Treatment Pathways for Active CLL

Treatment Pathways for Active CLL

This is the second in a series of slides from the recent CLL conference in Edinburgh that may be of interest to CLL patients.

This summarises current treatment options for active CLL and lists risk factors that would influence treatment decisions.

Abbreviations:

CIT = chemoimmunotherapy, eg FCR (fludarabine, cyclophosphamide, rituximab)

Allo SCT = allogeneic stem cell transplant with stem cells from another matching person – related or unrelated. In practical terms, it is uncommonly done, can cause GVH (graft versus host disease), and is recognised as a potential cure for CLL .

MRD = minimal residual disease, ie remission.


Wake-up call for cancer agency boss Diana Sarfati

Wake-up call for cancer agency boss Diana Sarfati

My colleague haematologist Ken Romeril of Myeloma NZ has an excellent article on stuff today calling out Pharmac and the new cancer agency on their failure to factor blood cancers into their plans.

Read it here.


'Take-out messages' from CLL Horizons

'Take-messages' from CLL Horizons

This is the first in a series of slides from the recent CLL conference in Edinburgh that may be of interest to CLL patients.

The important information here is that under half of people with CLL die primarily of that disease, while the rest die of other cancers, infections, or other diseases (comorbidities).  So, if you have CLL, it’s important to be checked regularly for other cancers, such as melanoma and other skin cancers, prostate cancer in men, breast cancer in women, and gastrointestinal (oesophageal, stomach, and colon) cancers and lung cancer, in both sexes. This relates to the fact that people with CLL have a reduced ability to control cancer in their bodies because of the impaired immune system that goes with the disease.

If you develop any infection, take it seriously, as if you have CLL you’re at higher risk of a serious episode of infectious disease or a fatal outcome, again because your immune system function is impaired. You may also need more prolonged antibiotic courses, with infective diseases in the context of CLL.

The third group of non-CLL causes of death in CLL, more than a quarter of cases, relates to pre-existing conditions such as heart disease, diabetes, and chronic obstructive pulmonary disease, which either precede or develop during the course of CLL, often independently. This is partly because approximately half of people with CLL are 70+ years old at diagnosis, and partly because a lot of  people with CLL, particularly the elderly patients, have a smouldering, relatively stable or only slowly progressive form of the disease. It also makes the point that important comorbidities need to be managed optimally in people with CLL.

Neil Graham


Study of Ibrutinib in CLL Shows a Benefit, but Raises Crucial Questions

Study of Ibrutinib in CLL Shows a Benefit, but Raises Crucial Questions

Efforts to target key mechanisms in the development of chronic lymphocytic leukemia (CLL), one of the most common lymphoid cancers, have led to several new treatments. Among these, ibrutinib emerged as a strong approach for patients who were too frail for aggressive treatment.1 But for healthier patients with CLL, the benefit of this drug remained unknown for a time.

A phase 3 study published in the New England Journal of Medicine showed a benefit for ibrutinib plus rituximab for these more fit patients.2 Although the data help clarify the potential role of ibrutinib in CLL, they also raise difficult questions about the future of this treatment approach.

The standard first-line treatment for otherwise healthy CLL patients 70 years or younger has been a chemoimmunotherapy regimen of fludarabine, cyclophosphamide, and rituximab (FCR). Patients with immunoglobulin heavy-chain variable region (IGHV)-mutated disease had particularly good results with this treatment: roughly half remained progression-free for up to 8 years after initial treatment. However, substantial toxic effects in the aftermath of treatment, including myelosuppression, risk of myelodysplasia, and infectious complications, have led researchers to explore other avenues of therapy — in particular, ibrutinib.

Ibrutinib inhibits Bruton tyrosine kinase (BTK), a B-cell signaling protein involved in B-cell development, differentiation, proliferation, and survival. After studies showed the drug to be effective for patients with relapsed CLL and then frail patients with untreated CLL, researchers have been eager to investigate its role in first-line therapy for younger patients.

Most studies so far have explored the use of ibrutinib as a monotherapy. This trial, however, led by Tait Shanafelt, MD, of Stanford University School of Medicine, California, combined ibrutinib with rituximab, and compared the regimen with the standard treatment of FCR.

The study began with 529 patients, all with previously untreated CLL. A total of 354 patients, all 70 years or younger, were randomly assigned to receive ibrutinib-rituximab treatment, consisting of 1 cycle of ibrutinib, followed by 6 cycles of ibrutinib-rituximab combined, and then ibrutinib alone, taken indefinitely until disease progression. The 175 patients in the control group received 6 cycles of FCR chemoimmunotherapy. The primary end point was progression-free survival (PFS), with overall survival (OS) as the secondary end point.

Patients in the ibrutinib-rituximab group received 1 dose of 420 mg per day of ibrutinib during day 1 to day 28 of each of the 6 cycles, until either their disease progressed or the side effects became intolerable. Alongside this dosage, they also received rituximab, during cycles 2 through 7. The FCR group received 6 cycles of FCR.

At a median follow-up of 33.6 months, Dr Shanafelt and the team found a benefit for the experimental treatment. At that point, 89.4% of patients in the experimental group had experienced no disease progression, compared with 72.9% in the control group. OS rates echoed the benefit: 98.8% of patients in the experimental group were still alive, compared with 91.5% of patients in the control group.

The researchers wondered if treatment efficacy would be different for patients with the IGHV-mutated CLL. Dividing the existing patients into 2 subgroups, they found that for patients carrying the mutation, the 2 protocols were nearly identical — and in fact, FCR proved 0.3% more effective. For those without the mutation, however, the ibrutinib-rituximab combination was superior to FCR: with 90.7% PFS at 3 years, compared with 62.5%, respectively. Patients in the experimental group without IGHV-mutated disease also experienced fewer serious infections.

Researchers concluded that treatment with ibrutinib-rituximab was superior to FCR with regard to both PFS and OS. They reported a 65% lower risk of progression and an 83% lower risk of death. This superior PFS was also present in high-risk subgroups, including patients with Rai stage III or stage IV disease, chromosome 11q22.3 deletion, and unmutated IGHV.

Study coauthor Jacqueline Claudia Barrientos, MD, associate professor at the Feinstein Institutes for Medical Research in New York, emphasized that the study does not provide any evidence that the addition of rituximab improved outcomes or remission duration beyond what is achieved by ibrutinib alone. Because the study didn’t include an ibrutinib-monotherapy arm, there’s no way to know. “I don’t believe that we should move to using combination ibrutinib plus rituximab for frontline except in specific cases, such as uncontrolled autoimmune complications or in a patient with a very aggressive disease that requires combined therapy because monotherapy is taking too long to work,” Dr Barrientos said.

She also pointed out that widespread use of ibrutinib as a frontline treatment would raise several issues. Although ibrutinib appears to cause less myelosuppression than FCR, she said, “there are still other issues that can affect quality of life.” These include bleeding, joint pain, diarrhea, cardiac arrhythmias, and other side effects. Dr Barrientos noted that because ibrutinib needs to be taken indefinitely, sorting out these complications is vital.

Cost is another concern. Again, the long-term nature of ibrutinib therapy is the issue: the drug may be too expensive to sustain treatment. In a 2015 paper in the Journal of Oncology Practice, Dr Shanafelt discussed the potential financial burden that would confront the movement toward novel targeted agents, such as ibrutinib, for frontline treatment of CLL.3 This shift, Dr Shanafelt wrote, “will dramatically increase individual out-of-pocket and societal costs of caring for patients with CLL. These cost considerations may undermine the potential promise of these agents by limiting access and reducing adherence.”

Nitin Jain, MD, associate professor of medicine at MD Anderson Cancer Center, Houston, Texas, who was not involved with the study, was optimistic about the findings. The results, he said, were not just statistically significant but also clinically significant.  “This study establishes a new treatment paradigm for younger patients with CLL,” he says. However, he emphasized that this benefit is restricted to patients with IGVH-unmutated disease, per the study findings.

As Dr Jain sees it, the study is just one more piece of the puzzle showing how ibrutinib and new drugs may best benefit patients with CLL. “Several ongoing randomized studies are evaluating combinations of targeted therapies with chemoimmunotherapy,” Dr Jain noted. “The results of these studies will further help define the optimal frontline approach for patients with CLL.”

Disclosure: The study was supported by the National Cancer Institute and Pharmacyclics. Some of the authors of the study reported receiving payments from the pharmaceutical industry. For a full list of disclosures, please refer to the original study.

References

  1. Burger JA, Tedeschi A, Barr PM, et al. Ibrutinib as initial therapy for patients with chronic lymphocytic leukemiaN Engl J Med. 2015;373(25):2425-2437.
  2. Shanafelt TD, Wang XV, Kay NE, et al. Ibrutinib–Rituximab or chemoimmunotherapy for chronic lymphocytic leukemiaN Engl J Med. 2019;381(5):432-443.
  3. Shanafelt TD, Borah BJ, Finnes HD, et al. Impact of ibrutinib and idelalisib on the pharmaceutical cost of treating chronic lymphocytic leukemia at the individual and societal levelsJ Oncol Pract. 2015;11(3):252-258.


CLL Horizons and workshop – an update

CLL Horizons and workshop – an update

I’ve just returned from attending two back-to-back conferences on CLL in Edinburgh. The first was the international  CLL Advocates Network (CLLAN) Horizons conference for CLLAN members. The second was the 2019 International Workshop on CLL (iwCLL), a major medical and scientific meeting. Both conferences were excellent.

Horizons focused on CLL patient advocacy group models from around the world, what made them work, where improvements could be made, and where the future was heading. There was a lot of discussion on sharing of resources amongst the various groups, so as not to “reinvent the wheel”, and you will soon see examples of this here on our site.

Psychosocial support provision, use of social media to communicate among individuals and groups, examples of successful advocacy, and the various ways in which advocacy groups can make positive contributions to research were major components of the formal presentations. There were also several presentations about the current state of the science and medical therapeutics of the disease CLL.

I was invited to present the story of a new advocates’ group, on how we’re developing CLLANZ and lessons learned, as well as the future role of the organisation. Click below to view my presentation.

The iwCLL meeting (attended by close to 2000 delegates) covered in great detail the science and the medicine of CLL in 2019, and the directions investigative science and medical therapeutics will take in the next few years.

I will be sharing specific aspects of interest  from the conference presentations with you on this website , over the next few weeks, linked to areas of research and treatments

Best wishes

Neil Graham


Neil Graham video

Submission to Pharmac to call for a revision of CLL treatment decision

Submission to Pharmac to call for a revision of CLL treatment decision

Dr Neil Gram writes on behalf of CLL patients to ask Pharmac to revise the decision to fund only venetoclax for the treatment of CLL, by funding ibrutinib as an essential treatment for CLL, in addition to venetoclax. While we welcome the fact that a new era treatment for CLL has at last been funded, we have serious concerns about the limitations of the chosen medicine and its inability to meet the needs of all CLL patients, in particular those with severe CLL.

Click here to view the letter sent to Pharmac on 12 September 2019


New Therapies for Blood Cancers Hold Promise

New Therapies for Blood Cancers Hold Promise

This article was originally published on BioSpace

Blood cancer is actually a term applied to three different types of cancer – leukemia, lymphoma and myeloma. For centuries, these cancers had virtually no possibility of survival. Even as recently as the 1960s, the five-year survival rate for leukemia was 14%. By 2010, it had increased to 61%. Similar gains have been made in the survival rates for lymphoma and myeloma, with Hodgkin lymphoma reaching a five-year survival rate of 88% in that year. The story of the science behind the gains in survival rates and the development of ever-more effective therapies is the story of advances in the field of immunotherapy and personalized medicine taking place at centers such as Abramson at UPENN and Dana-Farber in Boston.

Bone Marrow Transplants

The first significant increases in survival rates occurred in the early 1980s, with the introduction of chemotherapy and bone marrow transplants. In a UPENN CureTalks interview in 2017, Dr. Carl June of UPENN described the two-step process. First, the patient’s immune system received super-lethal doses of chemotherapy. Then, bone marrow from a sibling was transplanted into the patient. When the result was a better survival rate, the increase in survival was attributed to the super-lethal dose of chemotherapy administered prior to the transplant. When the procedure was performed on identical twins and researchers discovered that increased survival did not occur, researchers had to rethink their premise. They realized that the source of the survival increase lay in the differences in the marrow of the non-identical sibling rather than in the process of destroying the patient’s immune system before the introduction of new bone marrow.

This better understanding of the cause of increased survival rates from bone marrow transplant therapy, combined with the significant downside arising from graft vs host disease, led June to explore the possibility that patients could receive the benefits of a bone marrow transplant without an actual transplant. He studied the possibility that a patient’s own immune system could be used as a weapon. The outcome of this work was the development of CAR-T cells, approved for use by the FDA in 2017.

CAR-T

CAR-T therapy is the first personalized cancer therapy to be approved by the FDA. The process has been licensed by Novartis. They have manufactured CAR-T cells for patients in their FDA-approved facility. With CAR-T, a patient’s own T-cells are filtered, along with white blood cells, through the leukapheresis process. A viral vector is used to recognize the targeted cells – cells with cancer and other cells expressing a specified antigen. These “reprogrammed” cells are then introduced back into the patient’s blood.

According to June, it is not at all uncommon for a high fever to occur during the time when the CAR-T cells are annihilating the cancer cells. This fever has shown no lasting effect. It is a side effect that indicates that the process is working. For two of the first three participants in the clinical trials held at Penn in 2010, the survival rate for chronic lymphocytic leukemia (CLL) was eight years as of 2018.

Immune Checkpoint Inhibitors

Another FDA-approved immunotherapy agent is used in patients with recurring Hodgkin lymphoma (HL). The FDA approval occurred in 2016, but a study underway in 2019 at Dana-Farber by Dr. Margaret Shipp’s team is investigating the mechanism that causes two proteins, PD-L1 and PD-L2, to overproduce on HL cells. They’ve found that the proteins work with a protein on the T-cells that keeps the T-cells from attacking the HL. By blocking PD-1, it is possible to expose the HL to the T-cells. The use of these checkpoint inhibitors holds promise for those with HL that has reoccurred or not responded to the first therapy.

BiTE

Until recently, a patient’s immune system was reprogrammed to fight a single target – an antigen. Dr. Daniel D’Angelo of Dana-Farber describes BiTEs (bispecific antibodies) as a way to cut out the middle step. Rather than attack first one, and then the other, the BiTE attaches to both a T-cell and a tumor cell at the same time. This FDA-approved therapy is being used to treat acute lymphoblastic leukemia (ALL) but shows potential for the treatment of other cancers.

The potential advantage of BiTEs over CAR-T cell therapy lies in the fact that BiTEs are not patient-specific: There is not the need to remove and reprogram T-cells for reintroduction into the patient’s blood. Currently, BiTE is being used with patients who have multiple myeloma (MM) and have relapsed. Early results are promising. In one clinical trial, some patients showed no trace at all of cancer after treatment. The next step is to see how long this remains the case, as well as whether or not different delivery times or the use of BiTE in conjunction with CAR-T will make a difference in the outcome.

Under Study

At the ASH Annual meeting held at Abramson Cancer Center, two new studies were described.

One study is designed to determine the best time to introduce CAR-T therapy in multiple myeloma (MM). It will identify T-cell biomarkers that help to predict the outcome from CART-BCMA therapy (Abstract #1974 and Abstract #1886). The other explores the combination of CAR-T cells and the tyrosine kinase inhibitor ibrutinib in chronic lymphocytic leukemia (CLL). Initial results show that the use of both in combination will lead to deep and sustained remission (Abstract #298).

The current work is already leading to new avenues of investigation. Improved blood cancer therapies are one part of the advances being made in targeted, personalized therapies.


Ibrutinib Combo in Chronic Lymphocytic Leukemia is Superior, but Costly

Ibrutinib Combo in Chronic Lymphocytic Leukemia is Superior, but Costly

This article was originally published on the Cancer Network

In the first-line setting, ibrutinib plus rituximab had a superior survival benefit to standard chemoimmunotherapy for patients with chronic lymphocytic leukemia (CLL), according to an interim analysis of a phase III randomized clinical trial published in the New England Journal of Medicine.

Study researchers also noted that “indefinite” use of ibrutinib therapy has been associated with “substantial expense.” According to the IBM Micromedex, the estimated average wholesale price per month for ibrutinib alone is more than $13,324. A 2018 study found that at current prices, ibrutinib was not cost-effective as first-line treatment for CLL patients older than 65 years of age with a 17p deletion.

The trial enrolled 529 patients between March 2014 and June 2016 who were 70 years of age or younger with treatment-naïve CLL. Patients were randomly assigned in a 2:1 ratio to receive either 6 cycles of ibrutinib plus rituximab followed by continuous administration ibrutinib until disease progression (n=354) or 6 cycles of standard chemoimmunotherapy (n=175), which consisted of fludarabine, cyclophosphamide, and rituximab. Follow-up was a median of 33.6 months.

At 3 years, patients who received ibrutinib plus rituximab had a statistically higher progression-free survival (PFS) rate and 65% lower risk of disease progression or death compared with patients who received standard chemoimmunotherapy (89.4% vs 72.9%; HR=0.35; 95% CI, 0.22–0.56; P<0.001). Patients who received ibrutinib plus rituximab also had a significantly higher overall survival (OS) rate and an 83% lower risk of death compared with patients who received standard chemoimmunotherapy (98.8% vs 91.5%; HR=0.17; 95% CI, 0.05–0.54; P<0.001).

Overall, both the ibrutinib plus rituximab and chemoimmunotherapy groups had approximately an 80% incidence of adverse events of grade 3 or higher. There was, however, a difference in infection complications of grade 3 or higher, with the ibrutinib plus rituximab group having a lower incidence compared with the chemoimmunotherapy group (10.5% vs 20.3%; P<0.001).

The incidence of adverse events of grade 3 or higher (regardless of attribution) was similar in the two groups (in 282 of 352 patients [80.1%] who received ibrutinib–rituximab and in 126 of 158 [79.7%] who received chemoimmunotherapy), whereas infectious complications of grade 3 or higher were less common with ibrutinib–rituximab than with chemoimmunotherapy (in 37 patients [10.5%] vs. 32 [20.3%], P<0.001).

“I don’t think one hundred percent of people should be getting ibrutinib as frontline therapy,” Joshua Brody, MD, director of the Lymphoma Immunotherapy Program at the Icahn School of Medicine at Mount Sinai Hess Center for Science and Medicine in New York, told Cancer Network.

On the basis of the study results, he explained the ibrutinib combination is “definitely” a “reasonable” option and “better” than fludarabine, cyclophosphamide, and rituximab, but it’s not “definitely” better than rituximab plus bendamustine, which is the other chemoimmunotherapy regimen commonly used in this patient population.

previously published trial in treatment-naive CLL patients found a PFS benefit among those who received ibrutinib monotherapy or ibrutinib plus rituximab when compared with rituximab plus bendamustine. However, no OS benefit was seen for the ibrutinib-containing regimens.


Government unveils national cancer agency and $60 million injection into Pharmac

Government unveils national cancer agency and $60 million injection into Pharmac

This article was originally published on the New Zealand Herald

The Government has today unveiled plans to establish a national cancer agency, which will be led directly by experts of the deadly disease, and a $60 million injection into Pharmac.

Key announcements:

• Cancer Control Agency to abolish postcode lottery.• World-leading public health physician and cancer epidemiologist Professor Diana Sarfati has been appointed as the Ministry of Health’s interim National Director of the cancer control agency.

• A $60 million funding boost to Pharmac, $20 million this year and $40 million in 2020/21.

• A new system to fast-tracking Pharmac’s drug funding decision process.

Until today, decisions about how to tackle New Zealand’s cancer “crisis” came from bureaucrats within the Ministry of Health.

By December 1, the Government has promised decisions will come from a team of top cancer specialists who will report directly to Health Minister David Clark. That is the date the agency will officially be up and running.

World-leading public health physician and cancer epidemiologist Professor Diana Sarfati has been appointed as the Ministry of Health’s interim national director of the agency.

“This is huge for New Zealand. It’s the biggest change in cancer care in at least 15 years, if not ever. When the UK appointed a national cancer director there was an unprecedented improvement and survival rates increased dramatically,” Cancer Society of New Zealand medical director Chris Jackson said.

It comes after a powerful public movement started by dying dad Blair Vining who launched a petition calling for a national cancer agency to hold District Health Boards to account and put an end to postcode lottery.

His petition gained more than 140,000 signatures from New Zealanders across the country.

One of the main aims of the plan is to have equitable cancer survival rates across New Zealand by 2030 – including across geographic areas and across ethnicities. Māori cancer outcomes will be one of the first priorities as Māori have higher rates of cancer and poorer survival rates overall.

Funding decisions will be made with an “equity first” methodology, the plan says.

For example, the national bowel screening programme, which is still being rolled out, makes screening free for people aged 60-74.

But because Māori people tend to develop bowel cancer at an earlier age, the plan suggests the screening programme could be made free for Māori ten years earlier, between the ages of 50-74.

Another aim is for New Zealanders to suffer from fewer preventable cancers.

Lung cancer is the top of the list, with prevention strategies including promotion of vaping and the finalisation of a Smokefree 2025 Action Plan.

The plan also highlights improved detection and management of Hepatitis A, B and C, reducing HIV transmission, increasing the uptake of the HPV vaccine and addressing Helicobacter pylori infection in priority populations.

Skin cancer will also be a target, with promotion of sun safety – particularly among children – and sunscreen could also be regulated as a therapeutic product, the plan says.

A programme will also be developed to prevent work-related cancers.

Another aim of the plan is to improve survival rates once people have cancer, with an emphasis on better, earlier screening, and improved treatment once diagnosed.

Strategies including increasing the age of free breast screening from 70 to 74 years old, progressing the national bowel screening programme and exploring bringing in HPV screening as part of the cervical screening programme.

The radiation and oncology workforce could also see a boost to its workforce and resources.

Fast-track diagnostic pathways will be developed for “priority cancers”, and there would be a national agreement on the scope and distribution of specialist cancer services.

“Quality performance indicators” will be introduced under the plan to ensure specific cancers are being diagnosed and treated consistently across New Zealand.

Bowel cancer has been used as a test case for QPIs with the first results published for diagnosis and treatment in March this year. The Bowel Cancer Quality Improvement Report compared DHBs on measures such as death rate after surgery, length of stay in hospital and where at least 12 lymph nodes were examined.

By early 2020 prostate, lung and neuro-endocrine tumours will also have similar reports published.

Health Minister Dr David Clark said the Government has listened to calls for strong central leadership and will deliver the promised Cancer Control Agency by December 1, 2019.

“Cancer care is woven into so much of the work that our public health service does, so while the agency will have its own chief executive, it makes sense for it to be housed within the Ministry of Health.

“I’m also pleased to announce that leading public health physician and cancer epidemiologist Professor Diana Sarfati has been appointed interim National Director of Cancer Control, starting immediately. She will lead work to improve the quality of treatment.

“An immediate priority will be establishing quality performance indicators for specific cancer types. This will mean we can measure progress towards consistent care across DHBs.

“We are also combining the four current regional cancer control networks into a National Network to help remove regional variations in care,” Clark said.

More Pharmac funding welcomed

Pharmac has welcomed the $60m funding injection, which includes $20m for this year and $40m for 2020/21. That’s on top of $10m announced in this year’s Budget.

That brings Pharmac’s annual medicines budget to over $1 billion, Pharmac board chair Steve Maharey said.

In last year’s Budget, the Government increased Pharmac’s funding by more than 13 per cent, from about $870m to $985m. That compares to increases of 2.4 per cent and 6.3 per cent in National’s last two years in government.

Pharmac announced this afternoon it was proposing to funding three new medicines to treat ovarian cancer (olaparib, known as Lymparza), breast cancer (fulvestrant, known as Faslodex) and leukaemia (Venclexta – used to treat chronic pymphocytic leukaemia).

It is also proposing making contraceptives Mirena and Jaydess available to more people, and making the meningococcal ACWY vaccine free for people in close living situations like hostels and army barracks.

The medicines could be available from November if consultation feedback is positive.

Pharmac said it was also looking to get the best deal for New Zealanders for a particular type of advanced breast cancer.

Two registered medicines palbociclib (Ibrance) and ribociclib (Kisqali) could be suitable, experts believe.

Pharmac said it had issued a request for proposals and one of these medicines could be available from April next year.

Prime Minister Jacinda Ardern said from next year Pharmac will also speed up its decision-making by considering applications for funding while Medsafe assesses the safety of new medicines.

“Rather than waiting until that work is complete as it does currently. Work on options for early access to new cancer medicines is also progressing well,” Ardern said.

New Zealand’s history of tackling cancer:

1999

– Labour Government announces plans are under way for first ever cancer plan.

2003 – Cancer control strategy released included cancer prevention, screening, early detection, treatment, rehabilitation, support and palliative care.

2005 – Labour Government establishes national agency known as Cancer Control Council, formally Cancer Control of New Zealand, to provide independent advice free from political interference.

2014 – National Party-led Government introduces three-year cancer plan, including a faster cancer treatment target requiring most patients to start treatment within 62 days of diagnosis.

2015 – National disestablishes Cancer Control Council, saying it is no longer necessary as it has been superseded by new plan.

July 2017 – Pre-election, Labour promises to set up a National Cancer Agency, with $10 million to establish the agency and a further $10m to get work under way.

2018 Labour-led Government ends public reporting of DHBs’ faster cancer treatment target results, although the data is still collated.

Jan 31, 2019 – Melissa Vining blasts Health Minister David Clark for not following through on promise to establish cancer agency.

Clark announces the Government’s plan to tackle cancer is under way and he expects to see a draft by the end of June.

May 6, 2019 – Herald starts investigation revealing hundreds of Kiwi cancer sufferers have received large taxpayer-funded payouts after being let down by the public health system.

June 28, 2019 – Blair Vining launches petition calling for a national cancer agency to hold District Health Boards to account and improve the health care system.

June 29, 2019 – Herald reveals Prime Minister’s letter to Blair’s daughter Lilly Viningsuggesting agency is not part of the Government’s plan.

More than 650 New Zealanders gathered in Invercargill to join Vining as he handed over a petition to National’s Michael Woodhouse.

July 7, 2019 – Vining’s petition closes to the public.

Today – Government’s unveils plans to establish a national cancer agency lead by experts of the deadly disease.