Shadowing Practice: Personalised Cancer Care - Prof Mark Middleton - Learn English Speaking with Video

Kies een oefenmodus

Elke modus opent een volledig scherm oefenruimte.

312 zinnen

Als zinnen te kort of te lang zijn, klik op Bewerken om ze aan te passen.

So we're going to talk about personalized cancer care

and the focus is going to be on what we're doing clinically to change what patients across the street

and here experience if they come to have their cancer care here in Oxford.

So the key to personalized cancer treatment, and I'll come back to the difference between care and treatment in a minute,

is really about giving the right treatment, and that today in cancer treatment consists largely of surgery,

of radiotherapy, or of giving drugs to the right patient.

And we rely upon a series of tests, which Dr. Xu's going to talk about some of them later, and I'm going to mention during my talk,

in order to make sure we choose the right patient.

Then the other thing we have to do is to give it at the right time.

Most of the treatments that we use for cancer have quite significant side effects

or time to recover from that in the case of surgery.

And so we're always having to balance the risks of what we do, which can sometimes prove fatal,

with the risks of doing nothing or doing something else.

And I guess that's what we mean by personalized cancer treatment.

Personalized cancer care is slightly different.

The right treatment obviously is implicit in choosing the right person to give that to, but it also has to be delivered in the right context.

And what do I mean by that?

Well, and it has to have the right support.

Sorry, my slow reveal of my slide isn't working quite as well as I'd hoped.

So the right context means about that being a shared decision between us as clinicians and the patient,

not merely about us handing out a ticket by road as you come through the door, you know, line one, line two, line three and so forth.

And it also means perhaps considering whether we need to leave the concept of the hospital behind,

you know, how much of this treatment really needs to be delivered in big centers here in a highly specialized manner.

What can we do at home?

What can we do closer to home if we can't actually do it at home?

and then what support can we offer in delivering that so that it's truly about care, not just about handing out treatment, take it or leave it,

and then leaving patients and their families to get on with it.

And that's about having the right information so that patients can make the informed choices.

And it's also about having the right psychological support in and around the treatments that we offer,

both from the clinicians offering the treatment informally from professional psychologists and psychiatrists,

and also the right psychological support out and about away from the hospital, either through peer support by meeting other patients in the same position

or other families who faced similar decisions and dilemmas about their treatment,

not just about handing out the drugs, the radiotherapy, the surgery.

Having said all that, most of what I'm going to talk about this evening is the drugs, the surgery, the radiotherapy.

Because of the way in which the Biomedical Research Centre is set up and the things that we're researching at the moment, that is the major focus of what we're doing.

But I wouldn't want to give the impression that as a trust, as a university, we're not interested in the whole of cancer care,

and in fact we've been joined recently by Professor Mike Sharp, an expert in the psychological aspects of cancer treatment from the University of Edinburgh,

who's overhauling the way in which we provide a lot of the support

and building research into psychological support into a lot of what we do.

So we already deliver personalized cancer treatment.

If you are diagnosed with a cancer and come to the hospital, you aren't given the same treatment just because you have cancer.

The way in which we personalize it at the moment is based upon how old you are, how fit you are, what your gender is sometimes,

and also principally where we found the tumor and where it started in the first place.

So when we talk about cancers we often show slides such as this saying, you know, what's the most common cancer in a given situation?

You know, for men it's prostate cancer, for women it's breast cancer.

And we all think in terms of the treatment with I have breast cancer, I have lung cancer, I have bowel cancer and so forth.

And that's because that's the way the treatment's set up.

Partly because the surgeries are different, because the drugs are different, because the radiotherapy is different.

So one could argue that we already have personalized cancer treatment in the NHS today.

But what we have is very, very broad brush.

And what I want to talk about is the ways in

which we're trying to move on from that and to provide something that's very much more individualized,

not quite down to the level of each patient as a true individual having something that's absolutely tailored,

but certainly moving away from groups of dividing cancers up into groups of 10

or 20 or 30 groups and starting to think about 100, 1000, 10,000 groupings.

So if you take a very rare tumor, sarcoma, which is treated mostly here at the Nuffield Orthopedic Centre

and is too rare to even feature on this top 10 slide here,

then we already know that that is now over 100 different types of cancer.

all of which have a hundred different types of behavior, a hundred different types of outlook, and therefore the idea that we put everybody in a sarcoma box

and treat them all in the same way simply doesn't hold water.

So from that, the question is, well, how do we then define these hundred different groups?

Because until we've defined them, we aren't in a position to start to sort out what the best approach to treating them is

and to therefore looking after the patient who has that particular type of cancer.

So one of the principal ways in which we're starting to change that, and Dr. Su is going to talk about that later, is genetics.

And through detailed genetic analysis, and Chris alluded to the fact

that we use what's called next generation sequencing now to get

a more detailed genetic profile of the cancer as part of what we do.

And this is already routine in some areas like sarcoma, in the blood cancers in particular, a variety of tests are used as a matter of course

in order much better to define what the appropriate approach to treatment might be.

We also have to consider in this the patient

because important aspects of our treatment now use the patient as our principal weapon against the cancer.

In particular what I'm talking about here is immunotherapy.

We all have functioning immune systems that keep us alive from attack from bugs, outside poisons and so forth.

And increasingly we're starting to see that there's a way of harnessing

that to treat cancers as foreign and undesirable and use the immune system to eradicate them.

And I'd argue that that's probably the purest type of personalized therapy that you can have.

There's been a lot in the press recently about major breakthroughs in my particular field, which is melanoma.

and clearly this is going to play out quite considerably over the next decade or so, and have a very, very large impact on the sorts of treatment that we offer here in Oxford,

and indeed worldwide for cancer.

But I'm not really going to talk about that much today because this is at a very,

very early stage and not something that we can really go into too much detail at the moment.

We're just starting out on that journey.

The other way in which we define cancers and have done for many, many years in the pathology lab is to look at the levels of particular proteins on the cell surfaces.

This tells us a little bit by one remove about how the cancer is likely to behave.

It can also allow us to use our current sorting method as effectively as possible

because by seeing what proteins are in a cell, we can sometimes tell where it came from in the first place.

So if we find a tumor in the lung, this is the method that we currently use to tell whether it's a primary lung cancer, so it's started in the lung,

or whether it's perhaps a breast cancer or a bowel cancer that's traveled there.

It's therefore secondary and demands a different approach.

The other way in which we look at this is to look at things like cell shape and cell behavior.

And cell behavior in particular is important.

We have very, very sophisticated scanners now to look at the shape of what's going on inside us,

but they increasingly pick up lumps that we're not really sure what they mean.

And by looking at how the cell behaves, in particular what its metabolism is doing, using PET scans and so forth,

that can give us a handle on whether we're looking at something that's really a problem

or whether this is an incidental finding that could be left to one side, not a cancer, as one example.

But also how cells behave, as I'll show you later, is also an indicator of how we might approach treating them.

So just to touch briefly on the genetics, this is an example going back to what we talked about, a hundred different types of sarcoma.

What you can see here in A, C, D and E, ignore the bottom line which is a slightly different bunch, is a bunch of sarcomas,

100

and this is looking at chromosomal rearrangements, if you look at the lines inside the circles here, you can see that the key point I'm trying to make is they're all radically different.

101

And therefore the assumption

102

that we can manage all of these in the same way is probably not valid and something that we need to reconsider.

103

The main way though at the moment in which we look at the differences between particular tumors is down the microscope,

104

looking at the shape, the organization of the cells, but we are conscious of the fact

105

that whilst doing this we leave a lot of information behind

106

because we only make a relatively cursory inspection and usually focus down on one,

107

two, half a dozen proteins in order to tell us what to do.

108

The purpose of this slide isn't to illustrate anything other than the fact that very, very detailed looking at the proteins and starting to go back right to the beginning

109

and look at everything and not throw away a lot of the information that we've previously ignored

110

is leading to new insights about how best to look after patients and whether to start treatment at all in some instances.

111

And we're starting to harness the power of computers and machine learning in order to do that.

112

So as we gather more information and we don't throw it away, it very, very soon gets beyond our ability to process it.

113

We simply can't understand it.

114

So, what we can do though is use machines to learn

115

which aspects are important and rather than our biases

116

that we arrived at when we first looked at the slide down the microscope, we can get the machine to tell us whether there are better markers that we can look at in doing this,

117

that give us better quality information about the patient.

118

So that's really a brief synopsis of the ways in

119

which we're trying to describe the tumors better so that we can target our treatments more effectively.

120

But that gives rise to a different question which is how does cancer treatment improve?

121

And I just wanted to touch on that briefly.

122

So if you read the papers, then cancer treatment improves in giant leaps through magic bullets.

123

And that's a horrible mixed metaphor, I apologize for that.

124

And here's the poster child of the magic bullet.

125

So in chronic myeloid leukemia, it's long been known that there's been a rearrangement in chromosomes.

126

If you start on the left, you've got the normal chromosome 9, the normal chromosome 22.

127

When they break and rearrange, this forms a fusion called the Philadelphia chromosome, which gives rise to an active protein that changes cell behavior

128

and is responsible for what we call in the jargon the malignant transformation and the cancerous nature of the leukemia cells.

129

And about ten years ago we found a drug imatinib that can essentially counteract this overactive protein.

130

And it can make the chronic myeloid leukemia go into remission, it can hold it in remission for a time,

131

and new developments in next generations of drugs have extended the time in which that can be held.

132

So this is the archetypal Daily Mail, Daily Express, Daily Telegraph, Daily whatever your favorite read is,

133

view of how we make changes in cancer.

134

But in fact, for every poster child like this, there's another non-poster child that gets slightly glossed over.

135

And rather than rain on anybody's parade other than my own, I'm going to take an example from my field to show

136

perhaps a slightly more mundane reality with some of these magic bullets.

137

So we have a similar situation in melanoma where about half

138

of patients in their melanoma we can find in this case a mutation in a gene

139

which leads to an overactive protein called BRAF.

140

and about five years ago the news broke through clinical trials of a drug now called Vemurafenib

141

which can inhibit this overactive form of BRAF.

142

So when BRAF is mutated and overactive it makes the cell grow.

143

If you switch that off you remove the growth driver to the melanoma cell.

144

And that had very, very spectacular effects.

145

So, on the left you see a PET scan, it's like the old-fashioned PET scan showing very,

146

very metabolically active tumors in a patient who's standing facing the camera.

147

You can see the brain,

148

the heart, and the bladder in outline within that because they're metabolically active in their own right.

149

But all the other dark spots on the left-hand picture are either small amounts of bone marrow or active areas of tumor.

150

And a couple of weeks after starting on the drug, this is what's happened to the scan on the right-hand side.

151

So it's a very, very spectacular effect.

152

The tumors shrink with this.

153

The patient feels better.

154

But that effect is lost very rapidly within months.

155

And that's the reality for almost all of the patients whom we treat with this drug.

156

And I'll come back to this later on in the talk about why

157

that might be and what we can do to try and tease some of that out.

158

But what this means is that cancer treatment doesn't really undergo revolutions.

159

It, you know, these magic bullets aren't out there all the time.

160

And actually the way in which we make pro, progress is, more prosaic.

161

And in fact, one of the biggest contributions

162

that Oxford's made to cancer care is actually by synthesizing the results of hundreds if not thousands of researchers around the world,

163

in particular in the field of breast cancer.

164

at the Clinical Trial Support Unit which is in the Richard Dole building across the street, they've brought together the results of all the breast cancer studies

165

that have been done and asked a series of questions

166

and made some definitive observations about the best ways in which to treat particular types of breast cancer.

167

And this example here looks at the chances of a breast cancer coming back in women who've either had breast conserving surgery,

168

BCS here, if you look at the left hand curve, or some radiotherapy on top of that.

169

What you can see is a very much diminished chance, that's ten years, of the cancer coming back,

170

if you have a radiotherapy on top of the surgery.

171

Perhaps more surprisingly, because this is a treatment that's local, it's applied only to the breast, not all over the body,

172

this also has an impact upon the chances of dying of breast cancer further down the line.

173

But the thing I want to draw your attention to, rather than those results and that observation, is the fact

174

that this is a result that's come from looking at over

175

10,000 women who took part in 17 different trials around the world.

176

So this wasn't a magic bullet, an observation, suddenly it's all going away.

177

This is years and years of incremental work.

178

And the same is true, and this is again from the same group,

179

looking at whether adding chemotherapy in a similar situation has the same effect.

180

And again, this is now long-term outcome from over 100,000 women in over 100 different studies.

181

It makes very clear what you can get out of conventional chemotherapy, but it also makes it very clear

182

that you have to be in this for the long term in order to be absolutely clear

183

that what you're doing is helpful.

184

So, cancer treatment evolves, it's evolution not revolution, and the reason I've stuck up Chris Hoy there is really,

185

it's a similar approach, if you like, to the British Olympic cycling team.

186

The way they said they set out to be the best in the world was that no gain was too small, half of 1% was good enough,

187

because by the time you added up all the halves of 1%, you got something tangible and substantial.

188

So, bearing that in mind, what are we doing then in this long game in order to improve things for patients?

189

Well, if we take another step back, at the moment the way in which we cure cancer is by cutting it out, by and large.

190

That's responsible for the majority of cures.

191

This is now about curing, not just treating.

192

And then for the substantial part of the rest of the patients who are cured, that's done by using radiotherapy.

193

Drugs contribute only a relatively modest part of cure, and that's really only in a relatively narrow group of cancers,

194

affecting children, germ cell cancers, hematological cancers, blood cancers.

195

But you wouldn't believe that from reading about how cancer treatment evolves in the press.

196

So I want to take a little bit of time to talk about what we're doing with surgery

197

and with radiotherapy to make that personal to each individual patient.

198

Obviously surgery to a certain extent is personal, you get a bespoke operation every time.

199

We follow procedures and protocols to make that operation as safe and as effective as possible but as you'd anticipate, when a surgeon is cutting a tumor out,

200

he or she does that on a very individual basis.

201

However, that doesn't mean there isn't room for improving the personalization and making it truly more effective, and a lot of the attempts

202

that we have done to move this on over the years

203

have been based around doing less damage as we go about that process.

204

taking less normal tissue along with the tumor

205

and being much clearer about what does and doesn't work

206

and making sure that we only get really aggressive with our operations when that's truly effective.

207

And one of the approaches within the Biomedical Research Center

208

that we're pioneering to try and improve upon this is fluorescence image guided surgery.

209

So what you can see, probably not very well, and I apologize for that, in the left-hand panel on the top is what the surgeon sees with the naked eye,

210

with a very powerful light

211

when they're looking inside an abdomen trying to identify where the cancer is and to decide where to do their operation.

212

Now, using fluorescent tags that pick out cancer cells, you can get the image on the right.

213

You do have to turn the main light off in theater, so it's a slightly surreal experience and a little bit alarming,

214

the idea that people are wielding knives in the dark,

215

but it does mean that you can pick out much more accurately where the cancer is

216

and guide your surgery much more effectively for that reason.

217

And this is now being used in gynaecological surgery.

218

I think this was the only picture we thought we could show that wouldn't necessarily be off-putting.

219

And this is a reality in operating theaters across the street at the Churchill Hospital.

220

And it's being used to guide the extent of surgery for women with ovarian cancer.

221

And at the moment this is at the stage of proof of principle.

222

Assuming that we can prove this principle, which I think we're reasonably confident we can, what we'll then need to do is to construct clinical trials

223

to show whether doing this improves the outcome for patients beyond conventional surgery.

224

So turning to radiation treatment, the problems there are very similar.

225

Both surgery and radiation are extremely effective at getting rid of cancer, but the trick is not to damage the patient in the process.

226

And with both treatments, the bigger the amount of radiation, the bigger the surgery you do,

227

the more likely you are to create damage that then becomes permanent permanent

228

and has a real impact on patients' lives as increasingly they survive and live beyond their cancer.

229

So I've talked a little bit about how radiotherapy, how surgery is becoming more personalized,

230

more individualized to the patients by individual planning and so forth.

231

I think we've also covered a little bit about how functional imaging, I'm going to talk about that for a couple of minutes

232

means that how the tumors behaving can also guide what we do

233

and allow us to think about new ways of combining treatments to make the existing ones more effective.

234

And then finally, I think we can talk about how by using our molecular understanding of cancers, we can divide them into much smaller groups,

235

which mean that we can give treatments much more precisely in a way

236

that allows us to have greater confidence that they're likely to be successful in the longer term.

237

So this is work in breast cancer from Professor Adrian Harris, one of my colleagues in medical oncology.

238

We've known for a long time that an anti-blood vessel treatment called Avastin can be very effective in breast cancer.

239

But as we've used it more and more, we've found it to be less and less effective.

240

And so what's clear from this is that there are a group of women who do benefit from the drug,

241

drug, but as you widen the women that you give it to, that group doesn't change and so the overall impression is the drug is less effective.

242

So the question becomes how do you choose who should get this drug?

243

Because it has side effects, we could use other drugs instead of it

244

and therefore it's not just a question of whether you give it and if it doesn't work well so what?

245

And that's even before you get on to the issue of cost.

246

And so what Professor Harris described was three different ways in which breast cancers respond,

247

which are shown here, to the Avastin.

248

So on the left-hand side you see a picture of a tumor in a breast, the tumor, the breast is blue,

249

the tumor is yellow or red according to the leakiness of the blood vessels in the tumor, and then the effect of the Avastin in each case.

250

So on the top what you see is the effect that we're looking for,

251

which is the blood vessel abnormality essentially being corrected by the Avastin.

252

Below you see two ways in which it doesn't work terribly effectively.

253

Bottom right what you're seeing is the tumor basically ignoring the Avastin,

254

And what you're seeing on the left is that the central part of the tumor is responding,

255

but the growing rim of the tumor around the edge is effectively ignoring the Avastin, and so that's unlikely to have a material effect upon how the tumor behaves

256

and improve the treatment that's been given with surgery and chemotherapy alongside this.

257

Now those are the clearest examples, indicated by the arrows really,

258

of a whole different series of responses that we can measure by using MRI scanning.

259

But more importantly, what we can then do is having seen this on our MRI scanner,

260

this was done in ladies who are going to have surgery for their breast cancer anyway, anyway, we can then go in and take a sample of the tumor

261

and look at what genetic changes are happening and how the genetics in each tumor differs according to the response of the,

262

to the treatment.

263

And what we can then do is to categorize those genes as shown here

264

and then link them back to the pictures that have been taken in order to define,

265

well, in order to detect what defines who responds best to the treatment.

266

In the interest of time I'll skip on from that though.

267

So that's just an example really of how the genetic side of things is linking in with the imaging

268

and allowing us to look at how tumors function and relate

269

that to their genetics and then

270

that gives us a clue as to what particular aspects of

271

a tumor need to be in place for a particular treatment to work

272

which is in itself interesting

273

because it allows us to choose whom to give a treatment to

274

but it also tells us why it doesn't work in the other people

275

and suggests ways in which we could perhaps make it work by manipulating tumor behavior in the future.

276

So, to come back to genetics now for the last couple of minutes that I'm going to talk, and then I'm going to hand over to Dr. Xu.

277

Our concepts of site-specific cancer are changing rapidly rapidly, we can now divide up things like lung cancer,

278

like melanoma, into different groups based purely on the genetics.

279

And here are a number of mutations that can be found in lung cancer.

280

Now, in some tumors, lung cancer, melanoma, there are 30,000 genetic abnormalities if you sequence the whole genome of a cancer.

281

So one of the issues we struggle with is what are the driver mutations, the mutations that dictate cancer behavior, as opposed to the passenger mutations or changes,

282

the ones that are just there for the ride

283

that really are irrelevant to how the tumor's going to behave and therefore how it's best treated.

284

And that's a significant work in progress.

285

But these ones here, KRAS, EGFR, EM4ALP, these are all abnormalities that we can target with drug treatments at the moment.

286

So this isn't a theoretical exercise, this is a clinical reality that's defining who gets what drug

287

and how we get the best possible response for the least possible side effects for our patients.

288

And that's summarized really at the moment we have four genes in solid tumors as opposed to blood tumors

289

that we look at in detail as part of our routine

290

testing for these groups of patients to tell us what to do if the spread of the tumor throughout the body.

291

But we've gone beyond that and extended the range of mutations quite considerably that we look at as a matter of routine,

292

because it's not just a question of seeing something that we can throw a drug at.

293

What's going on elsewhere in the tumor, those other 30,000 events, or in this case a rather smaller number, because that's what we can get a handle on at the moment,

294

also tell us about the chances of treating the index mutation.

295

You know, how is that going to work out?

296

So it's not just a question of focusing on one thing, knocking it off, because then you've got, you know, the question becomes what's the next thing, what's the next thing after that, and so forth.

297

If we come back to the drug vemirafenib that I talked about at the beginning, which targets this BRAF mutation, and which, you know, as I showed with the PET scan,

298

what happens is it works very, very well, and as this graph shows, much more effectively than chemotherapy with decarbazine as a means of holding the tumor in check.

299

But the key thing to notice here on this curve, which shows the proportion of patients on each drug whose tumor is under control, with everybody under control at the beginning,

300

very quickly within nine months, nobody's tumor is under control.

301

So this resistance that I showed with the PET scans developing in everybody.

302

And what we understand from that is if we look at BRAF here in the middle of this signaling pathway,

303

all the orange bits, all the writing in black is showing ways in which resistance can develop.

304

So by understanding and looking at the mutations right across the piece,

305

we can start to pick out who benefits from the drug either transiently for the long term, and also how that changes.

306

None of this is set in stone.

307

This all changes as patients are on treatment, so we don't just measure once but we go back and we measure time and again.

308

And hopefully in time this will become slick enough and quick enough

309

that it will allow us to alter what we do as we go along, rather than waiting for the tumor to come back in order to change our treatment.

310

So what I'm going to do now I think is break off there

311

and hand over to Dr. Xu to talk a little bit more about some of this some of this

312

and then I'll come back for a couple of minutes.

App downloaden

Alles wat je nodig hebt om vloeiend te spreken

AI UitspraakScoor elke zin

IPA OefeningBeheers elk geluid

WoordenschatBouw je woordenschat op

WoordenspelLeren terwijl je speelt

Scan QR

Download on theApp Store Get it onGoogle Play

FOR YOU

Aanbevolen Video

21 zinnen

Behind the Scenes: Diagnostic Angiogram with Dr. Oliveira | Riverside Neuroscience

IELTS PrepTOEFL PrepUniversity Students

850 zinnen

Race Against Time To Start Major Operation | UK Hospital Documentary | Full Episode

IELTS PrepTOEFL PrepUniversity Students

Woordenschat en spreektips bij deze les

Deze video bevat 312 zinnen en 5017 woorden om na te spreken. Het gesproken deel duurt 29:45. De spreker praat in een natuurlijk tempo van ongeveer 169 woorden per minuut, dicht bij een alledaags gesprek. 86% van de woorden hoort bij de 3.000 meest gebruikte Engelse woorden; de rest kun je beter vooraf bekijken.

Belangrijke woorden in deze video

15 woorden uit de video die het leren waard zijn, met uitspraak en betekenis:

Woord	Uitspraak	Betekenis
tumor zelfstandig naamwoord	/tuː.məɹ/	tumor, gezwel
breast zelfstandig naamwoord	/bɹɛst/	borst
mutation zelfstandig naamwoord	/mjuˈteɪʃən/	mutatie
lung zelfstandig naamwoord	/ˈlʌŋ/	long
scan werkwoord	/skæn/	afspeuren
define werkwoord	/dɪˈfaɪn/	bepalen, determineren
genetics zelfstandig naamwoord	/dʒəˈnɛt.ɪks/	genetica, erfelijkheidsleer
genetic bijvoeglijk naamwoord	/d͡ʒəˈnɛt.ɪk/	genetisch
slide zelfstandig naamwoord	/ˈslaɪ̯d/	glijbaan, schuifaf
bullet zelfstandig naamwoord	/ˈbʊlɪt/	kogel
ignore werkwoord	/ɪɡˈnɔː/	negeren
psychological bijvoeglijk naamwoord	/ˌsaɪ.kəˈlɑː.d͡ʒɪ.kl̩/	psychologisch
chemotherapy zelfstandig naamwoord	/ˌkiːməʊˈθɛɹəpi/	chemokuur, chemotherapie
increasingly bijwoord		in toenemende mate
gene zelfstandig naamwoord	/d͡ʒiːn/	gen

Phrasal verbs die je zult horen

Woord	Uitspraak	Betekenis
go back werkwoord		teruggaan
set up werkwoord	/ˌsɛt ˈʌp/	bereiden, voorbereiden
come back werkwoord		terugkomen
get on with werkwoord		aan de gang gaan met, doorgaan
go away werkwoord		weggaan
pick up werkwoord		oppakken, optillen
stuck up bijvoeglijk naamwoord		hooghartig, zelfingenomen
throw away werkwoord		weggooien

Grammatica in deze video

De structuren die de spreker het meest gebruikt, met de exacte woorden uit de video:

Structuur	In de video
Present perfect have/has + voltooid deelwoord — iets uit het verleden dat nu nog telt	we've been joined · have personalized · we've defined
Lijdende vorm be + voltooid deelwoord — het gaat om wat er gebeurt, niet om wie het doet	be delivered · is set · we've been joined
Betrekkelijke bijzinnen who / which + zin — extra informatie over een persoon of ding	sarcoma, which is · field, which is · line which is

Uitspraak om op te letten

De spreker gebruikt 81 samentrekkingen en verkorte vormen, zoals we're, I'm, doesn't. Spreek ze kort uit, zoals je ze hoort.

De “th”-klanken: chemotherapy /ˌkiːməʊˈθɛɹəpi/, theater /ˈθi(ə)tɚ/, gather /ˈɡæðɚ/, theoretical /ˌθi.əˈɹɛt.ɪ.kəl/, pathway /ˈpæθˌweɪ/
De klanken “sh” en “zh”: mutation /mjuˈteɪʃən/, radiation /ˌɹeɪ.diˈeɪ.ʃən/, observation /ˌɑbzɚˈveɪʃn̩/, essentially /ɪˈsɛnʃəli/, impression /ɪmˈpɹɛʃn̩/
Lange woorden — let op de klemtoon: psychological /ˌsaɪ.kəˈlɑː.d͡ʒɪ.kl̩/, chemotherapy /ˌkiːməʊˈθɛɹəpi/, radiation /ˌɹeɪ.diˈeɪ.ʃən/, essentially /ɪˈsɛnʃəli/, apologize /əˈpɑləˌd͡ʒaɪz/

Zo oefen je met deze video

Luister de hele video één keer zonder te spreken en noteer de woorden die je niet kent.
Begin op 0,75× snelheid, spreek zin voor zin na en ga terug naar normale snelheid zodra het makkelijk gaat.
Neem jezelf op en vergelijk met het origineel; let daarbij op woorden als tumor, breast, mutation.

Wat is de Shadowing-techniek?

Shadowing is een wetenschappelijk onderbouwde taalleermethode die oorspronkelijk is ontwikkeld voor professionele tolkentraining en gepopulariseerd door polyglot Dr. Alexander Arguelles. De methode is eenvoudig maar krachtig: je luistert naar native Engelse audio en herhaalt het onmiddellijk hardop — als een schaduw die de spreker volgt met slechts 1–2 seconden vertraging. In tegenstelling tot passief luisteren of grammaticadrills, dwingt shadowing je hersenen en mondspieren om echte spraakpatronen tegelijkertijd te verwerken en te reproduceren. Onderzoek toont aan dat het de uitspraaknauwkeurigheid, intonatie, ritme, verbonden spraak, luisterbegrip en spreekvaardigheid aanzienlijk verbetert — waardoor het een van de meest effectieve methoden is voor IELTS Speaking-voorbereiding en echte Engelse communicatie.

Shadowing-techniek: lees de volledige stap-voor-stap-gids →

Shadowing Practice: Personalised Cancer Care - Prof Mark Middleton - Learn English Speaking with Video

Kies een oefenmodus

App downloaden

Dr Joseph Kwan | Cleveland Clinic London Neurological Rehabilitation

The Reason Why Cancer is so Hard to Beat

Are We Eating Better – C1 English Listening Test

What is Nuclear Medicine | Dr. Paulien Moyaert

Personal Assessment | IELTS LISTENING TEST | SECTION-2

Speaking P3 audio 1

Land of the Lions | Making Nature: How we see animals

The Latest Developments in Age Reversal Research

Latest advances in AVM treatment - Uday LIMAYE

Essentials: Understanding & Healing the Mind | Dr. Karl Deisseroth