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It's time for another column to be written.
I take a sip of my Gatorade. I remember my trainer telling me not to drink it unless I'm working out. I glance down and realize what I'm wearing: an Oregon Ducks sweatshirt. I'm still psyched about the outcome, as all of us "fans" are.
The Oregon Ducks ran up, over, and around the Oregon State Beavers in the latest edition of the Civil War, winning by a final score of 48-24.
Despite my enthusiasm, I was skeptical writing about the game. I could try to write like a devoted fanatic, you know the kind I'm thinking about- the people that buy the cardboard cut outs of their favorite players, flaunt the flags on their car every month of the year and buy Christmas wreaths with the theme of their favorite team.
I couldn't have been a fanatic behind the masked identity of the keyboard, but then I realized my position too, as I wore my sweatshirt in the midst of indifferent fans.
I know close to nothing, at least if you compare me to life-long football lovers. Don't get me wrong. I like the sport. I like the University of Oregon.
And yet, I am not the first opinionated and annoyed columnist to label the Ducks' fans as a "bandwagon" fan base.
Faced with the realization of my lack of knowledge of football and the Ducks' pride (a very consistent occurrence on both parties), I ask myself, what makes a true fan?
Usually impassioned flip floppers sporting painted chests cite reasons such as "My uncle lives there," "My dad went to school there," or "I appreciate the enthusiasm from the mascot and cheerleaders." This is an unfortunate outcome of sudden and widespread fame.
Many claim they are faithful fans, but at the mention of the word "faithful", we find the heart of the issue.
Many of us readily attribute this word to our own fandom but it is something that can only be tested by time.
Quick! Who was the Ducks 'starting quarterback and running back in 2007?
For those of you still thinking, instead of using this time to search your brain or check your smartphone, use it to adopt some humility. In no way does this mean you are less worthy as fans but we can come to the realization that there is a lot to learn- myself included- in becoming a true follower of the Oregon Ducks. No more band-wagon-ing.
In case you didn't know, it's national hyphen day.
Many Duck fans have remained patient through an existence mainly marked by irrelevance and exclusion. I doubt the newcomers quick to show elitism and arrogant opinions are appreciated. For those who have yet to suffer through season like those in the early 90's, or more recently 2004 and remain true, maybe you should wait to show enthusiasm until you've learned what it means to bleed green and gold- despite success and fame.
I am not advocating a lack of enthusiasm. The lightning quick success and play style of the Oregon Ducks is something worth cheering for, but just as lightning is a symbol of power and speed, it is also one of brevity, staying only as long as the realization of its arrival.
True fans don't bandwagon. You stick with the team through the suspense, the perfect plays, the brutal hit to the birdcage, the cheerful chop block, the unforgettable false start, the dynamic down and out, the terrific tackle … it's also national alliteration day.
True fans who move to another city don't change their allegiance to the team in that area. I mean really- you need to be a fan of your hometown.
By all means if you move, go to the games, but you can't pick them as your new team. Like your spouse, it's 'till death do us part." This rule's exception is given if a family member plays professionally for a team from another city.
Even if your favorite player is traded away, signs elsewhere as a free agent, or whatever else leads him to another jersey, you cannot start supporting their new team.
The arrogance of that is like being a Broncos' fan now that Peyton was traded, which is quite possibly the case for many new fans of the team.
The bottom line is that in time the day will come. Yes, a day will come again, perhaps sooner than we think, when the University of Oregon will finish a season outside the top 10, the top 25 even. So the question remains: will you still be there? Or will your fanaticism disappear in a flash?


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Microsoft BitLocker
We're experiencing a very frustrating issue with Microsoft BitLocker on our Dell Latitude E-Series laptops. The problem is that occasionally and for no discernable reason, the TPM module for the laptop gets disabled in the BIOS. This causes the system to prompt for a BitLocker Recovery Key at boot, rendering the system useless until the user contacts the help desk.
I'm hoping to compare notes with other institutions that are using TPM with hard drive encryption so we can try to isolate a cause for our problem. For anyone using hard drive encryption (BitLocker or otherwise) with TPM, would you mind giving me a little info about your deployment and experiences?
· What laptop make and model do you use? Approximately how many are in your environment?
· What hard drive encryption technology are you using?
· Have you experienced the problem describe above, where the TPM module of the system is disabled for no apparent reason?
· How long have you had hard drive encryption deployed?
If anyone has any recommendations in troubleshooting this issue, I'm eager to hear it. Thank you for your time and insight.
Matt Giannetto
Director of IT Security
Montgomery County Community College
email@example.com | (215) 619-7442
The Internet is a dangerous place.
Be suspicious. Be aware. Think security.
Montgomery County Community College is proud to be designated as an Achieving the Dream Leader College for its commitment to student access and success.
We have had Bitlocker deployed for a few years now with minimal issues. On a few very rare occasions, we have had the machine boot and prompt for the code. When this has happened, I have just re-encrypted the machine and all is well. Are you deploying chipset software on machines through WSUS that might over wright BIOS information? We have 60ish deployed with varying models and types.
Todd Clementz
Systems Engineer
Knowlton School of Architecture
The Ohio State University
Direct Line: 614.292.8544
Helpdesk: 614.292.8612
On Tue, 29 Nov 2011 13:43:46 EST, Matt Giannetto said: > * Have you experienced the problem describe above, where the TPM > module of the system is disabled for no apparent reason? On the Dell E-series, the TPM will drop back into the disabled state if the NVRAM battery is disconnected or dies. And sometimes you need to disconnect the battery to clear up NVRAM corruption. You can see where this is heading...
· What laptop make and model do you use? Approximately how many are in your environment? Dell Latitude (100)
· What hard drive encryption technology are you using? WinMagic SecureDoc
Have you experienced the problem describe above, where the TPM module of the system is disabled for no apparent reason? The issue you are having with Bitlocker sounds very similar to the issue I had last Spring with our Dell Latitude Series laptops. I traced my issue back to the use of docking stations and Windows hardware profiles. I could never find a solution to the issue, so the College purchased a 3rd party encryption program.
· How long have you had hard drive encryption deployed? Just starting to deploy the encryption software.
Chuck Thomas
Network Administrator
Wor-Wic Community College
32000 Campus Drive
Salisbury, Maryland 21804
Voice: 410.334.2931
Email: email@example.com
Web Site: http://www.worwic.edu

subset: commoncrawl


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Green Lava Studios
Green Lava Studios is a Costa Rican independent game studio, making games from the tropical forest. Our team is always aiming to create games with unique gameplay and engaging stories.
To make you feel awesome with our games!
- "GameMaker Game of the Year" – Fenix Rage, 2014.
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More about us…
Want to know more about us? Maybe you would like to read our story: click here


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Hotel Accommodation near Place Paul Mistral
Search 12 hotels near Place Paul Mistral
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Trending now in Grenoble
Hotels within 0.5 kilometer of Place Paul Mistral
- Most bookedCitadines City Centre Grenoble
205 people looked at this hotel in the last hour
Most recent review
"We stayed 1 night on our way from Paris to Nice. It was just a few hours in the hotel room, but everything was as expected. Parking in the basement parking lot was very convenient since street partaking is very difficult in the middle of the city."
A Traveller, Jul 2016, US
27 people looked at this hotel in the last hour
Most recent review
"Generally V good Staff V helpful and friendly and English speaking. Breakfast staff new so a little chaotic but helpful"
A Traveller, Sep 2016, GB
21 people looked at this hotel in the last hour
Most recent review
"Wonderfully modern hotel with large rooms. The location is good, about a 10 minute walking distance to the old town and major attractions."
A Traveller, Jun 2016, AU
18 people looked at this hotel in the last hour
Most recent review
"Hotel was clean, comfortable, and very nice. Air conditioning worked, hotel staff were nice and helpful, and overall a great impression. The hotel is within walking distance to the main ciry square, and we walked to and from the train station, though you may want to take the tram which is extreme..."
A Traveller, Sep 2016, CA
11 people looked at this hotel in the last hour
Most recent review
"The staff are nice and helpful. The room was amazing..I could sleep all day in that beautiful cloud of a bed..the tv had english channels and the overall impression of the room is cosy! The bathroom was nice but could've had better pressure from the showerhead, but it was hot and did the job! "
A Traveller, Sep 2016, AU
- La Bulle PlaisirNo Guest Reviews yet
5 people looked at this hotel in the last hour
Hotels within 1 kilometer of Place Paul Mistral
120 people looked at this hotel in the last hour
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"Location and neighbourhood are good, in Grenoble's eco-quarter. Surrounded by park and a square with fountains. Mountains all around. Good modestly priced restaurants, grocery stores and other shopping nearby. Can easily walk to tram lines and buses and the older part of the city. We really enjoy..."
A Traveller, Aug 2016, CA
115 people looked at this hotel in the last hour
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"Comfortable clean hotel, well equipped kitchenette and bathroom. Reception staff English were speaking and helpful. Opposite tram stop could be noisy on that side of hotel, great views of the city. Go for superior studios more spacious. Great reasonably priced base for exploring all Grrnoble has ..."
A Traveller, Sep 2016, GB
35 people looked at this hotel in the last hour
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"Very nice location, in a beautiful old building with modern facilities."
A Traveller, Oct 2016, CA
26 people looked at this hotel in the last hour
Most recent review
"Would recommend this hotel. Convenient for the centre of town. No external noise. Helpful, friendly staff."
A Traveller, Oct 2016, GB
- Palais des Congres Alpexpo
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Clarion Hotels Cleburne hotels are provided below. Search for cheap and discount Clarion Hotels hotel rates in Cleburne, TX for your upcoming individual or group travel. We list the best Clarion Hotels Cleburne lodging so you can review the Cleburne Clarion Hotels hotel list below to find the perfect place.
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This information is about chronic lymphocytic leukaemia (CLL), a type of low-grade non-Hodgkin lymphoma.
On this page
This information is about chronic lymphocytic leukaemia (CLL), which is a type of low-grade non-Hodgkin lymphoma. It aims to answer the questions people ask about CLL and about the form of CLL known as 'small lymphocytic lymphoma' or SLL:
- What is chronic lymphocytic leukaemia (CLL)? (page 1)
- Who gets CLL and why? (page 2)
- How does CLL affect the body? (page 2)
- What are the symptoms of CLL? (page 3)
- What are the tests for CLL? (page 3)
- What are the 'stages' of CLL? (page 4)
- What can I expect to happen if I have CLL? (page 4)
- How is CLL treated? (page 5)
- What happens after finishing a course of treatment? (page 12)
- Living with CLL (page 12).
What is chronic lymphocytic leukaemia (CLL)?
Chronic lymphocytic leukaemia (CLL) is a type of blood cancer that develops from blood cells called lymphocytes. It is called a 'leukaemia' because the cancerous lymphocytes (or 'CLL cells') are found in the blood and in the bone marrow. It is described as 'chronic' because it lasts for a long time.
Technically speaking, CLL is actually a type of low-grade non-Hodgkin lymphoma and in some people the CLL cells are not found in the blood in large numbers, but rather they are found mainly in lymph nodes. This is then called small lymphocytic lymphoma or SLL because the abnormal lymphocytes are small in size and found in the lymph nodes rather than the blood. CLL and SLL are two forms of the same illness and they are treated in the same way.
If you have SLL, the information here will therefore apply to your illness too. Both forms will be described together as 'CLL' unless there is something different about the SLL form that is important to highlight.
Who gets CLL and why?
Over 3,000 people in the UK are diagnosed with CLL each year – it is the commonest type of leukaemia in adults. It has been estimated that there are around 30,000 people living with CLL in the UK.
CLL can affect adults of any age but it is more common in older people. The average age for developing CLL is 72 and only 1 in 10 people are under the age of 55 when they are diagnosed. It is more common in men.
Although it has been noticed that people with CLL are more likely than other people to have a family member with CLL or with another type of lymphoma, it is not an 'inherited' disease. Most people who have a relative with CLL will never develop it themselves.
It is not known what causes CLL. You can't catch it from, or pass it on to, someone else. Nothing you have done will have caused the CLL to develop.
How does CLL affect the body?
CLL is different from most other types of lymphoma because it usually affects mainly the blood and bone marrow.
CLL cells can also collect in lymph nodes, in the spleen and in the liver. When the CLL cells are mainly present in the lymph nodes or the spleen, the CLL is called 'small lymphocytic lymphoma' or SLL.
If CLL cells collect in the bone marrow in large numbers they can stop the bone marrow from making enough healthy blood cells. This can cause:
- a lack of red blood cells (anaemia), which can lead to tiredness, weakness or breathlessness
- low numbers of platelets (thrombocytopenia), which can cause unexplained bruising or bleeding
- low numbers of infection-fighting white blood cells called neutrophils (neutropenia), which can mean you have frequent or persistent infections.
CLL also stops the immune system from working properly, so that it:
- doesn't react against bacteria and viruses as well as it should, making you more likely to have infections
- can start to react against your body's own blood cells – this is called 'autoimmunity' and it may cause:
- a type of anaemia called autoimmune haemolytic anaemia (AIHA) if the red blood cells are attacked
- a bleeding condition called immune thrombocytopenic purpura (ITP) if platelets are attacked.
Your body can also sometimes react to the CLL by releasing chemicals that cause tiredness, weight loss and sweating.
It is these effects that CLL has on the body that cause the symptoms of CLL.
What are the symptoms of CLL?
In more than three-quarters of people with CLL the illness is discovered quite by chance, for example when a blood test is done to check for something else.
Many people have no symptoms at all.
As the cancerous cells build up in the body, some people will start to notice symptoms such as:
- tiredness and a feeling of being generally weak or unwell
- swelling of lymph nodes, often causing lumps in more than one place (such as in the neck, armpits or groin)
- swelling and tenderness in the upper left-hand side of the abdomen and sometimes symptoms of indigestion or of feeling full after eating only small amounts of food (if the spleen is swollen)
- repeated infections
- breathlessness
- a tendency to bruise or bleed easily
- night sweats
- weight loss.
What are the tests for CLL?
CLL is suspected when blood tests show that there are large numbers of lymphocytes in the blood. CLL is diagnosed by looking at these abnormal lymphocytes under the microscope and by testing the proteins on the surface of the lymphocytes.
The SLL form is diagnosed by taking a biopsy from a lymph node and finding these same abnormal lymphocytes.
Further blood tests are done before treatment is started, including tests on the CLL cells to look at their chromosomes and genes (cytogenetic tests).
Other tests that are sometimes done before treatment is started include a bone marrow biopsy and a CT scan (a computed tomography scan).
Your examination and test results will be used by your medical team to give your CLL a 'stage'.
We have more information about tests for lymphoma, which you can read on our website at www.lymphomas.org.uk. You can also print this information at home or ask our helpline to send you copies – email firstname.lastname@example.com or ring 0808 808 5555.
What are the 'stages' of CLL?
Knowing the stage of a lymphoma helps doctors decide when and how to treat you. Most doctors in the UK use a system called the Binet staging system to stage CLL. This system is based on how many groups of lymph nodes are swollen and your blood cell counts:
- Stage A – fewer than three groups of swollen lymph nodes can be felt by your doctor
- Stage B – three or more groups of swollen lymph nodes can be felt by your doctor
- Stage C – there are reduced numbers of red blood cells and/or platelets in your blood (however many swollen lymph nodes there are)
You might hear doctors talk about another staging system called the 'Rai staging system'. This has five stages (0 to IV) and is more commonly used in the USA.
What can I expect to happen if I have CLL?
CLL is only rarely curable (see later sections on Radiotherapy and Allogeneic stem cell transplantation). It is nearly always an illness that you live with for many years.
Like other types of low-grade non-Hodgkin lymphoma, CLL is a chronic illness that flares up from time to time, with periods of being in remission in between.
In many people, CLL will be very slow-growing. If you have this type of CLL, you will probably go for long periods of time without needing any treatment – often for several years.
Other people have a faster-growing form of CLL. If this applies to you, you are likely to need courses of treatment more frequently.
Prognostic factors
There are certain things about your CLL that will give your doctor an idea of how quickly it will grow and how long it is likely to be before you need treatment. These are called 'prognostic factors' and include:
- your age, general health and any other illnesses you have
- the stage of your CLL
- the number of lymphocytes in your blood
- how quickly the numbers of lymphocytes in your blood are increasing
- whether your blood tests show low numbers of red blood cells and platelets
- whether you have particularly swollen lymph nodes
- what changes have happened to the genes and chromosomes of the abnormal lymphocytes.
The medical team will take all these factors into account when your treatment is planned.
In a few people (about 1 in 10 people) the CLL can start to change over time and grow more quickly. This kind of change is called 'transformation'. CLL can transform into:
- another type of leukaemia called B-cell prolymphocytic leukaemia
or into
- a faster-growing type of lymphoma – usually diffuse large B-cell lymphoma (or, less commonly, Hodgkin lymphoma).
When CLL changes into a diffuse large B-cell lymphoma, this is called Richter syndrome.
Symptoms that might suggest that CLL has transformed are:
- feeling much more unwell, sometimes with fevers, sweating and weight loss
- sudden swelling of lymph nodes
- abdominal pain and/or tenderness due to swelling of the spleen.
Further tests (such as a lymph node biopsy and more blood tests) would be needed to work out whether your CLL has transformed. If it has, you would be treated with the treatments that are normally given for these faster-growing lymphomas.
We have more information on transformation.
We have more information about transformation, which you can read on our website at www.lymphomas.org.uk. You can also print this information at home or, if you prefer, our helpline can send you a copy – email email@example.com or ring 0808 808 5555.
Before you read more about CLL and its treatments, you might find this overview of CLL by Dr George Follows helpful. It was filmed in Cambridge in June 2014 at a CLL Support Association meeting.
Video courtesy of CLL Support Association
How is CLL treated?
If the CLL isn't causing troublesome symptoms and the blood counts are not causing concern, you will not need any treatment at first. This approach is called 'active monitoring' or 'watch and wait'.
Treatment is usually only started if the CLL becomes active – for example if it begins to cause:
- severe symptoms such as fevers, sweating, fatigue or weight loss
- rapidly rising numbers of lymphocytes in your blood
- very enlarged lymph nodes, spleen or liver
- low blood counts due to bone marrow failure.
Treatments for CLL aim to:
- reduce the numbers of CLL cells in your blood, lymph nodes, spleen and bone marrow
- relieve your symptoms.
If the CLL is refractory (meaning that it doesn't respond well when it is treated) or if it relapses (meaning that it becomes active again later on), you can be given another course of treatment, which may be a different type of therapy.
People with CLL usually have several courses of treatment over a period of many years, with periods of watch and wait between them.
Watch and wait
Until your CLL becomes active you will not have treatment, but you will have check-ups every 3–12 months at your GP surgery or in the hospital outpatient clinic. At these check-ups your doctor will:
- ask how you are feeling and about any symptoms you have
- examine you
- do blood tests.
The doctors will be able to tell from these check-ups if you need treatment for your CLL.
Although you won't have any treatment for the CLL itself while you are on watch and wait, you will have treatment for low blood counts if these are caused by autoimmunity (see later section on Supportive treatments).
We have more information on watch and wait.
We have more information about watch and wait, which you can read on our website at www.lymphomas.org.uk. You can also print this information at home or, if you prefer, our helpline can send you a copy – email firstname.lastname@example.com or ring 0808 808 5555.
The chemotherapy drugs that are used most commonly to treat CLL are:
- chlorambucil
- fludarabine
- cyclophosphamide
- bendamustine.
- is a gentle form of treatment that has fewer side effects than other forms of chemotherapy
- is especially suitable for people with a milder form of CLL
- can be given again if the CLL comes back
- might be given in combination with an antibody therapy
- is given as tablets, usually for 7 days every month for 6–12 months.
Fludarabine and cyclophosphamide:
- are usually given together as FC, and usually also with the antibody rituximab in a combination called FCR
- can only be given to people who are medically fit enough for this stronger type of treatment; in particular, their kidneys have to be working relatively well because fludarabine cannot be given to anyone with severe kidney problems
- are given either as tablets for 5 days or intravenously (into a vein) for 3 days, once a month, for up to six cycles; the rituximab is given intravenously.
- can be given to people who cannot have fludarabine
- can be given if a course of chlorambucil hasn't controlled the CLL
- is given with the antibody rituximab in a combination called R-bendamustine
- is given intravenously on the first 2 days of each cycle; this is repeated every month for up to six cycles.
Note: after you have had treatment with fludarabine or bendamustine you must be given specially prepared 'irradiated blood' if you need to have blood transfusions in future. This is so that you don't develop a rare but serious complication of blood transfusion called 'transfusion-associated graft-versus-host disease'.
We have further information about chemotherapy and about the side effects of chemotherapy.
We have more information about chemotherapy for lymphoma and its side effects and about irradiated blood, which you can read on our website at www.lymphomas.org.uk. You can also print this information at home or, if you prefer, our helpline can send you copies – email email@example.com or ring 0808 808 5555.
Antibody therapy
Antibodies used to treat CLL now include:
- rituximab
- alemtuzumab
- obinutuzumab
- ofatumumab.
Rituximab (MabThera®):
- is given with chemotherapy in FCR, R-bendamustine or R-chlorambucil
- is given intravenously over several hours on the first day of each treatment – the first dose may be split over 2 days if the number of lymphocytes in the blood is above a certain level.
Alemtuzumab (MabCampath® or Campath):
- works well for people whose CLL is mainly in the blood and bone marrow
- can be given to people whose CLL hasn't responded to treatments containing fludarabine (eg FCR)
- is a good treatment for people whose CLL is 'difficult to treat' with chemotherapy because their CLL cells show certain genetic changes in cytogenetic tests (you might hear these called 'deletion 17p' or 'p53 mutation')
- can be given together with high doses of steroids to people whose CLL shows genetic changes that make it difficult to treat and who also have large lymph nodes
- is given three times a week for up to 3–4 months – either intravenously or subcutaneously (injected just under the skin).
- can be given to people who have CLL that hasn't responded to or can't be treated with fludarabine or alemtuzumab
- can be combined with chemotherapy drugs such as chlorambucil
- is awaiting approval for funding in England and Wales from the National Institute for Health and Clinical Excellence (NICE) as an initial treatment for people who can't have fludarabine, bendamustine or alemtuzumab (given with chlorambucil).
Obinutuzumab (Gazyvaro®, previously called GA101):
- can be given with chlorambucil to older people with CLL who might not be able to have more intensive treatments
- is awaiting approval for funding in England and Wales from NICE as an initial treatment for people with CLL who cannot have fludarabine or bendamustine (given with chlorambucil).
We have more information about antibody therapy and the side effects of antibody therapies.
We have more information about antibody therapy and its side effects, which you can read on our website at www.lymphomas.org.uk. You can also print this information at home or, if you prefer, our helpline can send you copies – email email@example.com or ring 0808 808 5555.
In CLL, steroids are given:
- to treat low blood counts caused by autoimmunity
- before starting chemotherapy, to treat low blood counts caused by bone marrow failure (where there are large numbers of CLL cells in the bone marrow)
- alone, or with rituximab, in people who cannot have chemotherapy
- instead of (or as well as) alemtuzumab in people who haven't responded well to standard chemotherapy.
We have more information on steroids and on their possible side effects.
We have more information about steroids, which you can read on our website at www.lymphomas.org.uk. You can also print this information at home or, if you prefer, our helpline can send you a copy – email email@example.com or ring 0808 808 5555.
Radiotherapy is not often used to treat CLL. It might be used to treat:
- early-stage SLL where there is just one area with swollen lymph nodes – radiotherapy has the potential to cure this form of the illness if it has been diagnosed and treated at such an early stage
- large lymph nodes in people with CLL who can't have chemotherapy or antibody therapy or who haven't responded to these treatments.
We have more information about radiotherapy and the side effects of radiotherapy.
We have more information about radiotherapy and its side effects, which you can read on our website at www.lymphomas.org.uk. You can also print this information at home or, if you prefer, our helpline can send you a copy – email email@example.com or ring 0808 808 5555.
Splenectomy or splenic radiotherapy
A few people with CLL need to have their spleen removed if autoimmune complications of CLL (AIHA or ITP) are causing severe symptoms and haven't responded to other treatments such as steroids or rituximab. This operation is called a 'splenectomy'. A splenectomy is rarely needed to treat the CLL itself.
Occasionally, frailer patients may benefit more from splenic radiotherapy than splenectomy or chemotherapy.
We have more information on splenectomy and the precautions you need to take if you have had this operation.
We have more information about splenectomy and on the precautions you need to take if you have had this operation on our website (www.lymphomas.org.uk). You can print this information at home or, if you prefer, our helpline can send you a copy – email firstname.lastname@example.com or ring 0808 808 5555.
Allogeneic stem cell transplantation
An allogeneic stem cell transplant is the only treatment given for CLL that is aiming to cure the disease (apart from radiotherapy in early-stage SLL).
An allogeneic stem cell transplant is a challenging and risky treatment. Usually only relatively young, fit people whose CLL has a high risk of getting worse would be offered this treatment (for example people with a p53 deletion or people who do not respond well to FCR treatment).
The transplant is more likely to be successful if the CLL is in a good remission after a course of chemotherapy.
We have more information on allogeneic stem cell transplantation.
We have more information about allogeneic stem cell transplantation, which you can read on our website at www.lymphomas.org.uk. You can also print this information at home or, if you prefer, our helpline can send you a copy – email email@example.com or ring 0808 808 5555.
Newer 'targeted' treatments
There are several new treatments that are currently being tested as treatments for CLL. These work by targeting and interfering with important biological processes in the CLL cells – stopping them from multiplying or killing them.
As with any new treatment, they have been tested first in people with relapsed or refractory CLL, but some may one day be used as initial treatments for CLL. Some are only available in the UK in the setting of a clinical trial.
These drugs are often suitable for older or less fit people with CLL, in whom standard chemotherapy might be too intensive. Another advantage is that they can often be taken in tablet or capsule form.
Ibrutinib, idelalisib and ABT-199 are newer drugs that are showing particular promise.
Ibrutinib (Imbruvica®):
- has been used to treat people whose CLL has come back
- seems to work better than the standard treatments in people with genetic changes in their CLL cells that make the CLL difficult to treat using other treatments.
Idelalisib (Zydelig®, previously known as CAL-101 and GS-1101):
- has been used to treat CLL that has relapsed
- reduces the size of large lymph nodes quickly
- has shown promising results when given together with rituximab.
- has shown promising results in people with difficult-to-treat CLL.
Many of the new treatments are also being tested in combination with other, more established treatments – for example in combination with antibody therapy.
The UK Clinical Trials Gateway has a useful list of clinical trials of CLL treatments at www.ukctg.nihr.ac.uk.
The following video is a Q&A session on clinical trials with Dr George Follows.
Video courtesy of CLL Support Association
There is more information on newer drugs and on clinical trials on our website at www.lymphomas.org.uk. We also produce a booklet about clinical trials. You can print this information at home or, if you prefer, our helpline can send you copies – email firstname.lastname@example.com or ring 0808 808 5555.
Supportive treatments
'Supportive treatments' are treatments that help with the symptoms of CLL or with the side effects of the drug treatments you are having for the CLL. Examples of supportive treatments that you may need are:
- antibiotics and antiviral drugs to prevent or treat infections
- immunoglobulin replacement therapy – a transfusion of general immune antibodies prepared from blood donations (not to be confused with antibodies such as rituximab which are used as a specific treatment to target the CLL itself); immunoglobulin replacement therapy is given if your blood antibody levels are low and you have had a serious infection or repeated infections
- red blood cell transfusions and/or platelet transfusions – given if your blood counts fall because of bone marrow failure
- drug treatments for AIHA and/or ITP – steroids are usually given initially but there are several other drugs that can be given for these autoimmune complications.
There is more information on steroids and on transfusion of blood products on our website at www.lymphomas.org.uk. You can also print this information at home or ask our helpline to send you a copy – email firstname.lastname@example.com or ring 0808 808 5555.
What happens after finishing a course of treatment?
Most people will go back to a watch and wait approach after a course of treatment.
As an alternative to going back to watch and wait, some people who go into a good remission might be considered for an allogeneic stem cell transplant.
At some stage the disease is likely to flare up again and further treatment will be needed. What treatment is given next will depend on:
- how quickly your CLL has come back
- what treatment you had before
- how well your CLL responded to the earlier treatment.
The same treatment can often be given again.
Because no treatment works quite as well or for as long the second time around, sooner or later you will probably need different and possibly stronger treatments. Or you might be offered one of the newer targeted treatments.
The latest developments in treatment for relapsed CLL were discussed at the European Hematology Association conference in Milan in 2014. Dr Peter Hillmen summarised the latest research in this interview.
Video courtesy of Leeds Teaching Hospital
Maintenance treatment
In some other low-grade non-Hodgkin lymphomas it has been found that giving additional drug treatment after the main course of treatment is finished makes remissions last longer. This is called 'maintenance treatment'.
Maintenance treatment is still at an experimental stage in CLL. Drugs that are being investigated as maintenance treatments for CLL in clinical trials include rituximab, alemtuzumab, ofatumumab, lenalidomide, ibrutinib and idelalisib.
All these drugs have side effects, such as an increased likelihood of developing serious infections. This means that the risks and benefits of maintenance treatments will be carefully assessed in these research studies. Current national guidelines do not recommend the use of maintenance treatments for CLL.
Living with CLL
CLL is an illness that most people live with for many years. You might find our information on living with lymphoma on our website and in our booklet Living with lymphoma helpful. These cover the more everyday aspects of living with a chronic condition like CLL, such as how to cope with tiredness and other symptoms, your feelings and relationships, diet and exercise and other practical things like managing medical appointments, financial matters, travel and vaccinations.
You could approach the CLL Support Association for help and support. Other organisations that offer further information and support for people with lymphoma can be found on our page of Useful organisations.
Our information about living with lymphoma on our website can be printed off at home or you can ask the helpline to send it to you. If you would like a copy of Living with lymphoma, please ring the helpline on 0808 808 5555 or email firstname.lastname@example.com.
You could approach the CLL Support Association (www.cllsupport.org.uk) for help and support. On their website you can watch interviews with experts in the field of CLL, including two very helpful presentations by Dr George Follows ('An overview of CLL' and 'New treatments for CLL') that were filmed at their June 2014 conference. The website also hosts a film interview with Cambridge CLL and Lymphoma Nurse Specialist, Gwyneth Stafford about managing CLL symptoms.
Please ring our helpline on 0808 808 5555 if you would like details of other organisations that offer information or support for people with CLL.
Sources used
The following are a few of the sources we used to prepare this information. The full list of sources is available on request. Please contact us by email (firstname.lastname@example.com) or by ringing 01296 619409 if you would like a copy.
Brown JR, Porter DL, O'Brien SM. Novel treatments for chronic lymphocytic leukemia and moving forward. American Society of Clinical Oncology Education Book, 2014. 34: e317–e325.
Ghia P, Hallek M. Management of chronic lymphocytic leukemia. Haematologica, 2014. 99: 965–972.
Marcus R, Sweetenham JW, Williams ME (editors). Lymphoma: Pathology, Diagnosis and Management. 2nd edition. 2014. Cambridge University Press, Cambridge.
Oscier D, et al., on behalf of the British Committee for Standards in Haematology. Guidelines on the diagnosis, investigation and management of chronic lymphocytic leukaemia. British Journal of Haematology, 2012. 159: 541–564.
Hallek M. Chronic lymphocytic leukemia for the clinician. Annals of Oncology, 2011. 22 (Suppl 4): iv54–iv56.
With thanks to Dr George Follows, Consultant Haematologist and Clinical Lead for Lymphoma, CLL and clinical trials, Addenbrookes NHS Trust Hospital, Cambridge for reviewing this information.
We would also like to thank the members of our reader panel who gave their time to review this information.
Content last reviewed: November 2014
Next planned review: November 2017
If you would like a printed copy of any of our lymphoma information, complete our information order form and we will post it to you free of charge (UK, Channel Islands and Republic of Ireland only). If you live outside the UK, we recommend that you contact the lymphoma patient and carer organisation in your country as treatments and healthcare systems vary overseas.


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Q & A Library
Mistletoe for Cancer?What can you tell me about Iscador as a cancer treatment?
Answer (Published 12/20/2006)
Iscador is an extract of European mistletoe (Viscum album). The main proponents of Iscador for cancer treatment are anthroposophic physicians who follow the tradition established by Austrian philosopher Rudolf Steiner, a Christian mystic and student of eastern as well as western spiritual traditions. Anthroposophic medicine addresses both the spiritual and physical components of illness. Steiner's followers have created a network of schools, hospitals, and nursing homes throughout Europe and the United States.
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In the laboratory, mistletoe extracts have been shown to kill cancer cells and to stimulate immune cells that can help the body fight cancer. A few animal studies have suggested that the extracts may help reduce the side effects of chemotherapy and radiation. However, so far, the few human studies that have been performed haven't yielded conclusive findings.
The National Center for Complementary and Alternative Medicine (NCCAM) and the National Cancer Institute (NCI), both part of the U.S. National Institutes of Health, are sponsoring two clinical trials to test the efficacy of mistletoe extract. One will look at the combination of mistletoe and the chemotherapy drug gemcitabine for treatment of patients with advanced pancreatic, colorectal, non-small-cell lung, or breast cancer. The goal is to see whether the mistletoe helps patients better tolerate the chemotherapy or whether it stimulates immune system cells to more effectively combat the cancer. The researchers plan to recruit between 45 and 51 patients for the study. Find more information on this clinical trial here.
The other study is recruiting patients being treated with conventional chemotherapy for non-small-cell lung cancer to determine whether supplemental treatment with mistletoe improves immune function and quality of life. Find more information on this study here.
Iscador is said to be among the most widely used unconventional cancer treatments in Europe. It is approved by Germany's Commission E as palliative therapy for malignant tumors – that is, for treatment of symptoms, not as a "cure" for the disease. The extract is injected under the skin on a daily basis. You should be aware that Iscador is not available in the United States, except through clinical trials, and that it is dangerous to ingest any part of the mistletoe plant. All parts are toxic – they can cause blurred vision, nausea, and vomiting, stomach pain, diarrhea, irregular heartbeat, confusion, convulsions, disorientation and drowsiness. In some instances, consuming mistletoe has led to seizures and death.
I'm glad that mistletoe is being investigated seriously by the NCCAM and NCI. The study results should give us a much better idea of its usefulness in cancer treatment.
Andrew Weil, M.D.
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A portion of the original material created by Weil Lifestyle on DrWeil.com (specifically, all question and answer-type articles in the Dr. Weil Q&A Library) is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 United States License.


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On Saturday Magnus Carlsen increased his lead in the World Championship match against Viswanathan Anand to 4-2. In a quiet Ruy Lopez, the 22-year-old Norwegian equalized comfortably, got a slight initiative, won a pawn, then another one but the rook ending was probably still drawn. However, Anand again failed to find the best defense and had to resign at move 67.
And he did it again. With an almost unprecedented will to win, Magnus Carlsen ground down Vishy Anand in another rook ending to take a two-point lead in the match. The cold, engine-driven evaluations were constantly saying "draw", but the practical problems Anand had to solve again proved to be too much for the 44-year old Indian GM.
Avoiding the Berlin Ending with the move 4.d3 seemed like a good practical decision by the World Champion, and his 10.Bg5 got Carlsen thinking for 25 minutes. From move 15 onwards, it was clear that Anand was going to try his luck on the kingside. Step one was to try and land a knight on f5.
However, Carlsen found a number of excellent maneuvers and when all the minor pieces were traded it was clear that Black was at least equal. In fact, after 26...c4! it suddenly became clear that it was the Norwegian who was playing for a win.
With a timely exchange, Carlsen left his opponent with a bad pawn structure but the question was how he would improve further. "I thought I got a pretty solid position out of the opening. Then at some point I was little bit better but nothing much was going on." But then, Anand either "sacrificed or blundered" a pawn, as Carlsen put it at the press conference. Asked about his surprising 38.Qg3, Anand said: "What can I say, some days it just goes like that."
Carlsen obviously took the pawn, and it was clear that he was going to torture his opponent for quite some time. "After that I got a very good rook ending but I am not at all sure if it is winning," the challenger said. As he allowed h4-h5 Anand was well on his way to draw the game anyway, until Carlsen found one more miniplan. "I had one little trap, this Kf4-Ke3 etc. Fortunately he went for it."
Both players felt that it was all over when Black got Ke3 in, but analysis shows that there was still one more chance to draw with White, missed by Anand, on move 60.
Vishy Anand was clearly upset. "I mean, today was a heavy blow. I will not pretend otherwise. Nothing to be done, you just go on." A Norwegian journalist asked how he would deal with it, to which Anand answered: "Well you just do your best." The same journalist wanted him to elaborate on his answer, to which Anand answered: "Doing your best means doing your best. I dont know why you don't understand English?"
Sunday is another rest day. On Monday the second half of the match starts, with Vishy Anand again playing with the white pieces. He needs a win soon.
now its very difficult for anand...but i hope he can do it..i m crying for anand!!
Anand is no match for Carlsen after four hours of play and in endgames. Carlsen must has spend many hours on computers to master the endgame techniques. It would be incredible or near a miracle if somehow Anand can tie the score. But if there is one that can do it, it's him. Tomorrow game is crucial and he need to win tomorrow or else I believe it's over.
With all due respect to Anand, it seems like once he has determined that in the current position it is a draw, he seems to enter a shell where he thinks whatever happens he will not loose from this position. While this may be true against most players, clearly it is not true against the best in the world. After this match, if Anand still wishes to continue playing, I wish he goes back to the younger Vishy days when he was always hungry for a win and avoid draws as far as possible!
23.Qg4 this is an OLD trick by Anand to move Nf5. Magnus replied by taking the knight. So it end up in Rook game which favour Magnus. And 37...Re6 38.Qg3 Rxe4 39.Qxd6 Rxe3 makes matter worst for Anand. Cool play Magnus
No! No! No!
Anand you are better than this!!!!!
Don't let him beat you!!!!!
Come on and win, just do it!
If Anand loses this match then...
hope Anand gets secelected in the candidates
This match is over. Anand isn't coming back from this.
Really, "More later."
In last two games one thing is clear Carlsen achieved to force anand to have isolated pawns and this became the reason why Anand lost, in my opinion.Also Don't know why Anand forgets the necessity of passed pawn!, that's why his h pawn became isolated and black rook took advantage.
I still don't understand why Anand exchanged all the minor pieces in game six?! If he continue to play this way he has no chance at all.
The idea of 60.b4! is pushing two connected pawns as soon as possible. A quick draw was possible.
Everything was tied until this move, we can not say Anand was the loser all the time in the game.
Alien 2, "Game over man;Game over!!"
Anand's 60. Ra4 wasn't strong enough.
I't amazing how Carlsen is able to keep the pressure. He is forcing Anand to defend at his very best. However I still feel a GM of his level should be able to draw these endings, perhaps he has problems with the pressure of being the world champion..
Gurd almighty !!
Amazing win for Carlsen. Anand has to do something at like 2900 level to win the match. Carlsen will win.
Brilliant play by Carlsen after a mostly equal game. I dont think we will need all twelve games to officially declare Carlsen as the new WC! Thus begins the chapter (and possibly a very long one at the top) of arguably the greatest chess player of the new millennium.
Carlsen makes no mistakes ! Why ? Because he was not shaken ! Anand would have to bring him at the edge of unknown and beyond so Carlsen will show his human face ;)
I think in the first few games Magnus tried some socondary weapons just to see how prepared his opponent is and to put an element of surprised and then he had to switch to his primary weapons which he can manage very well. This means he is in full control of what is going on and he knows exactly how to deal with his opponents. Yes Anand missed some chances and walked in danger zones but all in all Magnus is a much better player. I think. He deserves to be the world champion.
Carlsen--- New era.. the wolverine of the chess world
by PeterDoggers - 41 hours ago
by PeterDoggers - 3 days ago
by PeterDoggers - 4 days ago
by PeterDoggers - 5 days ago
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The 2014 Stanley Cup Final features two superficially similar teams that clawed their way through the postseason in dramatically different ways.
Both the New York Rangers and Los Angeles Kings are built, at least theoretically, on size, defensive play, depth throughout the lineup and goaltending.
The Rangers' formula hasn't changed from the regular season. The team still leans heavily on goaltender Henrik Lundqvist and a defence that limits how many shots he faces, and it counted on balanced scoring from all four lines to make it this far.
The Kings, on the other hand, have seen their goaltender struggle and their defence corps decimated by injury. They have had to change and consequently arrive in the Final with a shockingly high-octane offence and a somewhat suspect defensive group (though, as always, head coach Darryl Sutter's group of forwards is as committed as any in the league).
What do they look like head to head? Read on to go through the depth charts of each team and see how they stack up.
Statistics courtesy of ExtraSkater.com or NHL.com unless otherwise noted.


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Barron's conducts an annual roundtable interview with seasoned money managers to gather insight into the markets and showcase some interesting investment opportunities. Midway through the year, Barron's publishes a follow-up to see how these managers' picks have performed and to see how expectations have changed. I was interested to see commentary by Meryl Witmer, general partner of Eagle Capital Management, about a company called Innophos Holdings (NASDAQ:IPHS), a producer of specialty phosphates.
This is what Witmer had to say about IPHS:
Innophos Holdings [IPHS] has 23 million shares and sells for 43. Innophos, along with its main competitor, ICL, are the two main producers of specialty phosphate products in North America. The majority of Innophos' business is specialty ingredients such as minerals fortification, leavening agents in bakery products and excipients in pharmaceutical tablets, which bind the ingredients. The company also makes additives for deli meats and abrasives in toothpaste.
Specialty ingredients usually account for less than 1% of the overall cost of a product. They deliver technical effects that are hard to replicate with substitutes, and it can take months to qualify a specialty phosphate in a product so it generally isn't worth switching suppliers. These attributes allow Innophos to pass through cost inflation in its key input, phosphate rock. It recently restructured its rock sourcing to have multiple suppliers and shorter lag times between price fluctuations. The company buys phosphate rock in Mexico and converts it to an intermediate product. It also buys intermediate product in the U.S. and processes it further into specialty ingredients. Innophos is working to shift some sales in Mexico to higher-value-added products.
How much does Innophos earn?
The company could earn about $4.70 a share of free cash flow in 2011 and about $5 in 2012. Reported earnings are about $1 a share lower. Innophos has a strong balance sheet with little net debt. It is worth about 12 times free cash flow. Our target price is $65.
Witmer's description makes IPHS sound extremely compelling: Ongoing sales of a consumable product with price-inelastic characteristics and high switching costs usually translates into a competitive moat that allows for persistent and strong returns. I decided to investigate further.
The first thing I do after I've found an interesting possibility is to rebuild the financial statements in my Excel model. At this stage, I want to know very little about the company's strategy or growth prospects so as to avoid bias when assessing the company's history; once I am done looking at the company's past performance, I'll then consider these things in formulating assumptions for different future scenarios.
To start, this is a young company. It was formed in 2004 and went public in 2006. This presents an immediate problem in that a short track record provides little insight into management's abilities. I like to look at companies that have been able to grow revenues for more than a decade without sacrificing return performance or free cash flows. For IPHS, it will be difficult to draw these conclusions.
The following chart shows the variability of the company's returns since inception (note, this is a zoomed-in version to give a closer look at quarterly returns):
[Click all to enlarge]
IPHS Returns, 2005 - 1Q 2011
The variability in these returns is significant, which makes it difficult to have any conviction about management's abilities. How about revenues and margins?
This chart provides a bit of evidence to suggest the company is doing something right. It's been able to maintain upward trending revenues despite the recession, but it seems it may have accomplished this through discounting, as its gross margin has contracted significantly since 2008, and seems to be approaching a more normal level in the high teens. You can tell that it has a highly variable cost structure, in that its margins largely move in sync – this is a good sign. Let's check to see whether these sales have been accomplished through looser customer credit, or some other financial shenanigan.
Everything looks good here. Days Sales Outstanding have been remarkably stable, and management is making the right moves by bringing inventory back into line after a drastic decline in revenue in 2009 caught it off-guard. Let's check free cash flow.
Unfortunately, unlike other companies we've looked at, IPHS has not had a stable relationship between revenue growth and free cash flow growth. To quantify this, free cash flow has averaged 9% of revenues over the last six years (using annualized figures), but the standard deviation of this relationship is a whopping 7.6%, making it more difficult to form expectations about how relationships will continue in the future.
One last thing to take a look at is the company's capital structure. The following chart shows how the company has been aggressively reducing debt, which is a good thing in that it reduces the overall riskiness of the enterprise.
Where does all of this leave us? As expected with a relatively young business, operations have been characterized by volatility, which introduces risks when we are forming expectations. On the plus side, management seems quite capable and focused on improving operations, as we see revenue trending upward, working capital declining, and debt being quickly being paid off. Given the company's relatively low share count, improvements in revenue should lead to a corresponding jump in EPS, which is a focal point of many investors and could lead to some upside if the company's earnings multiple remains stable (though, given its relatively high multiple, this will be contingent on future growth expectations remaining quite high). Unfortunately, it is difficult to draw conclusions about free cash flow, given the particularly intense volatility in that metric.
The final step is to value the company using different scenarios for its future growth and margins. Having done this, I believe the company looks fairly valued in the high $40s (as of June 27), and that any expected upside would be based on speculation about the company's future growth. Consequently, I don't believe this is a value opportunity, as it reflect a "heads I win, tails I lose" situation rather than the far more favorable "heads I win, tails I don't lose much."
An investment in IPHS necessitates a high level of insight into the company and industry, and extremely strong convictions about its future growth. I would rather find a situation where the company is immediately undervalued, rather than undervalued only if my best expectations come true.
Disclosure: None