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Denise Brock

Lung Cancer Video Library – Spanish Language: Video #37 Basics of Lung Cancer Staging

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GRACE Cancer Video Library - Lung

 

We are pleased to continue this series of informational videos for our Spanish speaking community.  GRACE is pleased to welcome Dr. Rafael Santana-Davila, Assistant Professor with the University of Washington School of Medicine and Seattle Cancer Care Alliance.  In this 37th video for the Spanish lung cancer video library, Dr. Santana-Davila joined GRACE to discuss the basics of lung cancer staging.  


 

 

 

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TRANSCRIPTS – Spanish and English
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Lo básico en los estadios de cancer de pulmón

Basics of lung cancer staging

 Dr. Rafael Santana-Davila

Chief of Hematology/Oncology and Medical Director, Memorial Cancer Institute,
Clinical Associate Professor of Medicine, Florida International University

 

Spanish TRANSCRIPT

Lo principal que nos preguntamos nosotros cuando vemos a un paciente con cáncer es en que estadio esta, que es básicamente que tan avanzado está el cáncer. Cuando el cáncer esta solo en el pulmón, no se ha ido a ningún ganglio linfático ni a otra parte del cuerpo, le llamamos estadio uno. Cuando el cáncer ha avanzado a ganglios linfáticos cercanos pero no al mediastino es estadio dos y cuando avanza al mediastino es estadio tres. Por último cuando ha avanzado a otros órganos, a la región pleural del pulmón o a otras partes del pulmón, le llamamos estadio 4.

En cáncer de células pequeñas es relativamente fácil diagnosticar en que estadio está, ya que si está solo en un pulmón le llamamos estado limitado y cuando está en varias partes del pulmón o en el otro pulmón u otras partes del cuerpo le llamamos estadio avanzado. 


 

 

English TRANSCRIPT

The main question to have when we see a cancer patient is in what stage he is, which is basically how advanced the cancer is. When the cancer is located just in the lung, has not affected a lymph node or any other organ is called stage one. When the disease has affected lymph nodes close to the cancer but not the mediastinum is called stage two, while the affection of the mediastinum is stage three. Finally, when the cancer has spread to other organs, the pleura of the lung or other parts of the lung is called stage four.

In small lung cancer cells is relatively easy to diagnose the stage because when it’s only present in the lung it’s the limited stage and when it is located in several parts of the lung, or in the other lung or other organs is the advanced stage.


Denise Brock

Lung Cancer Video Library – Spanish Language: Video #36 Treatment Options for Acquired Resistance to EGFR TKIs: T790M-Negative Disease

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GRACE Cancer Video Library - Lung

 

We continue to provide informational videos for our Spanish speaking community and welcome Dr. Luis Raez, MD FACP FCCP, Chief of Hematology/Oncology and Medical Director at Memorial Cancer Institute, and Clinical Associate Professor of Medicine at Florida International University.  Dr. Raez joined GRACE to discuss the basics of lung cancer.  In this 36th video for the Spanish lung cancer video library, Dr. Raez discusses treatment options for acquired resistance to EGFR TKIs: T790M-negative disease.


 

How Did You Like This Video?

Please feel free to offer comments and raise questions in our Discussion Forums.


 

TRANSCRIPTS – Spanish and English
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Opciones de tratamiento para la resistencia adquirida a los inhibidores de tirosinas cinasa del receptor del factor de crecimiento epidérmico (EGFR): enfermedad T790M negativo.

Treatment options for acquired resistance to tyrosine kinase inhibitor in the epidermal growth factor receptor (EGFR): T790 negative disease

 Dr. Luis Raez, MD FACP FCCP

Chief of Hematology/Oncology and Medical Director, Memorial Cancer Institute,
Clinical Associate Professor of Medicine, Florida International University

 

Spanish TRANSCRIPT

También cuando hablamos de resistencia a inhibidores de la tirosina cinasa, ya hablamos que para los pacientes con 790 hay un nuevo fármaco que se llama osimertinib. El problema es ¿qué hacemos con el resto de los pacientes? Como les decía 60% de los pacientes que están en inhibidores de la tirosina cinasa, van a tener la mutación 790, que, si ustedes saben la pueden encontrar en la sangre, la orina o en una nueva biopsia, y ahí vamos a poder usar el fármaco nuevo.

Pero, ¿qué hacemos con el 40% de pacientes que no podemos documentar la mutación?

Hay esperanza para estos pacientes porque sabemos hoy en día que para muchos de estos pacientes que no tienen esta mutación, el mecanismo de resistencia está a través de la vía MET. Entonces tenemos en investigación inhibidores de MET y de su vía, que podría ser una solución para salvar a estos pacientes. La otra opción es que algunos de estos pacientes, en un grupo pequeño como del 10% hacen carcinoma de pulmón de células pequeñas. En otras palabras, el tumor original que era carcinoma de células granes se transforma en carcinoma de células pequeñas, entonces estos pacientes no van a responder a ninguna terapia blanco existente porque no tenemos terapia blanco para carcinoma de células pequeñas y entonces hay que ponerlo en quimioterapia.

Por eso es tan importante hacer una biopsia, porque si no hacemos una biopsia cuando en el paciente falla el receptor de la tirosina cinasa nunca nos vamos a enterar que el paciente transformo a carcinoma de células pequeñas y nunca le vamos a dar la quimioterapia adecuada.

Al final, mientras estos descubrimientos y otros van avanzando lo que hay que hacer es poner a los pacientes en quimioterapia. Cuando un paciente falla y no podemos documentar la mutación 790, hay que ponerlo en quimioterapia o en un estudio clínico que el paciente pueda calificar.


 

English TRANSCRIPT

When we talk about tyrosine kinase inhibitors resistance, we know that for patients with the 790 mutation, we have the drug osimertinib. The problem is, what do we do with the rest of the patients? As I told you, 60% of the patients that are in tyrosine kinase inhibitors will have the 790 mutation that if we can find them in the blood, urine or in a new biopsy, we will be able to use the new drug.

But, what do we do with the 40% of patients in which we cannot verify the mutation?

There is hope for these patients because nowadays we know that most patients without this mutation have their resistance mechanism via de MET pathway. We have MET and their pathway inhibitors that could be the solution for these patients. The other option is that some patients, in a group of around 10%, make small cell lung cancer. In other words, the original large cell lung cancer transformed into small cell lung cancer. These patients will not respond to any existing targeted therapy because we don’t have a small cell cancer treatment, so we have to put them in chemotherapy. 

That is why it is so important to make a biopsy, because if we don’t make a biopsy when the patients fails with the tyrosine kinase inhibitors, then we will never know that the patient probably transformed into a small cell lung cancer and we will never give him the right therapy.

At the end, while these findings and more research is progressing, what we have to do is put the patients in chemotherapy. When a patient fails with the treatment and we cannot verify 790 mutation, we have to put him in chemotherapy or in a suitable clinical trial.


Denise Brock

Lung Cancer Video Library – Spanish Language: Video #35 Treatment Options for Acquired Resistance to EGFR TKIs: T790M-Positive Disease

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GRACE Cancer Video Library - Lung

 

We continue to provide informational videos for our Spanish speaking community and welcome Dr. Luis Raez, MD FACP FCCP, Chief of Hematology/Oncology and Medical Director at Memorial Cancer Institute, and Clinical Associate Professor of Medicine at Florida International University.  Dr. Raez joined GRACE to discuss the basics of lung cancer.  In this 35th video for the Spanish lung cancer video library, Dr. Raez discusses treatment options for acquired resistance to EGFR TKIs: T790M-positive disease.


 

How Did You Like This Video?

Please feel free to offer comments and raise questions in our Discussion Forums.


 

TRANSCRIPTS – Spanish and English
download transcripts
 

Opciones de tratamiento para la resistencia adquirida a los inhibidores de tirosinas cinasa del receptor del factor de crecimiento epidérmico (EGFR): enfermedad positiva en T790M

 Treatment options for acquired resistance to tyrosine kinase inhibitor of the epidermal growth factor receptor (EGFR): T790 positive disease. 

 Dr. Luis Raez, MD FACP FCCP

Chief of Hematology/Oncology and Medical Director, Memorial Cancer Institute,
Clinical Associate Professor of Medicine, Florida International University

 

Spanish TRANSCRIPT

Hablando de resistencia en el caso de los receptores de EGFR, hay una mutación nueva que aparece llamada T790M. Es la más popular y se calcula que a veces hasta en el 60% de los pacientes que están en inhibidores de la tirosina cinasa, van a desarrollar mutaciones resistentes en T790M y hay otro 40% con otras etiologías.

Es importante documentar que el paciente tiene esta mutación nueva 790 porque ya tenemos un tratamiento específico, que es el fármaco osimertinib que ya está disponible en Estados Unidos y Europa y próximamente en todo el mundo que es otro inhibidor de la tirosina cinasa. Es un fármaco bien tolerado, no es muy tóxico, se parece a otros inhibidores de la tirosina cinasa. Incluso les diría que es menos tóxica en a lo que se refiere a piel y sistema gastrointestinal.

Lo importante es diagnosticarlo porque si uno no puede probar que el tumor ha hecho una mutación 790, no podemos darle el fármaco. Este fármaco está aprobado específicamente para pacientes que tienen esta mutación. Así que yo creo que es importante que cuando en un paciente falla un inhibidor de la tirosina cinasa, que se le haga una nueva biopsia, una biopsia líquida o una muestra de orina para documentar que el paciente haya hecho una resistencia y que se le haya encontrado la mutación 790 que usualmente no está al comienzo y así poder cambiar la terapia.


 

 

English TRANSCRIPT

Talking about resistance in the EGFR receptor, there is a new mutation called T790M. It’s by far the most popular and around 60% that are currently in tyrosine kinase inhibitor, will develop resistant mutations to T790M, the other 40% will have other etiologies.

It is of great priority to document that the patient has this new 790 mutation, because we already have a new specific treatment. This is the drug osimertinib, a tyrosine kinase inhibitor, already available in United Stated and in Europe, and in the near future worldwide. I would even say that this drug is less toxic in the skin and in the gastrointestinal tract.

The important here is the diagnosis because if one cannot prove that the tumor has made a 790 mutation, then we cannot give him the drug. This drug is approved specifically for patients with this mutation. So, I think, it’s very important that when a patient fails with the tyrosine kinase inhibitor, we should make a new biopsy, a liquid biopsy or an urine test to document that the patient has developed resistance and that he has the 790 mutation which is usually not developed in the beginning. This way, we will be able to change therapy.


Dr West

EGFR Tyrosine Kinase Inhibitors for Patients with EGFR Mutations

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Back when I first started doing this, one of my earliest posts (see here) was on the question of whether EGFR tyrosine kinase inhibitors (TKIs) (see introduction to this work in prior post). My point, which is still true, is that EGFR TKIs aren’t only effective in a narrow population of patients, whether identified based on molecular or clinical variables. But in the more limited number of patients who have the “activating mutation” in the actual receptor, who might be expected to do especially well with an EGFR TKI, how do they do? How does a targeted therapy do in a precisely targeted population?

There are several studies that have now tested this by identifying patients who have an EGFR mutation and received an EGFR TKI. As shown in the table below, the results are very clear and consistent.

Prospective trials of EGFR TKIs in pts with EGFR Muts

(Click to enlarge)

Continue reading


Dr West

EGFR Inhibitors Iressa and Tarceva: A Tale of Two TKIs (Part I)

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I haven’t really covered the history or issues of directly comparing the two oral inhibitors of the epidermal growth factor receptor, or EGFR, which are Iressa (gefitinib) and Tarceva (erlotinib). This is really because over the last few years, gefitinib has had disappointing results in some important trials and is no longer readily used or available, while the remarkably similar drug Tarceva has been approved by the US FDA and is a standard treatment for patients with advanced NSCLC that has previously been treated with chemotherapy. So you already know where we are in the story in early 2007. While it appears that Iressa for lung cancer is no longer very relevent for clinical management of lung cancer in the US, several trials of Iressa are still emerging that compare it to chemotherapy, so it’s important to review the similarities and differences of Iressa and Tarceva as we consider whether the effects with Iressa can be generalized to the “class” of EGFR inhibitors.

We’ll step back for a moment to say that the molecular target for both drugs is EGFR, which is expressed on some normal body tissues, including skin (it’s an epidermal growth factor), but it’s also expressed on 40-80% of NSCLC tumors and many other kinds of cancers. In fact, in lab studies using test tube as well as animal models, activating the receptor leads to activities in cancer cells that lead to cancer cell growth and division, as well as decreased likelihood of the cancer cell dying and a higher chance of it invading tissues and spreading elsewhere in the body.

EGFR Mechanisms (click to enlarge)

In people, several types of cancers that have high degrees of expression of the protein on the tumor cells have been shown to be more aggressive and be associated with more aggressive behavior and worse survival outcomes. On the other hand, drugs that inhibit EGFR, which can be antibodies that block EGFR on the outside of the cell (such as Erbitux (cetuximab) and Vectabix (panitumumab) or tyrosine kinase inhibitors (such as Iressa and Tarceva) that act on the inside of the cell on the back end of the receptor, block the cancer-promoting effects of an activated EGFR molecule. So Iressa and Tarceva act on the same part of the EGFR molecule.

EGFR MoAbs vs TKIs figure Continue reading


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