The document discusses staging of lung cancer, including the TNM system for describing the size and extent of the primary tumor (T stage), involvement of lymph nodes (N stage), and presence of distant metastasis (M stage). It provides details on lymph node stations evaluated in lung cancer and proposals to further subclassify N1 and N2 stages based on number and location of involved lymph nodes. Accurate staging is important for prognosis and determining appropriate treatment options for patients with lung cancer.
This class covers what all physicians need to know about colorectal cancer (except prevention and screening, dealt with elsewhere). It is exceedingly simple, but accurate to the best of my knowledge. It is based on Harrison's 19th, Edition.
In this webinar our Medical Advisory Board member Dr. Dennis Ahnen will cover the basics of colorectal cancer – the hows, whats, and whys.
This August 2015 webinar is brought to you by Fight CRC’s Research Advocacy Training and Support (RATS) program. http://fightcolorectalcancer.org/do-something/support-research/research-advocacy-training-and-support-rats/
Each January, the best and brightest minds in colorectal cancer research meet at the Gastrointestinal Cancers Symposium. Fight Colorectal Cancer and the Colon Cancer Alliance are partnering to bring you the big news in colorectal cancer from the 2013 symposium.
Join us to learn more about these topics:
- Can aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) keep cancer from returning?
- The relationship of body mass index (BMI) and exercise in colorectal cancer
- What scientists are learning about how your immune system can fight cancer
- The latest on what biomarkers can tell us about your cancer
- Rectal cancer treatment that is based on your biological make-up
The webinar will be led by Dr. Richard Goldberg, an internationally renowned gastrointestinal oncologist who specializes in colorectal cancer. He is a tenured professor in the Department of Internal Medicine at The Ohio State University and serves as physician-in-chief at Ohio State’s Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James).
Presentación realizada por la Dra. Pilar Escudero del HCU Lozano Blesa, en el marco de la I Jornada de actualización e innovación en Oncología que tuvo lugar en el CIBA en enero de 2015.
Colon cancer screening recommendationsPennMedicine
Colon cancer screening recommendation presentation from Dr. Tracy d'Entremont, Director of Oncology Services at the Abramson Cancer Center at Valley Forge.
This class covers what all physicians need to know about colorectal cancer (except prevention and screening, dealt with elsewhere). It is exceedingly simple, but accurate to the best of my knowledge. It is based on Harrison's 19th, Edition.
In this webinar our Medical Advisory Board member Dr. Dennis Ahnen will cover the basics of colorectal cancer – the hows, whats, and whys.
This August 2015 webinar is brought to you by Fight CRC’s Research Advocacy Training and Support (RATS) program. http://fightcolorectalcancer.org/do-something/support-research/research-advocacy-training-and-support-rats/
Each January, the best and brightest minds in colorectal cancer research meet at the Gastrointestinal Cancers Symposium. Fight Colorectal Cancer and the Colon Cancer Alliance are partnering to bring you the big news in colorectal cancer from the 2013 symposium.
Join us to learn more about these topics:
- Can aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) keep cancer from returning?
- The relationship of body mass index (BMI) and exercise in colorectal cancer
- What scientists are learning about how your immune system can fight cancer
- The latest on what biomarkers can tell us about your cancer
- Rectal cancer treatment that is based on your biological make-up
The webinar will be led by Dr. Richard Goldberg, an internationally renowned gastrointestinal oncologist who specializes in colorectal cancer. He is a tenured professor in the Department of Internal Medicine at The Ohio State University and serves as physician-in-chief at Ohio State’s Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James).
Presentación realizada por la Dra. Pilar Escudero del HCU Lozano Blesa, en el marco de la I Jornada de actualización e innovación en Oncología que tuvo lugar en el CIBA en enero de 2015.
Colon cancer screening recommendationsPennMedicine
Colon cancer screening recommendation presentation from Dr. Tracy d'Entremont, Director of Oncology Services at the Abramson Cancer Center at Valley Forge.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Antimicrobial stewardship to prevent antimicrobial resistanceGovindRankawat1
India is among the nations with the highest burden of bacterial infections.
India is one of the largest consumers of antibiotics worldwide.
India carries one of the largest burdens of drug‑resistant pathogens worldwide.
Highest burden of multidrug‑resistant tuberculosis,
Alarmingly high resistance among Gram‑negative and Gram‑positive bacteria even to newer antimicrobials such as carbapenems.
NDM‑1 ( New Delhi Metallo Beta lactamase 1, an enzyme which inactivates majority of Beta lactam antibiotics including carbapenems) was reported in 2008
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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DISSERTATION on NEW DRUG DISCOVERY AND DEVELOPMENT STAGES OF DRUG DISCOVERYNEHA GUPTA
The process of drug discovery and development is a complex and multi-step endeavor aimed at bringing new pharmaceutical drugs to market. It begins with identifying and validating a biological target, such as a protein, gene, or RNA, that is associated with a disease. This step involves understanding the target's role in the disease and confirming that modulating it can have therapeutic effects. The next stage, hit identification, employs high-throughput screening (HTS) and other methods to find compounds that interact with the target. Computational techniques may also be used to identify potential hits from large compound libraries.
Following hit identification, the hits are optimized to improve their efficacy, selectivity, and pharmacokinetic properties, resulting in lead compounds. These leads undergo further refinement to enhance their potency, reduce toxicity, and improve drug-like characteristics, creating drug candidates suitable for preclinical testing. In the preclinical development phase, drug candidates are tested in vitro (in cell cultures) and in vivo (in animal models) to evaluate their safety, efficacy, pharmacokinetics, and pharmacodynamics. Toxicology studies are conducted to assess potential risks.
Before clinical trials can begin, an Investigational New Drug (IND) application must be submitted to regulatory authorities. This application includes data from preclinical studies and plans for clinical trials. Clinical development involves human trials in three phases: Phase I tests the drug's safety and dosage in a small group of healthy volunteers, Phase II assesses the drug's efficacy and side effects in a larger group of patients with the target disease, and Phase III confirms the drug's efficacy and monitors adverse reactions in a large population, often compared to existing treatments.
After successful clinical trials, a New Drug Application (NDA) is submitted to regulatory authorities for approval, including all data from preclinical and clinical studies, as well as proposed labeling and manufacturing information. Regulatory authorities then review the NDA to ensure the drug is safe, effective, and of high quality, potentially requiring additional studies. Finally, after a drug is approved and marketed, it undergoes post-marketing surveillance, which includes continuous monitoring for long-term safety and effectiveness, pharmacovigilance, and reporting of any adverse effects.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
3. Variable Low risk Intermediate risk High risk
Diameter 1.5 1.5-2.2 2.3+
Age cut-off 45 60
Smoking status Never Current 1pack/d Current 1+ pack/d
Smoking cessatin Quit 7+ yrs ago Quit 7- yrs ago Never quit
Nodule
characteristics
Smooth Scalloped Corona radiata or
spiculated
Solitary pulmonary nodule
Radiologic features likely to be benign
Stability over 2+ yrs.
Benign calcification: central nidus, multiple punctate, “bulls-eye” and popcorn
SPN/GGO
Stable over 2 yrs
Benign calcification
Less than 4 mm in diameter
Stop
High-risk of cancer
Tissue biopsy
Less than 8 mm
Repeat CT in 3 mo
8+mm/Low-Intermediate risk
of cancer
PET-CT
13. Trends in incidence of lung cáncer
- Women
GLOBOCAN, 20
http://globocan.iarc.fr/old/FactSheets/cancers/lu
14. Jemal A, Siegel R, Ward E et al. Cancer Statistics, 2009 CA Cancer J Clin 2009 59: 225-249
Mortalidad 1930-2005 USA: Hombres / Mujeres
Lung cancer
Projected life-time risk of developing
lung cáncer is 6% and 8% in females
and males, respectively (in the US).
Tobacco consumption closely parallels
lung cancer incidence 20 years later.
15. Jemal A, Siegel R, Ward E et al. Cancer Statistics, 2009 CA Cancer J Clin 2009 59: 225-249
Incidencia/Mortalidad USA: Hombres
16. Incidencia Mortalidad
Jemal A, Siegel R, Ward E et al. Cancer Statistics, 2009 CA Cancer J Clin 2009 59: 225-249
Incidencia/Mortalidad USA: Mujeres
17. Lung Cancer: Incidence and Mortality
New cases in 2013: 228,190
- 40% with stage IV disease at
presentation (~ 90,000)
~ 160,000 deaths in 2012,
comparable to prostate,
pancreas, breast, and colon
cancer combined
5-yr relative survival rate:
3.7% for patients with
distant-stage disease
NCI. Non-small-cell lung cancer treatment (PDQ®). ACS. Cancer facts & figures: 2012. CDC. Lung cancer
rates by race and ethnicity. Howlader N, et al. SEER cancer statistics review.
Estimated Cancer Deaths
by Site, 2012
Other Cancers Lung Cancer
180,000
160,000
140,000
120,000
100,000
80,000
60,000
40,000
20,000
0
Lung
cancer
Prostate
Pancreas
Breast
Colon
18. Incidencia y mortalidad por de cáncer en Colombia
Registro Poblacional de Cáncer - Calihttp://rpcc.univalle.edu.co/
Cáncer del pulmón
19. Risk Factors for Lung Cancer
Smoking
– Current: 2000%
– Former: 900%
– ETS: 30%
– 1 new mutation per 15 cigarettes smoked
Lung cancer deaths due to smoking
– ~ 91% males and 80% females[1]
Environmental factors[2]
– Second-hand smoke 3% to 5%
– Radon 3% to 5%
– Industrial pollution 0% to 5%
Radiation exposure Rare
– Asbestos, radon, radiation, silicosis, and berylliosis, nickel, chromium, mustard
gas, Polycyclic Aromatic Hydrocarbons, bischloromethyl ether
– Arsenic exposure, talc, obesity, genetic factors
1. CDC. Lung Cancer. 2011.
2. American Cancer Society. Lung Cancer. 2011.
30. Complexities of Lung Cancer Pathogenesis Result in
Diverse Histologic Subtypes
SCC
(~ 25%)
SCLC
(~ 15%)
LPA
(formerly BAC)
(~ 5% to 10%)
Adenocarcinoma(~
45%)
Large Cell
(~ 5% to 10%)
NOS
(~ 10% to 30%)
Reprinted by permission from Macmillan Publishers Ltd:
Sun S, et al. Nat Rev Cancer. 2007; 7:778-790.
Travis WD, et al. J Clin Oncol. 2013;[Epub ahead of print].
34. Kris MG, et al. ASCO 2011. CRA7506. Johnson BE, et al. IASLC WCLC 2011. Abstract O16.01
Lung Cancer Molecular Consortium Analysis in
Lung Adenocarcinomas
No Mutation
Detected KRAS
22%
EGFR
17%EML4-AKL
7%
Double
Mutants 3%
BRAF 2%
PIK3CA 2%
HER2
MET AMP
MEK1
NRAS
AKT1
Erlotinib
Gefitinib
Afatinib
Selumetinib
Crizotinib
35. How to handle small tissue samples in lung cancer
p63 and TTF1
H&E
SCC Non-SCC (Adeno)
Genomics
SCLC
NeuroEndocrine
EGFR
ALK/EML4
ROS1
BRAF
Her2
p63+ TTF1+
PD-L1 by IHC
(in advanced NSCLC)
PD-L1 by IHC
(in advanced NSCLC)
Chromogranin
Synaptophysin
38. T-descriptor
Every cm counts…
Previous (TNM 7th)
T1a
T1a
T1b
T2a
T2a
T2b
T3
Rami-Porta R, J Thoracic Oncol, 2015
Proposed (TNM 8th)
Up to 1 cm: T1a
>1-2 cm: T1b
>2-3 cm: T1c
>3-4 cm: T2a
>4-5 cm: T2b
>5-7 cm: T3
>7 cm: T4
International Association for the Study of Lung Cancer, 2015
39. T – Primary Tumour
Tx Primary tumour cannot be assessed
T0 No evidence of primary tumour
T1 Tumour 3 cm or less in greatest diameter surrounded by lung or visceral pleura, without evidence
of main bronchus
T1a(mi) Mininally invasive adenocarcinoma
T1a Tumour 1 cm or less in greatest diameter
T1b Tumour more than 1 cm but not more than 2 cm
T1c Tumour more than 2 cm but not more than 3 cm
T2 Tumour more than 3 cm but not more than 5 cm; or tumour with any of the following features:
Involves main bronchus (without involving the carina), invades visceral pleura, associated with
atelectasis or obstructive pneumonitis that extends to the hilar region
T2a Tumour more than 3 cm but not more than 4 cm
T2b Tumour more than 4 cm but not more than 5 cm
T3 Tumour more than 5 cm but not more than 7 cm or one tha directly invades any of the following:
chest wall, phrenic nerve, parietal pericardium, or associated separate tumour nodule(s) in the
same lobe as the primary
T4 Tumours more than 7 cm or one that invades any of the following: diaphragm, mediastinum,
heart, great vessels, trachea, recurrent laryngeal nerve, oesophagus, vertebral body, carina;
separate tumour nodule(s) in a different ipsilateral lobe to that of the primary
40. N-descriptor
No changes in the TNM 8th Edition…
Exploratory subgrouping (for future validation)
- N1a: Single N1
- N1b: Multiple N1
- N2a1: Single N2 (skip metastasis)
- N2a2: Single N2 + N1
- N2b: Multiple N2
Asamura H et al. J Thoracic Oncol, 2015, in press
International Association for the Study of Lung Cancer, 2015
41. YOUR LOGO
Lymph-node stations in lung cancer:
General Plan
Supraclavicular:
- Station 1
Superior mediastinal:
- Stations 2-4
Aortic:
- Stations 5/6
Inferior mediastinal:
- Stations 7-9
N1 nodes:
- Stations 10-14
http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
42. YOUR LOGO
N-stage in lung cancer
http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
43. YOUR LOGO
N-Stage in lung cancer
1. Station 1: Low cervical, supraclavicular, sternal notch lymph-nodes
2. 2L/2R: Upper paratracheal (R and L)
3. 4L/4R: Lower paratracheal
http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
44. YOUR LOGO
N-stage in lung cancer
3. Prevascular and Prevertabral nodes
Station 3 nodes are not adjacent to the trachea like station 2 nodes.
They are either:
3A anterior to the vessels or
3B behind the esophagus, which lies prevertebrally.
Station 3 nodes are not accessible with mediastinoscopy.
3B nodes can be accessible with endoscopic ultrasound (EUS).
http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
45. YOUR LOGO
N-Stage in lung cancer
2L/2R: Upper paratracheal (R and L)
3A: Prevascular
46. YOUR LOGO
N-Stage in lung cancer
4R. Right Lower Paratracheal
Upper border: intersection of caudal margin of innominate (left
brachiocephalic) vein with the trachea. Lower border:lower border
of azygos vein.
4R nodes extend to the left lateral border of the trachea.
http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
47. YOUR LOGO
N-Stage in lung cancer
4R.Lower Paratracheal
From the intersection of the caudal margin of innominate (left brachiocephalic) vein with the trachea to
the lower border of the azygos vein.
4R nodes extend from the right to the left lateral border of the trachea.
4L.Lower Paratracheal
From the upper margin of the aortic arch to the upper rim of the left main pulmonary artery.
Aortic Nodes 5-6
5. Subaortic
These nodes are located in the AP window lateral to the ligamentum arteriosum.
These nodes are not located between the aorta and the pulmonary trunk but lateral to these vessels.
6. Para-aortic
These are ascending aorta or phrenic nodes lying anterior and lateral to the ascending aorta and the aortic arch.
http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
48. YOUR LOGO
N-Stage in lung cancer
Aortic Nodes 5-6
5. Subaortic
These nodes are located in the AP window lateral to the ligamentum arteriosum.
These nodes are not located between the aorta and the pulmonary trunk but lateral to
these vessels.
6. Para-aortic
These are ascending aorta or phrenic nodes lying anterior and lateral to the ascending
aorta and the aortic arch.
49. YOUR LOGO
N-Stage in lung cancer
4R. Right Lower Paratracheal
Upper border: intersection of caudal margin of innominate (left brachiocephalic)
vein with the trachea.
Lower border:lower border of azygos vein.
4R nodes extend to the left lateral border of the trachea.
6. Para-aorticThese are ascending aorta or phrenic nodes lying anterior and lateral to the ascending aorta
and the aortic arch. http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
50. YOUR LOGO
N-Stage in lung cancer
7. Subcarinal nodes
These nodes are located caudally to the carina of the trachea, but are not associated with the
lower lobe bronchi or arteries within the lung.
On the right they extend caudally to the lower border of the bronchus intermedius.
On the left they extend caudally to the upper border of the lower lobe bronchus.
On the left a station 7 subcarinal node to the right of the esophagus.
10 Hilar nodes
Hilar nodes are proximal lobar nodes, distal to the mediastinal pleural reflection and nodes
adjacent to the intermediate bronchus on the right.
Nodes in station 10 - 14 are all N1-nodes, since they are not located in the mediastinum.
51. YOUR LOGO
N-Stage in lung cancer
8 Paraesophageal nodes
These nodes are below the carinal nodes and extend caudally to the diafragm.
On the left an image below the carina.
To the right of the esophagus a station 8 node.
10 Hilar nodes
Hilar nodes are proximal lobar nodes, distal to the mediastinal pleural reflection and nodes
adjacent to the intermediate bronchus on the right.
Nodes in station 10 - 14 are all N1-nodes, since they are not located in the mediastinum.
http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
52. YOUR LOGO
N-Stage in lung cancer
7. Subcarinal nodes
These nodes are located caudally to the carina of the trachea, but are not associated with the
lower lobe bronchi or arteries within the lung.
On the right they extend caudally to the lower border of the bronchus intermedius.
On the left they extend caudally to the upper border of the lower lobe bronchus.
On the left a station 7 subcarinal node to the right of the esophagus.
10 Hilar nodes
Hilar nodes are proximal lobar nodes, distal to the mediastinal pleural reflection and nodes
adjacent to the intermediate bronchus on the right.
Nodes in station 10 - 14 are all N1-nodes, since they are not located in the mediastinum.
53. YOUR LOGO
N-Stage in lung cancer
9. Pulmonary ligament nodes
Pulmonary ligament nodes are lying within the pulmonary ligament, including those
in the posterior wall and lower part of the inferior pulmonary vein. The pulmonary
ligament is the inferior extension of the mediastinal pleural reflections that surround
the hila.
http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
54. YOUR LOGO
N-Stage in lung cancer
Stations 10 - 14. N1 lymph-nodes
Hilar, lobar, segmental and subsegmental
Stations 10-14 are NOT mediastinal lymph-nodes.
http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
55. YOUR LOGO
N-Stage in lung cancer
http://www.radiologyassistant.nl/en/p4646f1278c26f/mediastinum-lymph-node-map.html (Accessed 2017)
56. M-descriptor
• M1a: as it is
• M1b: single metastasis in a single organ
• M1c: multiple metastases in a single organ or
in several organs
57. N – Regional Lymph Nodes
Regional lymph nodes cannot be assessedNx
No regional lymph node metastasisN0
Metastasis in ipsilateral peribronchial and/or ipsilateral hilar lymph nodes
and intrapulmonary nodes, including involvement by direct extension
N1
Metastasis in ipsilateral mediastinal and/or subcarinal lymph node(s)N2
Metastasis in contralateral mediastinal, contralateral hilar, ipsilateral or
contralateral scalene or supraclavicular lymph node(s)
N3
M – Distant Metastasis
No distant metastasisM0
Distant metastasisM1
Separate tumour nodule(s) in a contralateral lobe; tumour with pleaural or
pericardial nodules or malignant pleural or pericardial effusion
M1a
Single extrathoracic metastasis in a single organM1b
Multiple extrathoracic metastases in one or several organsM1c
International Association for the Study of Lung Cancer, 2015
58. STAGE T N M
Occult TX N0 M0
0 Tis N0 M0
IA1 T1a(mi)/T1a N0 M0
IA2 T1b N0 M0
IA3 T1c N0 M0
IB T2a N0 M0
IIA T2b N0 M0
IIB T1a-T2b N1 M0
T3 N0 M0
IIIA T1a-T2b N2 M0
T3 N1 M0
T4 N0/N1 M0
IIIB T1a-T2b N3 M0
T3/T4 N2 M0
IIIC T3/T4 N3 M0
IVA Any T Any N M1a/M1b
IVB Any T Any N M1c
International Association for the Study of Lung Cancer, 2015
59. 8th Edition of the TNM Classification
for Lung Cancer
N0 N1 N2 N3 M1a M1b M1c
T1a IA1 IIB IIIA IIIB IVA IVA IVB
T1b IA2 IIB IIIA IIIB IVA IVA IVB
T1c IA3 IIB IIIA IIIB IVA IVA IVB
T2a IB IIB IIIA IIIB IVA IVA IVB
T2b IIA IIB IIIA IIIB IVA IVA IVB
T3 IIB IIIA IIIB IIIC IVA IVA IVB
T4 IIIA IIIA IIIB IIIC IVA IVA IVB
International Association for the Study of Lung Cancer, 2015
62. If surgery is considered
Upfront assessment
Potentially resectable
Potentially resectable with
some risk of incomplete
resection
Not resectable
SURGERY IN STAGE III NSCLC
Eberhardt WEE, De Ruysscher D, Weder W, et al. 2nd ESMO Consensus Conference in Lung Cancer: locally advanced stage III non-small-cell lung cancer. Ann Oncol.
2015;26(8):1573-1588. doi:10.1093/annonc/mdv187.
63. If surgery is considered
Optimal pre-op work-up
Histopathology for PET-
detected isolated single met
Primary tumour of >3 cm large
axis, central tumours, cN1, CT-
enlarged lymph nodes with
small axis >1 cm
Symptomatic / High Risk (T4N2
PET-CT
Assessment of mediastinal
disease in PET+ or suspicious
lesions
Brain MRI
or N3)
SURGERY IN STAGE III NSCLC
Eberhardt WEE, De Ruysscher D, Weder W, et al. 2nd ESMO Consensus Conference in Lung Cancer: locally advanced stage III non-small-cell lung cancer. Ann Oncol.
2015;26(8):1573-1588. doi:10.1093/annonc/mdv187.
64. YOUR LOGO
Tratamiento de NSCLC temprano
(Estadíos I-IIIA)
CIRUGÍA EN NSCLC
• Se recomienda cirugía para T resecables (T1-T3), sin
compromiso mediastinal (N0-N1)
- Lobectomía o pneumonectomía (+ disección ganglionar
mediastinal).
- Considerar SBRT en casos selectos (No candidatos a
cirugía)
• No se recomienda cirugía para pacientes con T4, N2 o N3 -
Si no hay metástasis, proceder con quimiorradioterapia
(Cisplatino + Etopósido)
65. Physiologic staging
Appropriate FEV1
- Greater than 2L for pneumonectomy
- Greater than 1.5L for lobectomy
VOmax greater than 15 mL/(kg.min)
Surgery contraindicated in:
- AMI within the last 3 months
- AMI within the last 6 months (relative)
- Uncontrolled arrhythmias
- FEV1 less than 1L
- DLCO less than 40%
- Severe pulmonary hypertension
- pCO2 greater than 45 mmHg
67. YOUR LOGO
NSCLC: Prognostic Factors
Factors correlated with adverse prognosis in resected
patients
- Presence of pulmonary symptoms
- Large tumor size (>3 cm)
- Nonsquamous histology
- Metastases to multiple lymph nodes within a TNM-defined nodal station
- Vascular invasion
For patients with inoperable disease, prognosis is adversely
affected by poor performance status, weight loss of more than
10%, male gender
Advanced age alone has not been shown to influence
response or survival with therapy
NCI. Non-small-cell lung cancer treatment (PDQ®).
68. YOUR LOGO
Tratamiento de NSCLC temprano
(Estadíos I-IIIA)
RADIOTERAPIA ADYUVANTE
• Estadíos I, II, IIIA no quirúrgicos
• Luego de cirugía si márgenes comprometidos
• Luego de cirugía si ganglios linfáticos mediastinales
comprometidos (estadío IIIA).
69. YOUR LOGO
Tratamiento de NSCLC temprano
(Estadíos I-IIIA)
QUMIOTERAPIA ADYUVANTE
- Estadíos II-III (algunos incluyen Ib)
- Dupletas basadas en cisplatino x4 meses
73. Potentially resectable stage III, but high
risk of incomplete resection
Superior sulcus tumors
Induction ChemoRT followed by Surgery
POTENTIALLY RESECTABLE STAGE III NSCLC
74. Potentially resectable stage III, but high
risk of incomplete resection
Selected Central T3-T4 tumors
Induction ChemoRT followed by Surgery*
T4N0-1
Definitive ChemoRT
Surgery within 4 weeks after RT finished
POTENTIALLY RESECTABLE STAGE III NSCLC
Eberhardt WEE, De Ruysscher D, Weder W, et al. 2nd ESMO Consensus Conference in Lung Cancer: locally advanced stage III non-small-cell lung cancer. Ann Oncol.
2015;26(8):1573-1588. doi:10.1093/annonc/mdv187.
Eberhardt W, Gauler T, Pöttgen C et al. Phase III study of surgery versus definitive concurrent chemoradiotherapy boost in patients with operable (OP+) stage
IIIA(N2)/selected IIIb non-small cell lung cancer (NSCLC) following induction chemotherapy and concurrent CRTx (ESPATUE). J Clin Oncol 2014; 32(5s suppl): abstr
75. Unresectable Stage III disease
Unresectable stage III disease
Bulky and multiple mediastinal nodal involvement
Stage IIIB disease based on unresectable T4
Stage IIIB disease based on N3
Eberhardt WEE, De Ruysscher D, Weder W, et al. 2nd ESMO Consensus Conference in Lung Cancer: locally advanced stage III non-small-cell lung cancer. Ann Oncol.
2015;26(8):1573-1588. doi:10.1093/annonc/mdv187.
76. Unresectable Stage III disease
Unresectable stage III disease
Definitive Concurrent ChemoRT
Sequential ChemoRT
Palliative therapy
77. YOUR LOGO
The many faces of stage III NSCLC
Post surgical N2/N3+ disease - Adjuvant CT
- Consider adjuvant RT
Known N2/N3+ disease
- Definitive chemo RT with platin-based chemotherapy
- Consider chemo RT with platin-based chemotherapy followed by surgery (if
lobectomy is sufficient) in non-bulky N2 disease.
Superior sulcus tumors - Arise in the apex of the lungs
- Invade the 2nd and 3rd ribs, brachial plexus, subclavian vessels, stallate
ganglion and vertebral body
- Pancoast syndrome: pain in the shoulder or chest wall or radiate to the neck and ulnar
aspect of the upper limbs. - Horner’s syndrome
- Neoadjuvant Chemo-RT followed by surgery (if not N2/N3 disease)
- Excellent LT OS: 50+%
78. Stage IV - NSCLC – PS 0-1
NSCLC without “Driver” – PD-L1<50%
NSCLC
Squamous*
NSCLC
Non-squamous
CT with Platinum +
Pemetrexed or
Paclitaxel + Bevacizumab
CT with Platinum+
Gemcitabine or Paclitaxel
*Bevacizumab is contraindicated due to fatal bleeding
*Pemetrexed is ineffective in squamous histology
85. Inmunología tumoral
Cebado
(priming) y
activación de
las células T
Célula
tumoral
PD-1
PD-L1
PD-L2
Receptor de
células T
MHC-1
CD28
Shp-2
B7.1
Célula
DendríticaLinfocito T
CD8+/Citotóxi
co
Co-estimuladora CD28 Co-estimuladora B7.1
88. Inmunología tumoral
Activación
de la
respuesta
inmunológi
ca CD8
efectora
Célula
tumoral
PD-1
PD-L1
PD-L2
Receptor de
células T
MHC-1
CD28
Shp-2
B7.1
Linfocito T
CD8+/Citotóxi
co
Antígeno + MHC-
1
Receptor de células T (TCR)
+++
Respuesta inmune
antitumoral
Presente
91. Inmunología tumoral
Las células
tumorales
expresan PD-L1
(PD-L2) cuando
hay estimulación
continuada del
IFN-Gamma,
"apagando" al
linfocito T
Célula
tumoral
PD-1
PD-L1
PD-L2
Receptor de
células T
MHC-1
CD28
Shp-2
B7.1
Linfocito T
CD8+/Citotóxi
co
IFN-γ
IFN-
γR
PD-L1
PD-1
- - -
Respuesta inmune
antitumoral
Frenada
99. EGFR in NSCLC: two distinct
pathways
Nucleus
Adaptor
Survival
PIP2
PI3K
PIP3
PTEN
AKT
Apoptosis
regulators
Proliferation
Adaptor
Transcription
factors
MAPK
MEK
RAFGTP-RASGDP-RAS
Sordella, et al. Science 2004
ATP ATP
Greater signalling through the
MAPK pathway producing
excessive cell proliferation
Higher affinity for ATP than
mutant receptor, so greater
competition with EGFR TKIs for
binding sites; higher
concentrations needed to inhibit
Successful inhibition of wild-type
EGFR reduces proliferation and
halts tumour growth
Higher incidence of stable disease
EGFR
wild-type
100. EGFR in NSCLC: two distinct pathways
ATP
Nucleus
Adaptor
Survival
PIP2
PI3K
PIP3
PTEN
AKT
Apoptosis
regulators
Proliferation
Adaptor
Transcription
factors
MAPK
MEK
RAFGTP-RASGDP-RAS
Sordella, et al. Science 2004
ATP
Preferential signalling through the PI3K-
mediated anti-apoptotic pathway –
‘oncogene addiction’
Reduced affinity for ATP means EGFR TKIs
have less competition for binding sites;
lower concentrations sufficient to inhibit
Successful inhibition of mutated EGFR
produces ‘apoptotic shock’
Higher incidence of complete or partial
response
EGFR
mutation
+ve
101. EGFR mutation +ve NSCLC:
different epidemiology
Majority of mutations are exon 19
deletions or L858R point mutations
in exon 21
EGFR
Chromosome 7
Shigematsu, et al. JNCI 2005; Murray, et al. JTO 2008
n=3,303
Exons 1–16
Exon 17
Exons 18–24
Exons 25–28
Extracellular domain
Transmembrane domain
TK domain
Regulatory domain
EGFR transcript EGF protein
Exon 18 Exon 19 Exon 20 Exon 21
50
40
30
20
10
0
Incidence(%)
105. SEER Fact Sheet
Distribución porcentual del estadío a la
presentación y supervivencia a 5 años
de cáncer de pulmón
Estadío a la presentación
Supervivencia a 5 años
108. Carcinoma broncogénico de
células pequeñas (SCLC)
Generalidades
- Menos común que el NSCLC (1/6, aprox.)
- Mayor asociación con tabaquismo
- Diseminación a distancia mucho más precoz en la
historia natural
- El espectro más agresivo de neoplasias
neuroendocrinas
109. Carcinoma broncogénico de
células pequeñas (SCLC)
Patología –
- Carcinoma de células pequeñas (SCLC)
- Célula pequeña, redonda y azul.
- Tiñe positivo para cromogranina y sinaptofisina (marcadores
neuroendocrinos)
Patrones de diseminación
- Masa central con extenso compromiso hiliar y mediastinal.
- Metástasis al:
- Hueso,
- Hígado,
- Cerebro,
- Pulmón,
- Adrenales.
110. SCLC
Estadificación
- ESTADÍO LIMITADO:
- T1-4 (excluyendo derrame pleural) N0-3M0:
- Usualmente se puede cubrir en un campo de radioterapia.
- ESTADÍO EXTENDIDO:
- Estadío IV: M1, y estadío III con derrame pleural.
- Supervivencia a 5 años
- Estadío I:
- Supervivencia a largo plazo del 70% (luego de cirugía y quimioterapia).
- Estadío Limitado:
- Supervivencia mediana 4 meses sin tratamiento,
- Supervivencia mediana 17 meses
- Curación en el 5-10%.
- Estadío Extendido:
- Supervivencia mediana 2-4 meses sin tratamiento.
- Se incrementa a 8-10 meses con terapia actual
- Aproximadamente 3% se curan
111. Small-Cell Lung Cancer: work-up and management
CT-Chest/Abdomen + Brain MRI +/- Bone Scan
SCLC
Stage I All others
PET-CT + Brain MRI
Confirmed Stage I
Surgery + EP
Limited-Stage Extended-stage
EP + RT + PCI EP +/- PCI
EP: Etoposide + Cisplatin x4 months
70% LT survival Median OS: 20 months Median OS: 9 months