociatio, scientists have found aliquam aliam rationem loci et ad geneticae susceptione de pulmone cancer.
Cytochrome P450 A familia est momenti oxidative metabolismi enzyme involvit in in metabolismi de pluribus amet mauris. Familia membra habet multa, CYP1A1, CYP1B1, CYP2D6 et CYP2A13, multiple sites ut sunt super genes consociata cum periculo pulmonis cancer. Hoc ad metabolicae chimicis resultant facultatem environmental scelerisque et adduxistis in corpore sicut fumigantium istorum, populus cum pauper plus verisimile ad esse metabolismi facultatem, ut polycyclic aromatizans hydrocarbonum substantiae ut accumula (FI), pulmone TEXTUS, quae potest esse causa damnum.
In addition, a cohort study of 5,739 patients with sporadic lung cancer and 5,848 healthy controls controlled the genetic susceptibility site at the rs2736100 (TERT) site on chromosome 5, and the TT genotype at this site was associated with a high incidence of lung cancer. TERT is a telomerase reverse transcriptase, under physiological conditions, it inhibits tuberculum production, but mutants may lose or reduce the function of the enzyme, thereby prone to tumors.
Certe multae adhuc studia ad pulmonis cancer suscipiendi imperator, ubi pauci. Ideo creditum est quod per altiorem investigationem, Picea genes erit be identified magis pulmonis cancer, et illa necessitudine inter sensitivo situs, et si casus ferat etiam patefacturus erat paulatimque pulmonis cancer.
Subtilitas pulmonis cancer in medicina
“Precision medicine” is an emerging method of disease prevention and treatment, which is based on understanding the individual’s genes, environment and lifestyle. At present, precision medicine is the most mature, or the most effective, is cellula parva non-pulmonis cancer (NSCLC), which accounts for more than 80% of lung cancer. Surgery is still the most effective treatment, but it is only suitable for a small number of patients with non-localized metastases in NSCLC, and many patients will still relapse after surgery. In recent years, the role of epidermal growth factor receptor (EGFR) in the tumorigenesis of lung cancer and targeted therapy for EGFR are gradually being clinically recognized. Clinically reasonable screening of EGFR targeted therapy targets and determination of test results play an extremely important role in treatment The important role becomes the key to treatment. At the same time, KRAS and BRAF mutations and ALK gene rearrangement and the role of PD-L1 gene in lung cancer targeted therapy have also been gradually recognized clinically.
EGFR
Epidermal growth factor receptor (EGFR) and its family members play an important carcinogenic role by regulating cell proliferation, apoptosis, migration and tumor angiogenesis. Changes in EGFR signaling molecules involve the occurrence and development of various malignant tumors. Although the mechanism by which EGFR mutations cause cancer is not fully understood, it is clear that EGFR mutations can enhance tyrosine protein kinase activity.
In Civitatibus Foederatis Americae et Asia, circa XXXV% quod X% de aegris cum pulmone cancer est non-parva cellula EGFR mutationes. Hae mutationes maxime fieri in exons 10-35, XIX de quibus de XC% of mutations sunt exon exons et indice deletionum. XXI Filius L18R punctum mutationem. Hae mutationes crescat EGFR operatio enzyme, ex in in amni de activation signalling tractuum. In maxime casibus saepe comitatus per alia genera mutationes et mutationibus EGFR rearrangements, ut KRAS mutationum et rearrangements ALK.
At present, the molecular targeted drugs developed for EGFR are mainly divided into two categories: 1. Small molecule tyrosine kinase inhibitors (TKI), such as gefitinib and erlotinib, and icotinib independently developed in China , The three can inhibit the activity of tyrosine kinase in EGFR intracellular domain; 2. Monoclonal antibody drugs (mAb), such as cetuximab and panitumumab, both of which bind to the extracellular domain of EGFR, blocking depends on EGFR activation of the ligand. The above drugs block EGFR-mediated intracellular signaling pathways through intracellular and extracellular pathways, respectively, thereby inhibiting tumor cell growth and migration, promoting tumor cell apoptosis, and increasing chemotherapy sensitivity.
RADO
RAS is a common oncogene in human tumors. The genes associated with human tumors in the RAS gene family are composed of K-ras, H-ras and N-ras. Among them, K-ras (v-Ki-ras2 murine Kirsten sARCOMA virus oncogene The highest mutation rate of homologues is 17-25%; at the same time, the K-ras gene is also the oncogenic gene with the highest mutation frequency in all tumors, and about 10-20% of tumors are related to the abnormal activation of K-ras. Can control the path of cell growth; when abnormal, it causes the cell to continue to grow and prevent apoptosis, which in turn leads to cancer.
K-ras dapibus moderator est etiam a key in in amni de EGFR signaling pathway. Post gene mutationem de K-ras, id est semper esse activated state, et non est qui stabat super aquas fluminis signum affectus EGFR. In hoc statu, curatio cum medicinae EGFR targeted est irritum. Plurrimi vulgaris via carcinogenic mutations in gene est punctum K-ras mutationes in codons XII, XIII, et LXI ad N, termini, Lepisosteus XII mutationes sunt maxime communia.
FRATER
BRAF (Mus musculus SARCOMA filter toxin (v-L.) carcinogen homologum B1) gene est, iv
et hujusmodi sunt decurrent atque KRAS in EGFR signalling continuati semitae encodes est serine / protein MAPK in via. In RAS enzyme transduces ut signum de MEK1 / II, et sic fit particeps reguntur variis vicibus certe in cellula.
Investigationis coetus domi et foris referunt BRAF has diversas rationes mutationes in pulmone cancer. Hae mutationes occurrit maxime in regione activation exon XV: et circa XCII% of earum sitae sunt in MDCCXCIX sumptibus JG (T ad mutationem A): inde patet in substitutione glutamic acidum (V15E) est encoded valine. Aegris ut faciam hanc mutationem potest develop musculus medicinae ut cetuximab vi resistentiae coniunctas.
Verofinil is a non-receptor tyrosine kinase inhibitor that selectively inhibits the BRAF protein located at the entrance of the MAPK / ERK pathway. Approved for the treatment of malignant melanoma, it is the first approved tyrosine kinase inhibitor for tumors carrying the BRAF (V600E mutation) gene. Clinical trials have shown that the drug has an effective rate of 42.9% for patients with this melanoma, but is basically ineffective for those who have not been mutated.
ALK
The ALK (anaplastic lymphoma kinase) gene encodes a receptor tyrosine kinase and belongs to the insulin receptor superfamily. ALK proteins play an important role in brain development and can affect the nervous system of specific neurons. FDA approves ZYKADIA for patients with metastatic non-small cell lung cancer who have ALK positive progression or cannot use crizotinib, and crizotinib (XALKORI) is approved by the FDA for ALK positive non-small cell lung cancer patient. Rearranged ALK accounts for 5% of the incidence of NSCLC. In 2010, the New England Journal of Medicine reported that 82 of 1001 lung cancers were ALK-positive medications, with an effective rate of 60.8%. 347 patients with ALK positive (including platinum-based chemotherapy failure) randomized to receive crizotinib and chemotherapy significantly improved the proportion of tumor control.
Orci iudiciis et ostensum est, quod postquam per ceritinib per CLXXX aegris cum ALK, quoddam non-parva cellula pulmonis cancer, LX% de aegris qui effective medicamento reactiones, quae CXXI aegris qui antea accepimus crizotinib habebat responsionem rate de 180%, LIX non receperunt aliqua aegris qui habent curatio responsionem rate de 60%. PD-L121 PDCD55.4 (Progammed death59 cellula, PD69.5) gene encodes ad immunoglobulin genus typus ego transmembrane glycoprotein, quae consociata cum suis ligands PD-L1, PD- Compositum ex L1 machinationem inhibendi ius habet effectus super activation de lymphocytes, in mediis negans regulatory signum de immune responsio, et inducit T in apoptosis est anti-tumore cellulis. T cellulis per antigen Utilia PD1 quoque control nodorum lymphaticorum regulet BCL gene-II. Cumulus. Eam lascivio a munus in propria regulatory tumorigenesis, infectiones virales et autoimmune morbo. PD1 atque ligand PD-L1 quae ad co-stimulatory moleculo in domo B2. Hoc TEXTUS wide moleculo est expressio, et excelsum profile ad aliquid tumore cellam lineae expressio. Multa sunt studiis ostensum est quod immune est effugium ad mechanism de anorum. Signalling in viam suam, et mediante PD1 ligand PD-L2 unus ex decorum morbo curatio modos orci in immunological interveniret.
PD-L1
Protein molecules are hardly expressed in normal tissues, but they are ubiquitous on the surface of human lung cancer, ovarian cancer, colon cancer, renal cancer and melanoma. Studies have speculated that it can make tumor cells have the magical ability to escape immune response. . By inhibiting PD1 or PD-L1 to activate the anti-tumor activity of T cells and maintain its ability to detect and attack cancer cells, it can provide new ideas for cancer treatment. More than 200 patients with different types of tumors were enrolled in two different clinical trials. The largest cohort samples included melanoma and non-small cell lung cancer (NSCLC) patients. Both trials reported surprisingly long-lasting response rates (6–17% in the anti-PDL1 group and 18–28% in the anti-PD1 group), especially for melanoma patients (17% and 28% in both groups) , And the incidence of drug-related adverse events is also low (9% and 14% for grade 3 and 4 drug-related adverse events, respectively). More importantly, in the anti-PD1 group, the response rate of tumor patients with positive PD-L1 expression was 36%. It is worth noting that the trial purpose and sustained response rate of NSCLC patients also meet the trial requirements, and such patients are known for their resistance to immunotherapy. Hoc longe felicissimum est immunotherapy consilium omnium generum tumorum, cum rate of 10-15% responsionis tumore persistente.
As the concept of precision medicine continues to advance, the clinic has begun to use mutations to distinguish tumors rather than tissue sources. For example, if a gene mutation related to pectus cancer targeted medication is found in lung cancer, then this breast cancer medication may be used in the treatment of lung cancer; the National Cancer Institute (NCI) has initiated related clinical research (NCI-MATCH) . I believe that in the near future, this concept will be fully practiced in the clinic.
De pulmone cancer praeventionis
Ne pulmonis cancer quod physice activa et passiva fumigans negat praeter, inveterata pulmonis morbo attendentes ad actum et active, umbraticis et velit reducere caeli pollutio comparamus, et parentur post ullo spiramento ullo spiramento iusto medicinae screenings omni anno haberi. Et hoc est psallebat an maximus partes in diluculo popularis palam de pulmone cancer. Pro Ordinarius populus, qua parte sui non geneticae background et conscientiam sui ipsius, providebit fidem facit pro sano vitae.
