肺癌课件英文
肺癌-优秀医学PPT课件
侵蚀肋骨
周围型肺癌伴胸椎转移：左肺下野见一较大肿块影，密度均匀，边缘 模糊，第四胸椎骨密度减低，椎弓根显示不清。
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痰细胞学检查
鳞癌 小细胞癌
细支气管肺泡癌是肺腺癌的另一类型。这里是肺实变多病灶变异的粗略外观大多数右上肺叶呈现黑-白色到灰色外观。
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支气管肺癌(肺泡细胞型腺癌)
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大细胞型Large cell carcinoma
甚少见 半数起源于大支气管，细胞大胞浆丰富胞核形态多样，细胞排列不规则，分化程度低。 预后很差。 常发生脑转移后才被发现。
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周围型肺癌：右肺下叶背段见一球形肿块影；呈分叶状
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左肺上叶周围型肺癌 ：上叶尖后段见一较大肿块影， 密度均匀，边缘不规则，可见小毛刺。
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周围型肺癌：
肿瘤中心部分液化坏死，呈厚壁偏心空洞，内壁凹凸不平。
右肺下叶周围型肺癌：下叶背段见一较大肿块， 内可见一偏心小空洞伴有液平。
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血行转移 Hematogenous metastasis
是肺癌的晚期表现，病人预后差。 腺癌，小细胞癌血行转移较鳞癌更为常见。 癌细胞—肺V—左心大循环—全身（肝、骨骼、脑、肾上腺多见）。
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五、临床表现 CLINICAL SITUATION
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肺癌症状取决于发生部位、大小、是否压迫临近器官及有无转移。早期可无症状，而在X线体检时发现。中央型出现症状早。周围型较晚。
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杵状指趾和肥大性骨关节病
前者：发生快、疼痛剧烈、甲床周围出现红晕为特点。 后者：以长骨疼痛、骨膜增生、新骨形成或关节疼痛常同时伴发，多见于鳞癌。手术切除肺癌后症状立即减轻或消失。肿瘤复发又可出现。
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肺癌英文PPT演示幻灯片
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Pathology And Classification
According to the different principles of management,it is divided into two types.
SCLC:small cell lung carcinoma. NSCLC:non small cell lung carcinoma.
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Pathology And Classification
1. According to the position of tumor arising from ,it can be divided into two types .
Central type:Tumor arises from main bronchus, lobar and segmental bronchus . Peripheral type : Tumor arises beyond segmental bronchus .
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Clinical Features
(4).Horner’s syndrome.It is caused by invading the cervical sympathetic ganglia on the involved side the pupil is small ptosis of the up eyelids,retraction of the eyeball and no sweat of the face.
(5)Cardiac effusion
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Passive smoking is also a carcinogen factor.
肺癌PPT课件
• 痰细胞学检查
• 阳性率为60%左有，高者达80%以 上。其中，约2/3的病变位于中央， 在支气管镜能够观察到的范围内
• 胸水细胞学检查
• 与 痰一样，阴性结果并不重要，但 肯定的阳性发现却非常重要
• 常用三种方法 •灌注扫描 •检查肺癌的转移灶 •亲肿瘤扫描 •直接提示肺部肿瘤 •吸入扫描 •间接提示肺部肿瘤
FDG-PET在肺部肿瘤诊治中的应用：
确定肺内病变的存在及性质 对肺癌患者进行临床TNM分期。 发现常规检查未发现的亚临床转移病灶。 判断肿瘤对治疗的反应，指导治疗方案。 肿瘤局部复发的早期诊断。
纤维支气管镜检查
• 纤支镜检查除观察病灶外，主要目的在于钳 取组织进行病理检查以明确诊断 ;其对中央型 肺癌阳性率较高
• 胸内转移症状
• 胸水：血性胸水一般系肿瘤直接侵犯胸膜所致， 提示预后不佳
• 纵隔受累
• 压迫上腔静脉，引起上腔静脉综合征 • 压迫食管致吞咽困难 • 累及一侧喉返神经致声音嘶哑 • 肺尖部的肿瘤---Pancoast瘤，常常出现胸廓上口受累
的症状
*Pancoast瘤
支气管源癌，鳞癌为主，少数为小细胞癌。位 于肺尖部，常出现胸廓上口受累的症状，表现 为:1)胸腔上口软组织受累，合并邻近骨质破坏 和局部性疼痛;2)臂丛神经受累，引起患侧上肢、 手部疼痛，手部肌肉萎缩;3)支配头颈部同侧的 颈交感神经节受累，引起Horner综合征
某些金属和非金属物质 如铀、铬、镍、铍、氡、砷、锡、 石棉等有致癌作用。其中最重要的是石棉。石棉工人发生 肺癌的危险是普通人的6~10倍
大气污染 可使肺癌的发病率提高2~3倍:肺癌死亡率在城市 高于农村
2020年肺癌英文.ppt
Incidence and mortality
• Bronchogenic carcinoma has increased remarkable in
incidence and mortality during half of the century and has
become the most frequent visceral malignant diseases of men.The mortality of lung cancer hold the first place among all
Etiology
• 2.Atmospheric pollution.It was found that carcinogenic factor is benzpyrene .
• 3.Occupational factors. • 4Radioactivity in the atmosphere . • 5.Diets and Nutrition. • 6.Chronic irritation. • 7.Genetic factors.
Clinical features
• There are no symptoms of early lung cancer in some patients. • Symptoms caused by lung cancer are non-specific:perhaps an
audible wheeze or a slight cough,symptoms of infection (fever ,purulent sputum) , of obstruction (wheezing,dyspnea), or ulceration of bronchial mucosa (hemoptysis).
讲课肺癌英文演示文稿
讲课肺癌英文演示 文稿
What is Lung Cancer?
• Begins when cells in the lung grow out of control and form a tumor
Etiology and pathogenesis
• Cigarette smoking • Other factors include air
• According to histologic classification: Small cell lung cancer(SCLC) and Non-small cell
lung cancer(NSCLC). NSCLC includes Squamous cell carcinoma,
• it causes symptoms early in
• areas of scarring is associated with the occurrence of adenocarcinoma.
• Peripheral adenocarcinomas are usually wellcircumscribed, grey-white masses that rarely cavitate.
• Intercellular bridges and cellular pleomorphism
• squamous cell carcinoma usually occurs near the bronchi, the tumor can cause cough (sometimes a cough that is tinged with blood), shortness of breath, wheezing, and pneumonia in the area between the tumor and the edge of the lung
肺癌英文(课堂PPT)
Pathology And Classification
1. According to the position of tumor arising from ,it can be divided into two types .
Central type:Tumor arises from main bronchus, lobar and segmental bronchus . Peripheral type : Tumor arises beyond segmental breatures
(4).Horner’s syndrome.It is caused by invading the cervical sympathetic ganglia on the involved side the pupil is small ptosis of the up eyelids,retraction of the eyeball and no sweat of the face.
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Clinical features
1.Respiratory symptoms.
(1).Cough: (2).Hemoptysis: (3).Dyspnea.: (4).Wheeze or stridor: (5).Chest pain : (6).Fever:
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Clinical features
cell carcinoma).
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Pathology And Classification
According to the different principles of management,it is divided into two types.
SCLC:small cell lung carcinoma. NSCLC:non small cell lung carcinoma.
肺癌研究报告Lung cancer(英文)ppt课件
PPT学习交流
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Environmental Risk Factors Alcohol
Diet and Body Mass
Non-modifiable Risk Factors Age \Race \Sex
PPT学习交流
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Types
squamous cell carcinoma,squamous epithelium of the lungs or bronchi
An individual then has a better idea of
the value of different fors that are taken into
account include the person's general
health, medical problems that may affect
Small cell lung carcinoma (SCLC) accounts for approximately 20% of all primary lung cancers
The histologic distinction between nonsmall cell lung cancer and small cell lung cancer is extremely important. There are substantial differences between the two groups in both treatment and prognosis.
PPT学习交流
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Other symptoms that are
associated with lung
cancer include:
讲课肺癌英文 PPT
lung cancer(NSCLC). NSCLC includes Squamous cell carcinoma,
large cell carcinoma, adenocarcinoma, adenosquamous carcinoma.
Small cell lung cancer(SCLC)
• It arises from the submucosal glands,located in peripheral airways and alveoli
• Female
large cell carcinoma
• large nuclei,prominent nucleoli,abundant cytoplsma
neuroendocrine cells that are responsible for the production and secretion of specific peptide product.they may related to paraneoplastic syndrome.
• Cells are oval or vaguely spindleshaped ,have scant cytoplasm
大家学习辛苦了，还是要坚持
继续保持安静
Squamous cell carcinoma
• the most frequent form of the tumor(30-50 percent of all cases
原发性支气管肺癌中英文对照课件
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• 2 职业致癌因子
• 2 Occupation carcinogenic factor: Asbestos, Radon 3 空气污染
• 3 Air pollution • （1）室外大环境污染 • （1）Outdoor environment pollution • （2）室内小环境污染 • （2）Indoor environment pollution • 4 电离辐射
• （2）intermediate cell type
• （3）混合型
• （3）mixed type
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• Small cell carcinoma
– Rare in non-smokers – Large hilar mass – 70% present with overt metastasis – Very chemo-responsive… – Worst prognosis
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Squamous Cell Carcinoma
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Squamous Cell Carcinoma
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鳞癌
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Lung Cancer Pathology
• Adenocarcinoma
– Most common pathology(2nd in China) – “Non-smoker’s lung cancer” – Women – Peripheral (75%) – Aggressive metastases
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• Dominant oncogenes
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*Kras
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*Her-2/neu
肺癌PPT课件
麦细胞癌。
• 4.大细胞癌：此型.肺癌甚为少见。约半
数起源于大支气管。细胞大，胞浆丰富， 胞核形态多样，细胞排列不规则，呈片形 或条索状。大细胞癌分化程度低，常发生 脑转移，预后差。
• 此外，少数病例同时存在不同类型的 癌肿组织，如腺癌内有鳞癌组织，鳞癌内 有腺癌组织或鳞癌与小细胞癌并存，这一 类癌称为混合型肺癌。
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• 2.职业与肺癌：某些工业生产及矿区职 工肺癌的发病率较高，这可能是由于长期 接触石棉、铬、镍、铜、锡、砷、铀等放 射性元素有关。
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• 3.大气污染与肺癌：流行病学调查资料 表明，肺癌的分布规律是：工业发达、空 气污染严重的地区高于工业不发达地区， 城市居民高于农民，近郊高于远郊。这可 能是与煤和石油燃烧后释放出二氧化硫、 煤焦油、特别是3，4-苯丙芘等可致癌的有 害气体，直接作用于和环境空气接触面积 最大的肺脏，使其成为致癌因素的靶器官。
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• （二）组织学类型：肺癌的组织学分类 较为繁多，临床上通常分为：
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• 1.鳞状细胞癌（鳞癌）：在肺癌中最为 常见，约占50%，患者年龄多在50岁以上， 男性多于女性。大多起源于较大的支气管 鳞状上皮、近肺门多为中心型。虽然鳞癌 的分化程度不一，但在常见的各型肺癌中 此型生长速度较缓慢，病程较长；通常首 先经淋巴管局部转移较多见，血行远处转 移发生较晚。对放疗及化疗均较敏感，因 此其五年生存率相对较高。
肺癌
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• 肺癌(lung cancer)大多数发生于各级支 气管粘膜及其腺体的上皮细胞，亦称支气 管肺癌，(bronchopulmonary carcinoma) 临床上则通称为肺癌。
流行病学与病因
• 流行病学概况： • 近半个世纪以来，世界肺癌的死亡率
treatmentoflungcancer(肺癌的治疗方法)ppt课件
▫ 外科治疗是肺癌首选的， 主要的治疗措施
▫ 外科治疗能在最大范围内 切除病灶及引流的淋巴结 和受侵犯的临近组织，能 实现根治，是所有治疗中 效果比较显著的。
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2020/10/12
Treatment-Surgery
• 适合外科手术的患者
▫ 非小细胞肺癌I~IIIA期
如无手术禁忌，以手术为首选疗法 手术也参与一些中晚期治疗的综合治疗
Treatment
• 肺癌的治疗方法
▫ 手术 41 % ▫ 化疗 23% ▫ 放疗 11% ▫ 手术+化疗 4% ▫ 手术+化疗 3% ▫ 放化疗 12% ▫ 此外还有靶向治疗 ▫ 免疫治疗 ▫ 中药治疗等
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2020/10/12
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Treatment-Surgery
• Symptoms and signs that may suggest lung cancer include:
▫ coughing ▫ weight loss ▫ dyspnea (shortness of breath) 呼吸困难 ▫ chest pain ▫ hemoptysis (coughing up blood) 咳血 ▫ bone pain ▫ clubbing of the fingernails 杵狀指 ▫ fever ▫ fatigue ▫ superior vena cava obstruction 上腔静脉组赛 ▫ dysphagia (difficulty swallowing) 吞咽困难 ▫ wheezing 哮喘
• Up to 60% of patients have a new cough or a change in a chronic cough
肺癌幻灯英文版
Lung Cancer 101 and ASCO 2016 HighlightsDr. Jennifer Garst with ASCO slides by Dr. Jared WeissDuke Cancer Institute at Duke Cancer Center Raleigh8/20/2016Build Hope. Take Action.End Lung Cancer.Mission…..To save lives and provide support to thoseaffected by lung cancer through research,awareness, education, and access programsacross North Carolina.A Major Public Health Problem•Estimated 1.6 million deaths each year worldwide from lung cancer •In 2015:–Estimated 221,200 new cases of lung cancer expected to be diagnosed in US –158,000 Americans expected to die from lung cancer•Leading cause of cancer-related deaths in US men and women –More deaths from lung cancer than breast, prostate, colon, liver, melanoma, and kidney cancers combined•Need for better thought out, patient-driven studiesTorre LA, et al. CA Cancer J Clin. 2015;65(2):87-108.Siegel RL, et al. CA Cancer J Clin. 2015;65(1):5-29.USA DistributionWhat is lung cancer?Lung cancer is an uncontrolled growth ofabnormal cells that starts in the lungs.Cancer can develop with a mutation or error inthe lung cell’s DNA.DNA mutations can be caused by the normalaging process and through exposure to toxins like smoke, viruses, radon, and otherenvironmental factors. Cigarette SmokeLung Cancer Risk Factors•Current or past H/O smoking or second handsmoke exposure•Radon exposure•Previous cancer•Lung disease, COPD, pulmonary fibrosis •Toxic exposures: arsenic, chromium, asbestos, nickel,, cadmium, beryllium, silica, dieselfumes, viruses•Genetic risksWhat is lung cancer?It likely takes a series of mutations to create alung cancer cell. Cells may be pre-cancerous due to some mutations but continue to function like normal lung cells. As these cells divide, the mutations are passed down and can become augmented from other toxic exposures until the cells do not behave like normal lung cells andtake on the characteristics or “hallmarks” ofcancer.Hanahan D, et al. Cell . 2000;100(1):57-70. Self-sufficiencyin growth signalsEvading apoptosis Sustained angiogenesis Limitless replicativepotentialInsensitivity toantigrowth signalsTissueinvasion andmetastasisThe Hallmarks of Cancer: New Targets•228,190 new cases of lung cancer •159,480 deaths dueto lung cancer MenLung and bronchus 28%Prostate 10%Colon and rectum 9%Pancreas 6%Leukemia 5%WomenLung and bronchus 26% Breast 14% Colon and rectum 9%Pancreas 7%Ovary 5%Leading Sites, United States, 2013 EstimatesSiegel R, et al. CA Cancer J Clin . 2013;63(1):11-30.Cancer-Related DeathsCommon causesof US cancerdeaths, 2008 Rudin CM, et al. Clin Cancer Res.2009;15(18):5622-5625. Ever-SmokersNever-SmokersTypes of Lung Cancer •Non-Small Cell Lung Cancer –AdenocarcinomaSquamous cell carcinoma–Large cell•Small Cell Lung CancerNSCLC Stages at PresentationSubramanian J, et al. J Thorac Oncol. 2010;5: 23–28.Staging: NSCLCStage I:•≤ 5cm; no lymph nodes involvedStage II:•≤ 7cm, if ipsilateral hilar lymphnodes involved•>7cm, or local invasion, ormultiple nodules in same lobe ifno lymph nodes involvedStaging: NSCLCStage III:•Has not spread beyond lymphnodes in chest•May have metastases withinipsilateral lung•May have local invasion of majorstructuresStage IV:•Metastatic disease or disease withpleural effusionLess Invasive Lung Cancer Staging EndoBronchial Ultrasound (EBUS) Mediastinoscopy Use of an ultrasound-guided camera to biopsy lymph nodes around the airway with needle aspirationSurgical removal of lymph nodes from around the main airway ENDOBRONCHIAL ULTRASOUND EBUS is done under general anesthesia Angled, balloon-tipped ultrasoundbronchoscopeallowssimultaneousendoscopic andultrasound views Endoscopic viewUltrasound viewEBUS probe in the main airwayCurrent State of NSCLC •NSCLC: ~ 85% of lung cancers•Histology-directed therapy–Non-squamous: bevacizumab, pemetrexed–Squamous: nab-paclitaxel, nivolumab•Biomarker-directed therapy–Erlotinib, afatinib, gefitinib, crizotinib, ceritinib •Immunotherapy•Overcoming resistance–EGFR and ALK resistanceMore Choices = More Decisionspatients, providers, payersStrategies to ImproveOutcome of Lung Cancer Patients •Move away from approaching lung cancer as one disease•Develop treatment strategies for different subsets of lung cancer•Treatment improvements based on–Histology–Oncogenic alterations–ProteomicsFirst-line Second-line Third-line Maintenance Not approved 1970 1980 1990 2000 MedianOS (mos) 12+ ~ 6~ 2–4 BSC Single-agent platinum DoubletsBevacizumab + PC Carboplatin a1989 ErlotinibPemetrexed2004Docetaxel1999 PaclitaxelGemcitabine 1998 Vinorelbine 1994 Docetaxel 2002 Bevacizumab2006Gefitinib2003Standard Therapies a Label does not include NSCLC-specific indication. BSC = best supportive care;PC = paclitaxel/carboplatin; OS = overall survival. Adapted from Shrump, et al. Non-small cell lung cancer. In: Cancer: Principles and Practice of Oncology . 7th ed.Philadelphia, PA: Lippincott Williams & Wilkins:2005.Pemetrexed2008/2009Histology-directed therapyCisplatin a 1978History of Therapy in Advanced NSCLC: FDAApproval Dates 1970-20102010Erlotinib2010 ~ 8–10Maintenance Therapy Targeted TherapyALK TranslocationEGFR Mutation2011 2013History of Therapy in Advanced NSCLC: FDAApproval Dates 2011-2013Crizotinib 2011 Erlotinib 2013 Afatinib 2013MedianOS(mos)Targeted Therapy20-30+ monthsLung Cancer Mutation Consortium: Incidence ofDriver MutationsROS-1 1%Kris MG, et al. JAMA. 2014;311:1998-2006.Lung Adenocarcinoma MutationsRudin CM, et al. Clin Cancer Res. 2009;15(18):5646-5661.MATCH trial EGFR SignalingAdapted from Ciardiello F, Tortora G. N Engl J Med. 2008;358:1160-1174. gefitinib erlotinibEGFR MUT Disease Progressionon an EGFR TKI Molecular: •Unknown (other pathways) •EGFR T790M (exon 20) •MET amplification •PIK3CA •SCLC Clinical PD appearance: •Rapid disease PD globally •Slow growth globally •Growth in several areas, but not all T790M~ 40-55% T790M +EGFR amp~ 10% Other EGFR mut 1-2%SCLC w/PI3K ~ 4% SCLC~ 6% PIK3CA~ 1-2%MET amp~ 5% BRAF ~ 1%HER2 Amp ~ 8-13%EMT~ 1-2%Unknown~ 15-20%Camidge DR, et al. Nat Rev Clin Oncol. 2014;11(8):473-481.Osimertinib activity in patients with leptomeningeal disease from non-small cell lung cancer: <br />updated results from the BLOOM studyPresented By James Yang at 2016 ASCO Annual MeetingChanges in EGFRm DNA copy number in CSF <br />with osimertinib treatmentPresented By James Yang at 2016 ASCO Annual MeetingPhase I study (BLOOM) of AZD3759, a CNS penetrable EGFR inhibitor, for the treatment of non-small-cell lung cancer (NSCLC) with brain metastasis (BM) and leptomeningeal metastasis (LM)Presented By Myung-Ju Ahn at 2016 ASCO Annual MeetingThird Generation EGFR TKIs“3rd” Generation N RR* T790M- RR T790M+PFS ToxicityRociletinib (CO-1686)256 37% 53% ~ 8.0 mo Hyperglycemia AZD9291 253 21% 61% ~ 8.2 mo Diarrhea HM61713 (800 mg) 62 12% (300 mg)55% NR Dyspnea/rash EGF816X* 53 - 60% NR RashASP8273* 47 ~ 33% 61% NR Hyponatremia/diarrheaSequist L, et al. J Clin Oncol. 2015;33(suppl). Abstract 8001; Jänne PA, et al. N Engl J Med. 2015;372(18):1689-1699; Park K, et al. J Clin Oncol. 2015;33(suppl). Abstract 8084; Tan DS-W, et al. J Clin Oncol. 2015;33(suppl). Abstract 8013; Goto Y , et al. J Clin Oncol. 2015;33(suppl). Abstract 8014.Multiple other agents earlier in development*T790M - subgroups are very small. RR, response rate; PFS, progression-free survival.ALK Fusion Oncogenes and Downstream Signaling Shaw AT, Solomon B. Clin Cancer Re s. 2011;17:2081-2086.Alectinib versus Crizotinib in ALK Inhibitor Naïve ALK-Positive Non-Small Cell Lung Cancer:<br /> Primary Results from the J-ALEX StudyPresented By Hiroshi Nokihara at 2016 ASCO Annual Meeting J-ALEX Phase III Study DesignPresented By Hiroshi Nokihara at 2016 ASCO Annual MeetingPrimary Endpoint: PFS by IRF (ITT Population)Presented By Hiroshi Nokihara at 2016 ASCO Annual MeetingBrigatinib in Patients With Crizotinib-Refractory ALK+ Non–Small Cell Lung Cancer: First Report of Efficacy and Safety From a Pivotal Randomized Phase 2 Trial (ALTA)Presented By Dong-Wan Kim at 2016 ASCO Annual MeetingPFS by ArmPresented By Dong-Wan Kim at 2016 ASCO Annual Meeting Survival by ArmPresented By Dong-Wan Kim at 2016 ASCO Annual MeetingROS1 Rearrangement in Lung CancerJänne PA, et al. J Clin Oncol. 2012;30(8):878-879.Safety and Efficacy of Lorlatinib (PF-06463922) From the Dose Escalation Component of a Study in Patients With Advanced ALK+ or ROS1+ Non-Small-Cell Lung CancerPresented By Benjamin Solomon at 2016 ASCO Annual MeetingPhase I Design and Patient Population <br />of an Ongoing Phase I/II StudyPresented By Benjamin Solomon at 2016 ASCO Annual Meeting Clinical Activity: <br />Progression-Free Survival in ALK+ PatientsPresented By Benjamin Solomon at 2016 ASCO Annual MeetingMajority of ROS1 Patients Had a <br />Decrease in Target Lesion Size*Presented By Benjamin Solomon at 2016 ASCO Annual Meeting CNS Responses in ALK/ROS1+ Patients<br />with Measurable DiseasePresented By Benjamin Solomon at 2016 ASCO Annual MeetingOther Drugs That Target ALK and/or ROS-1 •1st-generation ALKCrizotinib( plus ROS-1)•2nd-generation ALK Inhibitors‒Ceritinib (LDK378)( plus ROS-1)‒ Alectinib (CH5424802)( no ROS-1 activity)•ALK/EGFR/ROS-1 Inhibitors‒Brigatinib (AP26113)(nearing approval process)Promising Others ALK/ROS-1: Lorlatinib, Ensartinib (X-396)in clinical trialsResistance: Cabozantinib (FDA approved medthyroid/renal), TPX-0005 (ALK/SRC) in clinical trialsResponse of An ROS1+ PatientBaseline 12 Weeks Crizotinib Bergethon K, et al. J Clin Oncol. 2012;30(8):863-870.Antitumor Activity and Safety of Crizotinib <br />in Patients with Advanced MET Exon 14-Altered <br />Non-Small Cell Lung CancerPresented By Alexander Drilon at 2016 ASCO Annual Meeting Slide 11Presented By Alexander Drilon at 2016 ASCO Annual MeetingAn Open-Label Phase 2 Trial of Dabrafenib in Combination With Trametinib in Patients With Previously Treated BRAF V600E–Mutant Advanced <br />Non-Small Cell Lung Cancer (BRF113928)Presented By David Planchard at 2016 ASCO Annual MeetingProgression-Free SurvivalPresented By David Planchard at 2016 ASCO Annual MeetingSlide 1Presented By D. Camidge at 2016 ASCO Annual Meeting Antibody Drug Conjugate: Sacituzumab Govitecan (IMMU-132)Presented By D. Camidge at 2016 ASCO Annual MeetingProgression-Free Survival and Overall Survival <br />(8 or 10 mg/kg; median of 3 prior therapies)Presented By D. Camidge at 2016 ASCO Annual MeetingImmunotherapy in NSCLC•Immunotherapy•Vaccines•Check-point inhibitors:•Preliminary evidence of activity with CTLA-4 andchemotherapy•Preliminary evidence of activity with PD-1 or PD-L1Lynch TJ, et al. J Clin Oncol. 2012. Genova C, et al. Expert Opin Biol Ther 2012. Brahmer JR et al NEJM 2012, Topalian S et al NEJM 2012PD-1, PD-L1 AntibodiesTarget AgentPD-1 Nivolumab (BMS-936558)Pembrolizumab (MK-3475)Pidilizumab (CT-011)AMP-224PD-L1 BMS-936559Durvalumab (MEDI4736)Atezolizumab (MPDL-3280A)PD-1, programmed death receptor-1; PD-L1, programmed death-ligand 1.Davies M. Cancer Manag Res. 2014;6:63-75; Brahmer JR. J Clin Oncol. 2013;31(8):1021-1028; Rizvi NA, et al. J Clin Oncol. 2014;32(suppl 15). Abstract 8007;Brahmer JR, et al. J Clin Oncol. 2014;32(suppl 15). Abstract 8021.CheckMate 012: Safety and Efficacy of First‐line Nivolumab and Ipilimumab in Advanced NSCLCPresented By Matthew Hellmann at 2016 ASCO Annual MeetingNivolumab Plus Ipilimumab in First-line NSCLC:<br />Summary of EfficacyPresented By Matthew Hellmann at 2016 ASCO Annual Meeting Nivolumab Plus Ipilimumab in First-line NSCLC:<br />Efficacy Across All Tumor PD-L1 Expression LevelsPresented By Matthew Hellmann at 2016 ASCO Annual Meeting•Immune responses are dynamic and evolve. •A single biomarker may not be the complete answer.•“Mutational Load” is a very important factor and may be a better predictor of response to a single PD-1 blockade.•Micro-environment influences responses to PD-1 blockade …....hypoxia, metabolism, genetics.ImmunotherapyConclusions:Small cell lung cancerSafety and efficacy of single agent rovalpituzumab tesirine (SC16LD6.5), a delta-like protein 3 (DLL3)-targeted antibody-drug conjugate (ADC) in recurrent or refractory small cell lung cancer (SCLC)Presented By Charles Rudin at 2016 ASCO Annual MeetingSCLC Kaplan-Meier Overall SurvivalPresented By Charles Rudin at 2016 ASCO Annual Meeting Favorable Comparison vs. Existing 2L and 3L CTXPresented By Charles Rudin at 2016 ASCO Annual MeetingLocal Consolidative Therapy (LCT) Improves Progression-Free Survival (PFS) in Patients with Oligometastatic Non-Small Cell Lung Cancer (NSCLC) who do not Progress after Front Line Systemic Therapy (FLST): Results of a Multi-Institutional Phase II Randomized StudyPresented By Daniel Gomez at 2016 ASCO Annual MeetingTrial DesignPresented By Daniel Gomez at 2016 ASCO Annual MeetingTrial DesignPresented By Daniel Gomez at 2016 ASCO Annual Meeting Prognostic Factors for PFSPresented By Daniel Gomez at 2016 ASCO Annual MeetingImproved Overall Survival in Lung Cancer Patients <br />using a Webapplication-mediated Follow-up compared to Standard Modalities: <br />Results of a Phase III Randomized TrialPresented By Fabrice Denis at 2016 ASCO Annual MeetingPhase 3 multi-centric randomized studyPresented By Fabrice Denis at 2016 ASCO Annual MeetingOverall Survival ImprovementPresented By Fabrice Denis at 2016 ASCO Annual Meeting Other « intensive » clinical follow-up studiesPresented By Fabrice Denis at 2016 ASCO Annual MeetingChallenges for the Next Decade•Expanding biomarker-directed therapy –Transitioning to multiplex testing–BRAF, Exon 14 MET, HER2•Defining role of immunotherapy •Squamous histology-directed therapy •Small cell lung cancer•Maintenance ‒ what surrogate can we use?Figure 6Source: Cell , Volume 144, Issue 5, Pages 646-674 (DOI:10.1016/j.cell.2011.02.013)Copyright © 2011 Elsevier Inc. Terms and ConditionsTrends Continuing as Screening for Lung CA Evolves •Earlier Detection–NLST Results finding survival benefitwith CT screening•Earlier Diagnosis–Navigational Bronchoscopy•More Treatment Options–Early stage Lung CA improvedprognosis, more flexibility withtreatment options tailored to patientDuke Raleigh Hospital Cancer CenterMultidisciplinary Lung Cancer Care TeamStanding: Brenda Wilcox , RN; Dr. Jennifer Garst; Lisa Dowd, NP; Dr. Albert Chang Seated: Dr. Catherine Chang, Dr. David White, Katherine Gillis, PA-CRadiation FieldsReferral: Fast andAppropriate•Medical oncologists – appropriate for every lung cancer patient•Thoracic surgeons – role intreatment for all stage patients–Best results from centers that do highernumber of thoracic surgeriesClinical Trials: The Road to New Therapeutic Advances •With the advances being made in lung cancer treatment, clinical trials are an attractivetherapy option•The family physician is often the most trusted – your advice carries a lot of weight!•You don’t need to know that there is a trial available, just plant the seed!Trends in Management of Lung CA HOPE Image GuidanceLess invasiveBetter OutcomesTargeted Therapy Earlier DetectionTeam HOPE•We all need a team of support: •Family and friends•Advocacy groups like LCI•Social media/blogs/ carebridges •Local medical team•Consulting medical team •Spiritual support and more…...Our “A” team: Jonathan Choe, PA-C, Vereterrica Rushdan, RMA, Jennifer Mizelle, RN, Elattmont Spiller, patient care coordinatorHeather Hooper, Executive Director Thank You to Our Staff!Lynne Ritter,Director of FinanceKhaki Stelten, Communications & Development Manager Jenni Danai Programs Manager Parker Shields Administrative & Program AssistantCynamon Frierson, Communication & Marketing ManagerWe are very much looking forward to partnering with you in the cause and making lung cancer awareness andresearch a priority.Together, there ’s always somethingwe can do!。
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and lung cancer risk was related to the type of tobacco, the age at which smoking began, the number of years of smoking, and the amount of smoking
Each cigarette
shortens a
•
smoker's life
by seven
minutes
Etiology
• The association between smoking and squamous cell carcinoma was significantly higher than that of adenocarcinoma
Etiology
4、Ionizing radiation：Large doses of ionizing radiation can cause lung cancer, different radiation effects are different
5、Diet and nutrition： Chronic food deficiencies of vitamin A and β carotene and trace elements (zinc(Zn), selenium(Se)) are prone to lung cancer.
Because vitamin A is an antioxidant.
Etiology
6、Others：
• The risk of lung cancer was significantly correlated with chronic bronchitis and tuberculosis.
Passive smoking for 15 minutes equals active smoking
Etiology
2、Occupational carcinogen:
• Confirmed carcinogens：Chromium, nickel, arsenic, beryllium, asbestos, soot, coal tar, mustard gas, isopropyl oil, dichloromethyl ether and ionizing radiation.
Overview
overview
• Bronchial cancer: lung cancer refers to the cancer originating in the bronchial mucosa or glands
• bronchial glands or alveolar epithelium, lung cancer is actually bronchogenic cancer
• The American cancer society lists tuberculosis as a risk factor for lung cancer.
Etiology
• Recent molecular biology studies have shown that the occurrence of lung cancer is closely related to the of some oncogenes and the of tumor suppressor genes.
Hale Waihona Puke Etiology★Passive smokers have a 50% increased risk of lung cancer
Definition: people who live and work around smokers unconsciously inhaling smoke particles and toxic substances.
Bronchogenic Carcinoma
Learning goals
➢Overview ➢Etiology ➢Classification ➢Clinical Features ➢Examination ➢Diagnosis and differential diagnosis ➢Staging of lung cancer ➢Treatment
• Smoking cessation for 10 years can reduce the incidence of lung cancer by 80 %
• The incidence of lung cancer 15 years after quitting was similar to that of nonsmokers
Globle Incidence of Cance
Etiology
Etiology
1、Smoking
★Smoking is the leading risk factor for lung cancer
other reasons
cigarethes 90%
Etiology
★Smokers are 10 to 13 times more likely to develop lung cancer than nonsmokers
overview
• Both morbidity and mortality rates are increasing significantly
• The incidence and death rate of male lung cancer ranks the first in the world.
Etiology
3、The air pollution：
• Outdoor environmental pollution：Industrial waste gas, highway asphalt, motor vehicle exhaust gas
Eiology
• Indoor environmental pollution：Such as kitchen small environment coal tar, soot,tobacco