Posts Tagged ‘Obama “Moonshot” program’

Cancer Policy Related News from Washington DC and New NCI Appointments

Reportor: Stephen J. Williams, PhD.

Biden to announce appointees to Cancer Panel, part of initiative to cut death rate

The president first launched the initiative in 2016 as vice president.

By Mary Kekatos

July 13, 2022, 3:00 PM




America This Morning

America This Morning

President Joe Biden will announce Wednesday his appointees to the President’s Cancer Panel, ABC News can exclusively reveal.

The Cancer Panel is part of Biden’s Cancer Moonshot Initiative, which was relaunched in February, with a goal of slashing the national cancer death rate by 50% over the next 25 years.MORE: Biden relaunches cancer ‘moonshot’ initiative to help cut death rate

Biden will appoint Dr. Elizabeth Jaffee, Dr. Mitchel Berger and Dr. Carol Brown to the panel, which will advise him and the White House on how to use resources of the federal government to advance cancer research and reduce the burden of cancer in the United States.

Jaffee, who will serve as chair of the panel, is an expert in cancer immunology and pancreatic cancer, according to the White House. She is currently the deputy director of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University and previously led the American Association for Cancer Research.

PHOTO: In this Sept. 8, 2016, file photo, Dr. Elizabeth M. Jaffee of the Pancreatic Dream Team attends Stand Up To Cancer (SU2C), a program of the Entertainment Industry Foundation (EIF), in Hollywood, Calif.
In this Sept. 8, 2016, file photo, Dr. Elizabeth M. Jaffee of the Pancreatic Dream Team attends Stand Up To Cancer (SU2C), a program of the Entertainment Industry Foundation (EIF), in Hollywood, Calif.ABC Handout via Getty Images, FILE

Berger, a neurological surgeon, directs the University of California, San Francisco Brain Tumor Center and previously spent 23 years at the school as a professor of neurological surgery.

Brown, a gynecologic oncologist, is the senior vice president and chief health equity officer at Memorial Sloan Kettering Cancer Center in New York City. According to the White House, much of her career has been focused on eliminating cancer care disparities due to racial, ethnic, cultural or socioeconomic factors.

Additionally, First Lady Jill Biden, members of the Cabinet and other administration officials are holding a meeting Wednesday of the Cancer Cabinet, made up of officials across several governmental departments and agencies, the White House said.

The Cabinet will introduce new members and discuss priorities in the battle against cancer including closing the screening gap, addressing potential environmental exposures, reducing the number of preventable cancer and expanding access to cancer research.MORE: Long Island school district found to have higher rates of cancer cases: Study

It is the second meeting of the cabinet since Biden relaunched the initiative in February, which he originally began in 2016 when he was vice president.

Both Jaffee and Berger were members of the Blue Ribbon Panel for the Cancer Moonshot Initiative led by Biden.

The initiative has personal meaning for Biden, whose son, Beau, died of glioblastoma — one of the most aggressive forms of brain cancer — in 2015.

“I committed to this fight when I was vice president,” Biden said at the time, during an event at the White House announcing the relaunch. “It’s one of the reasons why, quite frankly, I ran for president. Let there be no doubt, now that I am president, this is a presidential, White House priority. Period.”

The initiative has several priority actions including diagnosing cancer sooner; preventing cancer; addressing inequities; and supporting patients, caregivers and survivors.

PHOTO: In this June 14, 2016, file photo, Dr. Carol Brown, physician at Memorial Sloan Kettering Cancer Center, gives a presentation, at The White House Summit on The United State of Women, in Washington, D.C.
In this June 14, 2016, file photo, Dr. Carol Brown, physician at Memorial Sloan Kettering Cancer Center, gives a presentation, at The White House Summit on The United State of Women, in Washington, D.C.NurPhoto via Getty Images, FILE

The White House has also issued a call to action to get cancer screenings back to pre-pandemic levels.

More than 9.5 million cancer screenings that would have taken place in 2020 were missed due to the COVID-19 pandemic, according to the National Institutes of Health.MORE: Louisiana’s ‘Cancer Alley’ residents in clean air fight

“We have to get cancer screenings back on track and make sure they’re accessible to all Americans,” Biden said at the time.

Since the first meeting of the Cancer Cabinet, the Centers for Disease Control and Prevention has issued more than $200 million in grants to cancer prevention programs, the Centers for Medicaid & Medicare Services implemented a new model to reduce the cost of cancer care, and the U.S. Patent and Trademark Office said it will fast-track applications for cancer immunotherapies.

ABC News’ Sasha Pezenik contributed to this report.

Biden to tap prominent Harvard cancer surgeon to head National Cancer Institute

Monica Bertagnolli brings leadership experience in cancer clinical trials funded by the $7 billion research agency

headshot of Monica Bertagnolli


President Joe Biden is expected to pick cancer surgeon Monica Bertagnolli as the next director of the National Cancer Institute (NCI). Bertagnolli, a physician-scientist at Brigham and Women’s Hospital, the Dana-Farber Cancer Center, and Harvard Medical School, specializes in gastrointestinal cancers and is well known for her expertise in clinical trials. She will replace Ned Sharpless, who stepped down as NCI director in April after nearly 5 years.

The White House has not yet announced the selection, first reported by STAT, but several cancer research organizations closely watching for the nomination have issued statements supporting Bertagnolli’s expected selection. She is “a national leader” in clinical cancer research and “a great person to take the job,” Sharpless told ScienceInsider.

With a budget of $7 billion, NCI is the largest component of the National Institutes of Health (NIH) and the world’s largest funder of cancer research. Its director is the only NIH institute director selected by the president. Bertagnolli’s expected appointment, which does not require Senate confirmation, drew applause from the cancer research community

Margaret Foti, CEO of the American Association for Cancer Research, praised Bertagnolli’s “appreciation for … basic research” and “commitment to ensuring that such treatment innovations reach patients … across the United States.” Ellen Sigal, chair and founder of Friends of Cancer Research, says Bertagnolli “brings expertise the agency needs at a true inflection point for cancer research.”

Bertagnolli, 63, will be the first woman to lead NCI. Her lab research on tumor immunology and the role of a gene called APC in colorectal cancer led to a landmark trial she headed showing that an anti-inflammatory drug can help prevent this cancer. In 2007, she became the chief of surgery at the Dana-Farber Brigham Cancer Center.

She served as president of the American Society of Clinical Oncology in 2018 and currently chairs the Alliance for Clinical Trials in Oncology, which is funded by NCI’s National Clinical Trials Network. The network is a “complicated” program, and “Monica will have a lot of good ideas on how to make it work better,” Sharpless says.


One of Bertagnolli’s first tasks will be to shape NCI’s role in Biden’s reignited Cancer Moonshot, which aims to slash the U.S. cancer death rate in half within 25 years. NCI’s new leader also needs to sort out how the agency will mesh with a new NIH component that will fund high-risk, goal-driven research, the Advanced Research Projects Agency for Health (ARPA-H).

Bertagnolli will also head NCI efforts already underway to boost grant funding rates, diversify the cancer research workplace, and reduce higher death rates for Black people with cancer.

The White House recently nominated applied physicist Arati Prabhakar to fill another high-level science position, director of the White House Office of Science and Technology Policy (OSTP). But still vacant is the NIH director slot, which Francis Collins, acting science adviser to the president, left in December 2021. And the administration hasn’t yet selected the inaugural director of ARPA-H.

Correction, 22 July, 9 a.m.: This story has been updated to reflect that Francis Collins is acting science adviser to the president, not acting director of the White House Office of Science and Technology Policy.

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Intratumor heterogeneity challenge

Larry H. Bernstein, MD, FCAP, Curator



Intratumor Heterogeneity Poses Challenge for Cancer “Moonshot” Program

Intratumor Heterogeneity Poses Challenge for Cancer “Moonshot” Program

The tiny fraction of cells in a biopsy of a heterogeneous cancer may not be representative of the entire tumor mass, which means important disease features might be missed. [istock/Vitanovski]

  • Vice President Joe Biden, in describing the cancer research initiative President Obama asked him to lead, said “the goal of this initiative—this ‘moonshot’—is to seize this moment…to accelerate our efforts to progress toward a cure, and to unleash new discoveries and breakthroughs for other deadly diseases.”

    As he noted during his recent visit to the University of Pennsylvania’s Abramson Cancer Center to officially launch the initiative, however, he was “not naive about the likelihood of soon curing an entire group of diseases that have bedeviled humanity for centuries.” Rather, he said, the intention of the initiative is to accelerate progress already underway.

    Biden personally lobbied for a major increase in cancer research funding in the government spending bill that Congress passed in December, pledging to pursue an initiative to end cancer for the rest of his term and beyond. The bill will raise funding for the NIH by $2 billion, including a $264 million boost specifically for the NCI, the biggest increase for the institute in more than a decade. Scientists concur with the VP’s lack of naiveté.

    As Jose Baselga, M.D., Ph.D., the president of the American Association for Cancer Research and physician-in-chief and chief medical officer at Memorial Sloan Kettering Cancer Center (MSKCC), told The New York Times, “Cancer is way more complex than anyone had imagined in 1970,” reflecting many scientists’ sentiments that this kind of approach won’t succeed quickly or easily.

    Rebecca A. Burrell and colleagues, writing in the September 19, 2013, issue of Nature noted that the recently revealed genetic diversity both between and within tumors affecting key cancer pathways and driving phenotypic variation poses a significant challenge to personalized cancer medicine.

    Among the researchers focused on tumor heterogeneity is MSKCC biologist Scott W. Lowe, Ph.D., chair of the Cancer Biology and Genetics Program and the Geoffrey Beene Cancer Research Center, who commented in a MSKCC blog that “We are increasingly becoming aware of the problem of intra-tumor heterogeneity, the fact that one person’s tumor cells can vary depending on where in the body they are located. Even within the same tumor from the same patient, tumor cells might be subtly or even dramatically different. And there can be very important implications of this type of heterogeneity.”

    If doctors are dealing with a highly heterogeneous cancer, the tiny fraction of cells in the biopsy may not be representative of the entire tumor mass, which means important disease features could be missed. What this means in practical terms, said Dr. Lowe, is that “A potentially effective therapy could be overlooked because the indicator for that drug, such as a specific gene mutation, wasn’t found in the biopsy. Conversely, the wrong drug might be chosen if a biopsy reveals the presence of an indicator that isn’t actually that prevalent in the tumor.”

  • Cancer Therapeutic Challenges

    Recent investigations of tumor heterogeneity provide ample evidence of the challenges for cancer therapy and the scope of the problem. Particularly worrisome is the recent finding that post-treatment relapse among acute myelogenous leukemia (AML) patients is associated with the addition of new mutations and clonal evolution.

    Li Ding, Ph.D., and colleagues reported in the January 11, 2012 issue of Nature that they had sequenced the primary tumor and relapse genomes from eight AML patients and validated hundreds of somatic mutations using deep sequencing, allowing precise definition of clonality and clonal evolution patterns at relapse.

    The scientists pointed out the occurrence of novel, recurrently mutated genes (WAC, SMC3, DIS3, DDX41, and DAXX) in AML, as well as two major clonal evolution patterns during AML relapse. They discovered that the founding clone in the primary tumor gained mutations and evolved into the relapse clone, or that a subclone of the founding clone survived initial therapy, gained additional mutations, and expanded at relapse. In all cases, chemotherapy failed to eradicate the founding clone.

    The researchers concluded that comparison of relapse-specific vs. primary tumor mutations in all eight cases revealed an increase in transversions, probably due to DNA damage caused by cytotoxic chemotherapy. These data demonstrate, the authors said, that AML relapse is associated with the addition of new mutations and clonal evolution, shaped in part by the chemotherapy that the patients receive to establish and maintain remissions.

    A team working at Harvard and the Broad Institute sought to estimate the extent of clonal heterogeneity in multiple myeloma in a large-scale MM genome sequencing dataset that included untreated and previously treated patients. Jens G. Lohr, M.D., Ph.D., and colleagues, reporting results in the January 13, 2014 issue of Cancer Cell, performed a massive parallel sequencing of paired tumor/normal samples from 203 MM patients.

    Commenting on the study, co-senior author Todd Golub, M.D., founding core member of the Broad Institute, director of its cancer program, and professor of pediatrics at Harvard Medical School, said “What this new work shows us is that when we treat an individual patient with multiple myeloma, it’s possible that we’re not just looking at one disease, but at many. In the same person, there could be cancer cells with different genetic makeups. These findings indicate a need to identify the extent of genetic diversity within a tumor as we move toward precision cancer medicine and genome-based diagnostics.”

    The Cancer Cell authors identified significantly mutated genes and copy number alterations and discovered putative tumor suppressor genes by determining homozygous deletions and loss of heterozygosity. They reported their observation of frequent mutations in KRAS (particularly in previously treated patients), NRAS, BRAF, FAM46C, TP53, and DIS3 (particularly in nonhyperdiploid MM). Mutations were often present in subclonal populations, and multiple mutations within the same pathway (e.g., KRAS, NRAS, and BRAF) were observed in the same patient.

    These studies demonstrate how acquisition of genetic alterations over time leads to clonal evolution. Systemic treatment with chemotherapy may affect the fitness of some subclones more than others, and thus may alter the tumor composition by promoting particular subclones.

  • Understanding Glioblastoma

    Noting that accumulating evidence suggests that intratumor heterogeneity likely is the key to understanding Glioblastoma (GB) treatment failure, Andrea Sottoriva, Ph.D., and colleagues in the department of oncology at University of Cambridge developed a surgical multisampling scheme to collect spatially distinct tumor fragments from 11 GB patients.

    The authors reported their findings in the March 5, 2013 issue of PNAS. Their integrated genomic analysis, they said, uncovers extensive intratumor heterogeneity, with most patients displaying different GB subtypes within the same tumor. They also reconstructed the phylogeny of the fragments for each patient, identifying copy number alterations in EGFR and CDKN2A/B/p14ARF as early events, and aberrations in PDGFRA and PTEN as later events during cancer progression. Their clonal characterization of each tumor fragment at the single-molecule level detected multiple coexisting cell lineages.

    Taken together, the researchers concluded, their results reveal the genome-wide architecture of intratumor variability in GB across multiple spatial scales and patient-specific patterns of cancer evolution, with consequences for treatment design.

    Asked how his findings in MM and those of others with different tumors might immediately translate into practice for oncologists, Dr. Golub said that the notion of a yes or no answer, that is, whether or not a given mutation is present in a tumor, is too simplistic, particularly in interpreting clinical trial results testing targeted agents.

    “It is unreasonable to expect that an entire tumor would respond to a drug if the target of the drug is only present in a minority of the tumor cells,” he explained. “If the mutation, for example, is sub-clonal and the patient doesn’t respond clinically, it would be the wrong conclusion to say the drug is ineffective.”

    He added that what is needed is a quantitative approach to know in what proportion of the tumor the mutation is found.

    “For example, if a mutation is only present in a minority of the tumor cells, the drug might not be so good for the patient. But if the mutation were present in 100 percent of the cells, it’s a better choice,” he said. “Targeted agents that go after the least-heterogeneous aspect of the tumor might be a better choice.”

    The same goes for clinical trials as you might come to different results, continued Dr. Golub. In the MM study, for example, “we found that in some patients the BRAF mutation was clonal (present in all of the cells), but in some patients present only in a minority.” If you did a clinical trial of a BRAF inhibitor and you only enrolled sub-clonal patients, you might conclude that BRAF is not a good target in MM, “whereas, if you enroll only patients with clonal mutations in clinical trials, you might come to a completely different conclusion.”

    With respect to drug discovery, Dr. Golub is more optimistic about developing drugs that go after the founding mutations that will be present in all of a tumor’s cells. “Those will make the best therapeutic targets,” he said. “I am less optimistic about trying to pick off five sub-clones with a five-drug combination.”

    Beverly Mitchell, M.D., director of the Stanford Cancer Institute, David Rubenson, associate director for administration and strategic planning, and Daniel S. Kapp, M.D., professor emeritus of radiation oncology, posed some tough questions about the meaning of these findings for cancer therapeutics in the April 11, 2015 edition of The Scientist. These include whether intra-tumor heterogeneity implies that a single targeted therapeutic, while producing short-term responses, brings us any closer to enduring disease control. Or, they ask, do we simply need a better, or a second or third, targeted therapeutic?

    While uncertainties remain, they said, there is sufficient data for every major cancer research and treatment center to assess how intra-patient heterogeneity will affect research priorities, clinical trial design, and the patient’s choice of treatment.

sjwilliamspa commented on Intratumor heterogeneity challenge

Intratumor heterogeneity challenge Larry H. Bernstein, MD, FCAP, Curator LPBI Intratumor Heterogeneity Poses …

There are a few very important points here, and one commentary in which I would like to point to another post on this Open Access Journal in the Related section :

where my feeling was the most likely revolutionary achievement from Moonshot will be the closer collaboration of government, academia, industry, patient advocacy AND the PAYERS. This would be a goal I feel is much needed and one where VP Biden can make the greatest effect.

As to the points I was very interested in Dr, Golub’s remarks concerning shifting focus more on driver mutations than “end-stage” kinase mutations and relying on combination therapy. An initial hope of the personalized target medicine era was to remove the need for combination therapy as concerns over limiting toxicities and development of resistance is always a concern with more traditional chemotherapy, whether mono or combination therapy. However it is becoming clear, even with immune modulators and checkpoint inhibitors, that monotherapy may have limited efficacy.

That being said it appears that the VP and the Moonshot program is focusing on the new T cell engineered therapies (CAR-T and TCR) which have had much success with certain childhood lleukemia and just now adult leukemias. CAR-T are showing some promise with pancreatic which sees to be the first data out there with regard to solid tumors (although I feel pancreatic is a more “immune system available” tumor. And as CAR-T are engineered to a specific epitope expressed on tumor cells intratunoral heterogeneity will complicate the therapy. Indeed (as posted in this Online Journal) intra-tumoral heterogeneity is felt as another mechanism of resistance,

However the increased visibility to the cancer problem within government is a much needed boost and funds, hands, minds, and support can join together to at least address some of these issues which stymie the oncology field.

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