GRACE :: Lung Cancer

The Predicament of Poorly Differentiated NSCLC/NSCLC NOS

Dr West — Fri, 12 Mar 2010 19:43:47 +0000

A topic that came up in a recent expert round table case discussion was the issue of how to manage a patient with a lung cancer for which the pathology report says “NSCLC not otherwise specified (NOS)”, or “poorly differentiated NSCLC, NOS”. What does this actually mean, and what does it mean in terms of treatment options?

Tumors of pretty much all types are categorized by their tumor grade, how “differentiated” they are, which basically means, “how much do the cancer cells look like the cells they started out as?”. Different cells of the body start out as stem cells, which means that they’re not specialized to be any special kind of cell, like one that detects light in the back of the retina, lines the esophagus, or is optimized for lung function. Most cells of the body are differentiated, so that the appearance under a microscope shows that it’s a liver cell, part of the kidney filtering mechanism, heart muscle, etc.

Cancer cells, however, have mutations in them that make them grow and divide faster than other cells (that’s why they make a tumor that pushes other tissues aside), and they usually have several. As they grow and divide, they often make sloppy copies of their DNA that leads to more mutations. Cancers therefore are made of cells that may look a lot like the normal cells they originated from (well-differentiated), or they have lots of mutations that make the cells look so chaotic that they don’t look at all like the cells they started out as (poorly differentiated).

Today, oncologists want to know whether a non-small cell lung cancer (NSCLC) is an adenocarcinoma, squamous cell carcinoma, large cell neuroendocrine carcinoma, etc. But about 20% of the time on various studies, we get an answer back of “NSCLC not otherwise specified”. As explained by Dr. Matt Horton, expert lung cancer pathologist, a lung tumor may be classified as NSCLC NOS because of either of two reasons:

1) there isn’t enough tissue, because the biopsy material was very scant, or

2) the tumor is so poorly differentiated that even with all of the material in the world, a good pathologist couldn’t identify the underlying NSCLC histology

Dr. Horton says that many of the conclusions of NOS are because there isn’t enough pathology material to review, and now there is an ever-growing list of reasons for why we’d want to ensure that this isn’t a problem. First, knowing whether a cancer is a squamous cell carcinoma or an adenocarcinoma or another subtype is important for deciding whether it’s appropriate for patients to get Avastin (bevacizumab) (since the risk of serious or even fatal bleeding complications is considerably higher in patients with squamous NSCLC who receive an anti-angiogenic agent like Avastin) or Alimta (pemetrexed) (because the evidence shows that Alimta isn’t effective in patients with a squamous NSCLC). Second, there’s now a growing role for collecting enough tissue to due testing for specific mutations like EGFR, possibly an ALK rearrangement, and arguably K-RAS. With the field moving to molecularly-based treatment plans for specific molecular defects, and more clinical trials and treatments being dependent on molecular testing, it’s necessary to have tissue to do these studies on.

But sometimes even with a resected early stage cancer, a situation in which a pathologist has all of the tumor tissue he or she could want, it’s not possible to make a good histologic assignment because the cancer cells just look too chaotic under the microscope. A study from ASCO 2009 showed that, as you’d expect, expert pathologists from academic centers tend to have agreement in their interpretation of NSCLC subtype than community-based pathologists, but neither groups really agree consistently on poorly differentiated tumors. Essentially, this is just saying the same thing we’d say about interpreting ambiguous lesions on scans, or treating aggressive and resistant cancers: the hard ones are hard for everyone. In fact, there is also evidence that, stage for stage, patients with poorly differentiated cancers don’t tend to do as well as patients with better differentiated cancers. This is probably because they’re also more aggressive. The cancers that are so chaotic that experts can’t determine the histologic subtype are also likely to grow and divide very quickly, and be far less likely to have a specific mutation like EGFR or an ALK mutation driving them — instead, they’re driven by a combination of many, many mutations.

It’s worth noting that there are companies now studying the “molecular signature” of a poorly differentiated cancer that promises to clarify whether a tumor is actually a squamous NSCLC or adenocarcinoma or other squamous. Companies like Biotheranostics can do detailed molecular typing, and others exist as well. I don’t generally use these, because I think that there may well be something different about a cancer that requires this kind of assessment to know its histology than the ones that a pathologist can assign. I wouldn’t presume that a cancer that is so poorly differentiated that you need molecular testing to determine that it’s a lung adenocarcinoma will act the same as a better differentiated adenocarcinoma.

So practically speaking, what does it mean if a cancer is so poorly differentiated that you can’t assign a histology? First, these tend to be very unlikely to carry an EGFR mutation or ALK rearrangement, so I would favor chemo-based treatment and wouldn’t prioritize testing for every molecular marker under the sun early in the workup. As I mentioned above, these tumors have a tendency to be bad actors, but we still treat them basically the same as other NSCLC tumors. I personally am less enthused about using Avastin in patients with a very poorly differentiated tumor, though the ECOG study that showed a survival benefit with Avastin added to chemo included 20% of patients with NSCLC NOS, and they really didn’t have increased bleeding at all. Still, I’m a little more concerned that bleeding could be an issue, particularly if the cancer is in the central part of the chest and near any major blood vessels. That said, other experts, including ones included in the case discussion from the beginning of this post, are still comfortable giving Avastin to patients with NSCLC NOS, so it’s clearly a debatable question.

The other issue is whether to give Alimta to patients with a poorly differentiated NSCLC that can’t be assigned a histology. The approval of Alimta is now for patients with non-squamous NSCLC, and NSCLC still is considered non-squamous if it isn’t called squamous. Still, it’s not clear that patients with a very poorly differentiated cancer will benefit as much as the patients with a moderately differentiated adenocarcinoma. When other chemo agents commonly used for NSCLC aren’t dependent on the histology, I and I believe most oncologists favor an alternative to Alimta as a first line approach and tend to relegate it to a later choice. This isn’t the same situation as being potentially more dangerous than other options, but we’d always want to use agents with the best probability of success as our first treatment.

This is certainly a tough area, and it’s also a moving target. More and more of the field is becoming dependent on the tissue (”the tissue is the issue“), and we may move toward identifying particular mutations and genetic patterns associated with better results with chemo A vs. chemo B, but right now this is the state of the field.

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Case Discussion with Experts, Drs. Julie Brahmer & Greg Riely, Part 1

Dr West — Wed, 10 Mar 2010 03:47:40 +0000

Here’s a webinar case discussion I did with Drs. Julie Brahmer from Johns Hopkins in Baltime, and Greg Riely from Memorial Sloan Kettering Cancer Center in New York. They’re great thoracic oncologists as wellas friends, and they were kind enough to join me for discussion of several complex cases that don’t have clear answers and illustrate the reality that even when we know the evidence, there’s plenty of room for judgment.

Our first case is about a 63 year-old woman who has a poorly differentiated NSCLC that is just outside of the range we’d feel feasible for radiating, and it brings up issues related to trying to integrate chemo and possible radiation, the debatable role of agents like Avastin (bevacizumab) and Alimta (pemetrexed) for cancers that are hard to classify, and then how we approach managing patients who have responded well — observation or maintenance?

Here is the audio and video versions of the podcast, along with the associated transcript and figures.

rt-brahmer-riely-webinar-case-1-audio-podcast

rt-brahmer-riely-webinar-case-1-transcript

rt-brahmer-riely-webinar-case-1-figures

My thanks go out again to Drs. Brahmer and Riely for their time and thoughtful comments. You’ll hear more from them about a couple of additional cases in the next few weeks.

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Podcast of Q&A Portion from Molecular Markers Webinar with Dr. Pennell

Dr West — Sun, 07 Mar 2010 19:52:10 +0000

Here’s the podcast of the Q&A portion of the excellent webinar with Dr. Pennell on Molecular Markers in Management of NSCLC.

dr-pennell-molecular-markers-qa-audio-podcast

dr-pennell-molecular-markers-qa-transcript

dr-pennell-molecular-markers-qa-figures

Obviously, people may have additional questions about this topic but who weren’t able to attend the live program. If you’d like to ask a question about molecular markers in lung cancer after this point, Dr. Pennell and/or one of the other GRACE faculty will be happy to try to give our best answer.

By the way, thanks again to Response Genetics for their grant to support this educational program.

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Round Table with Drs. Anne Tsao and Alex Farivar, Part 2: Mesothelioma

Dr West — Fri, 05 Mar 2010 04:19:21 +0000

This is part 2 of my round table case discussion with Dr. Anne Tsao, a medical oncologist and thoracic oncology expert from MD Anderson Cancer Center in Houston, and Dr. Alex Farivar, a thoracic surgeon with expert training in mesothelioma at Swedish Cancer Institute in Seattle. This particular case covers a patient with a mesothelioma, cancer of the lining around the lung, which is also known as malignant pleural mesothelioma.

Here is the audio and video versions of the podcast, along with the transcript and figures.

round-table-with-drs-tsao-and-farivar-part-2-meso-case-audio-podcast

round-table-with-drs-tsao-and-farivar-part-2-meso-case-transcript

round-table-with-drs-tsao-and-farivar-part-2-meso-case-figures

By the way, my apologies for the poor audio quality, a combination of inadequate recording, passing buses outside of the public space we were in, etc. It’s audible and still useful to people who are interested in learning about this topic, but this recording is below the standard for which we’re striving. To be honest, part of the audio quality issue was that we went for a lower cost sound guy, and it shows. So please consider a contribution, because it goes for things like having our podcasts sound better. You get what you pay for, and we would prefer to do better than “shoestring budget” quality.

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Watching Small Lung Lesions Do Nothing: “Ground Glass Opacities” Don’t Progress Over Years If They’re Watched, Not Resected

Dr West — Wed, 03 Mar 2010 03:36:45 +0000

In one of my earliest posts about bronchioloalveolar carcinoma (BAC) (in the dark ages, pre-Twitter), I wrote on the subject of managing small BAC-type lesions, which tend to appear as small hazy areas called “ground glass opacities” (GGOs) and suggested that some of these cancers may be so indolent that they don’t need to be treated, even if they have the word “carcinoma” in the diagnosis.

(a representative GGO identified by arrow)

Now there is a proposal to change BAC to “adenocarcinoma in situ“, a pre-cancerous condition, reflecting the idea that these lesions have such a favorable prognosis that they shouldn’t necessarily be put in the same category as invasive lung cancers (pure BAC is a non-invasive lesion that shouldn’t be able to get into the bloodstream and spread outside of the lungs). And now, there’s a new article out of Japan that describes the experience of patients with BAC and multiple GGOs, some of which were resected and some not very accessible and some just watched. It turned out that just watching seemed to be a pretty good strategy.

The article out of Korea was published in the Journal of Thoracic Oncology and describes the experience of 73 patients with pathology-proven BAC, among whom 23 had other small GGOs identified pre-operatively. They followed patients after surgery for a median of 40 months and found that none of the patients with one or more identified small GGOs (<1 cm was their limit) showed any growth of these lesions; most stayed the same, and a few lesions actually regressed (they may not have been BAC and could have been inflammation or infection). They certainly had no impact on survival. Though the results are limited by the relatively short follow-up (just over 3 years of follow-up doesn’t mean people are out of the woods), they do suggest that it’s reasonable to use a watch and wait approach, at least for GGOs (which don’t have a solid component that suggests an invasive cancer) that are less than a centimeter (larger tumors are more likely to have some area(s) of invasiveness).

I’ve had several patients in whom there was one or a few growing lesions, perhaps with a solid component, along with several tiny background nodules that you aren’t sure how to manage. They may represent “multifocal BAC”, but often these areas are too small and inaccessible to sample. This work suggests that it’s appropriate to take your chances and ignore them.

In Japan and some other parts of Asia, the surgery they do for small BAC lesions is typically a wedge resection or segmentectomy rather than a full lobectomy, and this work is consistent with the idea that if you’re going to do surgery on small GGOs/proven BAC lesions, a complete lobectomy may remove far more good lung tissue than necessary.

To me, this work really raises the question of whether surgery is doing anything of value at all (at least if there are any other lesions left behind), if these lesions can sit there and do nothing for years at a time, and there’s only a finite amount of lung tissue someone can afford to lose to the scalpel or to disease (at some point in the future). While there is certainly a range of clinical behavior for BAC, I’m impressed with this evidence supporting a “less is more” approach and suggesting that these patients and their lesions may do well no matter what you do or don’t do.

Are we are Making Progress in Treating Non-small Cell Lung Cancer? You Bet! We all kno
BAC No More? The most e
A Disturbing Case of Needle Track Seeding from Biopsy of a Previously Resected NSCLC Tumor Several da

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Podcast by Dr. Camidge on ALK Rearrangements and a New Era of Molecular Oncology

Dr West — Fri, 26 Feb 2010 21:46:44 +0000

Last week, Dr. Ross Camidge from the University of Colorado joined me on a webinar entitled “One Size Does Not Fit All” in which he discussed the early work on ALK rearrangements and the novel agent PF-02341066 (now known as crizotinib) in particular, and the new era of molecularly defined practice of oncology in particular. This story has been widely considered to be among the most important in the field of lung cancer over the last few years, and Dr. Camidge did not disappoint.

Not only did many of the participants in the live program write comments here expressing their positive feedback on the great energy and overall quality of the program, but both our transcriber and the editor of our podcasts independently commented to me that they thought it was a terrific podcast and that they learned a lot (and they don’t have a special, vested interest in lung cancer issues).

Here’s the audio and video podcast links, as well as the transcript and the figures from the webinar:

dr-camidge-on-alk-inhibitors-and-molecular-oncology-audio-podcast

dr-camidge-on-alk-inhibitors-and-molecular-oncology-transcript

dr-camidge-on-alk-inhibitors-and-molecular-oncology-figures

Finally, I’d like to personalize this a bit, because one of the people who was mentioned in the podcast, Andy Hill, has also been featured in the local news in both Seattle (link to news report here) and Denver (link here) as a remarkable example of the promise of molecular oncology. He’s also been a dedicated and extremely helpful supporter of GRACE in terms of both financial support and participating in our recent programs and some meetings as we work on the future directions for our organization. So I’d like to dedicate the program to Andy and hope he continues to redefine the great success of this work in how well he does.

Speaking of which, we could really benefit from your support for these programs. This webinar wasn’t from a grant but rather from your contributions. I hope you find these activities helpful and will support them. I’d also encourage people to tell others, provide the link, if you know of anyone else who might benefit from learning the material in our educational programs. We’d hate to think of the Andy Hills out there who may miss a chance for a very helpful treatment because they simply didn’t know such a possibility might exist. And unfortunately, many oncologists are still not aware of these developments: the field is simply moving too quickly.

Comments or questions? We’d love to get your feedback.

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A New Series of March Webinars

Dr West — Thu, 25 Feb 2010 22:47:03 +0000

That short month of February makes it so that March really sneaks up on you! We’re just a few days from March and our first of several upcoming webinars I need to tell people about.

The first will actually be on Monday, March 1st (just 4 days from now), with Dr. Jared Weiss from University of Pennsylvania joining me at 8 PM EST/5PM PST for a discussion of two very different but timely topics. First, Dr. Weiss will cover the controversial and completely open question of what role EGFR inhibitors might play in early stage NSCLC, or whether we should even be talking about and checking for EGFR mutations in patients who don’t have advanced non-small cell lung cancer (NSCLC) (where most of the research and discussion has been concentrated). Next, I’ll turn to a debate that has been ongoing for decades in lung cancer: should the minority of patients with very localized small cell lung cancer (SCLC) undergo surgery? A very recent review of results from a large database put this topic back in the lung cancer news. So should SCLC ever be managed surgically? I’ll try to highlight the pros and cons.

Dr. Weiss and I will discuss our own perspectives on both of these issues and also leave time for questions from participants in the live online event. If you’re interested, you can’t beat the price of registration (free, though your financial support is very helpful), which is through this link: Register for the March 1 program with myself and Dr. Weiss

Oh, but it doesn’t end there. We received an educational grant from Eli Lilly in support of a couple of additional March webinars from terrific lung cancer leaders to cover very central topics in managing advanced NSCLC. On March 10th (again, 8 PM EST/5 PM PST), Dr. Suresh Ramalingam, medical oncologist and head of the Thoracic Oncology Program at Emory University in Atlanta, GA will cover “Personalized Therapy for First Line Treatment of Advanced NSCLC”. This approximately hour-long program will cover issues such as NSCLC histology (tumor subtype) safety concerns with anti-angiogenic agents, and the emerging work on molecular markers and how these factors lead to individualized recommendations for patients initiating treatment for advanced NSCLC, including an approximately 40-45 minute presentation, followed by time for questions from participants in the live program. Register for March 10th webinar with Dr. Ramalingam on Personalized Therapy Recommendations for First Line Treatment of Advanced NSCLC

A week later (Wednesday, March 17th at 8 PM EST/5 PM PST), medical oncologist Dr. Mark Socinski, who leads the world-renowned lung cancer program at the University of North Carolina at Chapel Hill, will cover “Optimizing Timing and Choice of Treatment after First Line Treatment of Advanced NSCLC”. Like the first line discussion by Dr. Ramalingam, this will be an approximately 40-45 minute presentation followed by Q&A, and Dr. Socinski will focus on the evidence supporting which agents are our strongest treatment options and how we might consider the question of whether patients should transition straight from first line to later treatment or whether a break from treatment might be a good idea. Register for March 17th webinar with Dr. Socinski on Timing and Treatment Choice after First Line Treatment for Advanced NSCLC.

Registration for each of these live events is limited, and we also know that the timing doesn’t work well for everyone who might want to be there, so all of these activities will be turned into podcast materials for people to refer to at any time in the future.

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Round Table Discussion with Experts: Indolent BAC in an Elderly Man

Dr West — Tue, 23 Feb 2010 06:09:45 +0000

This is the first part of a case presentation I did with two great colleagues: Dr. Anne Tsao, who is a medical oncologist and lung cancer expert at MD Anderson Cancer Center in Houston, and Dr. Alex Farivar, who is a terrific thoracic surgeon at my own institution, Swedish Cancer Institute in Seattle.

This case is an elderly gentleman who has a very indolent but growing lung lesion. His story brings up questions of how concerned to be in following a nodule in a patient of advanced age and with competing medical issues, whether surgery that is less than a lobectomy might be considered, as well as the systemic therapy options for bronchioloalveolar carcinoma.

Here are the audio and video versions of the podcast, along with the transcript and figures.

expert-round-table-tsao-and-farivar-pt-1-bac-audio-podcast

expert-round-table-tsao-and-farivar-pt-1-bac-figures

expert-round-table-tsao-and-farivar-pt-1-bac-transcript

I hope that’s helpful. We’ll provide info on a couple of additional cases from this discussion in the future.

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Loading the Dice: Comparative Trials of EGFR Inhibitors in Patients with EGFR Mutations (or, When Bad Trials Happen to Good People)

Dr West — Sat, 20 Feb 2010 05:30:55 +0000

The IPASS trial that randomized Asian never-smoking or light previously smoking patients with previously untreated advanced NSCLC to either standard chemo or the epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) inhibitor Iressa (gefitinib) is widely considered among the most important and standard-changing trials of the last few years in the field of lung cancer. Nevertheless, it’s important to bear in mind that patients were identified for enrollment on that trial based on clinical factors, with about a third of the 1217 enrolled patients having their tumors analyzed for EGFR mutation status. The post-hoc results for that molecularly defined subset was the most interesting component of the trial, demonstrating that the patients with an EGFR mutation had a very significantly longer progression-free survival (PFS) with Iressa than with the standard chemo combination of carbo/taxol (paclitaxel). In contrast, the exact opposite was true for patients who were Asian never-smokers with an adenocarcinoma but didn’t have an EGFR mutation.

That comparison of chemo vs. an EGFR inhibitor in a clinically selected population was a perfectly appropriate question when the study was designed and enrolled, since we didn’t have evidence that one approach was superior to another in clinically or molecularly selected populations. This line of inquiry has been taken one step further by work from the North East Japan Gefitinib Study Group from Kobayashi and colleagues that tested Iressa against chemo in 200 previously untreated patients with advanced NSCLC who were prospectively selected for having an EGFR mutation. It was designed to enroll 160 patients per arm, but an interim analysis showed that the results were so overwhelmingly more favorable for recipients of Iressa that the trial was closed early because it was felt to be unethical to continue to randomize patients if the answer to the question was already clear. Although overall survival was not mature and wasn’t shown, preliminary results of this trial presented at ASCO 2009 revealed that the patients on the Iressa arm had a far superior response rate (74.5% vs 29%, p < 0.001) as well as PFS (10.4 vs. 5.4 months, p < 0.001). The curves for the latter are shown below.

(click on image to enlarge)

Along with this trial, a remarkably similar European trial is being completed that randomizes a population of previously untreated patients with an EGFR mutation to either erlotinib or cisplatin/docetaxel.

Between the recently closed Japanese trial and the ongoing European trial with a very similar design, I would say that there’s no more need for a new trial comparing an EGFR inhibitor to chemo in patients with an EGFR mutation. Still, there’s a new one recently activated, this time with a new agent known as BIBW 2992, or “Tovok”, from the large German pharmaceutical company Boehringer Ingelheim. BIBW 2992 has been hailed as a next generation targeted agent because it inhibits both EGFR (also known as HER-1) and another sibling receptor called HER-2 or HER2/neu, which is a very important target in breast cancer). Last year, some data emerged from a single arm trial of BIBW 2992 in patients with an EGFR mutation, and this showed that patients in this small trial had responses about half the time, which is similar to the results we’ve seen with the currently widely used EGFR TKIs Iressa and Tarceva, or perhaps less impressive. Still, the company wasn’t aiming high, and they achieved their modest goal of ballpark comparability with our currently available agents when the dice were loaded in their favor.

(this is how I think of this work)

Now, Boehringer Ingelheim is trying to run a trial called LUX-Lung 3, in which 330 patients with a lung adenocarcinoma and a proven EGFR will now be randomized 2:1 to their oral EGFR/pan-ERB inhibitor BIBW 2992 or cisplatin/alimta (pemetrexed). In a not very shocking turn of events, they’re having trouble getting patients enrolled globally, but especially in the US. After all, this is very similar to a trial that was closed in Japan because it was felt unethical to continue to randomize EGFR mutation positive patients to standard chemo.

While I can see why this trial would be helpful to the sponsor company, I can’t imagine a patient sending their tissue, learning that they have an EGFR mutation, hearing the rationale for giving a first line EGFR inhibitor and then willingly signing up to get chemo. What oncologist would feel comfortable randomizing such a selected patient to this? Even more impressive to me is that the principal investigator in the US is Mark Kris, Chief of the Thoracic Oncology Division at Memorial Sloan Kettering Cancer Center and one of the strongest proponents for aggressive EGFR mutation testing and first line use in the population of patients with an EGFR mutation. I believe that Dr. Kris is more likely to spontaneously burst into flames than to publicly declare that feels comfortable with the randomization in this trial and thinks it’s a perfectly great idea for previously untreated patients with advanced NSCLC who have an EGFR mutation to then knowingly have an EGFR inhibitor withheld. Tellingly, he hasn’t enrolled a patient of his own…

This is a trial that does not answer a relevant scientific question anymore. The proper trial for today would be one in which BIBW 2992 is directly compared to one of the more established EGFR TKIs to see whether it provides any improved outcomes, or if it happens to have activity in patients who have already received and progressed on gefitinib or erlotinib. But that trial isn’t being done, and instead the company is trying to get a drug approved by doing a trial that has essentially already been done and is known to subject some of the patients to a suboptimal treatment. Thankfully, doctors and patients are voting with their feet.

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Webinar with Dr. Ross Camidge: Learn about his Experience Treating Patients with EML4-ALK Translocation

Dr West — Mon, 15 Feb 2010 16:40:49 +0000

I just wanted to offer a reminder that Dr. Ross Camidge, medical oncologist and lung cancer expert from the University of Colorado in Denver, is going to be speaking with me during a webinar this Wednesday, 2/17, at 8 PM EST/5 PM PST. Among the topics we’ll cover is the EML4-ALK translocation, which is widely considered to be among the most exciting developments in the lung cancer field over the last several years.

Dr. Camidge was kind enough to agree to give a primer on the new and emerging story of EML4-ALK and the investigational drug PF-02341066, which Dr. Camidge was one of the first people to use in lung cancer patients. He’s currently treating some patients having sensational responses, so he can tell us more from the perspective of someone who has been directly involved with the research program.

We’re also going to cover a bit on the question of the role of surgery in more locally advanced NSCLC that is treated initially with chemo and radiation. I’ll present some background on this, including a new article that is coming out describing this experience. I’ll also invite Dr. Camidge to give some of his thoughts on this work as well.

Otherwise, we’re going to try to leave some time for questions on these subjects from people participating in the webinar. If you’re interested in being one of those people, please register for the Feb 17th webinar; registration is free but limited.

And because we know that some people who are interested in these topics may not be able to make the live event, we’ll also make this webinar into a podcast or two, so that people can access it later.

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