Palbociclib plus cetuximab shows antitumor activity among head and neck cancer subset

Source: www.healio.com
Author: Adkins D, et al.

A combination of palbociclib and cetuximab demonstrated substantial antitumor activity among patients with platinum- or cetuximab-resistant HPV-unrelated head and neck squamous cell carcinoma, according to results of a multigroup phase 2 trial published in The Lancet Oncology.

“Currently, effective therapeutic options for patients with cetuximab-resistant HNSCC are few. Traditional chemotherapy has marginal activity, with 6% of patients or fewer achieving a tumor response,” Douglas R. Adkins, MD, professor in the oncology division of the department of medicine at Washington University School of Medicine in St. Louis, and colleagues wrote. “The most effective therapy for these patients might be pembrolizumab [Keytruda, Merck] or nivolumab [Opdivo, Bristol-Myers Squibb], which have resulted in responses in 11% to 16% of patients and median OS of 6.9 months to 8 months. Novel treatment strategies are needed for patients with recurrent or metastatic HNSCC.”

The combination of the cyclin-dependent kinase (CDK) 4/6 inhibitor palbociclib (Ibrance, Pfizer) and epidermal growth factor receptor inhibitor cetuximab (Erbitux, Eli Lilly) appeared safe and tolerable in the phase 1 portion of the multicenter trial, conducted across eight U.S. university sites.

For phase 2, Adkins and colleagues divided 62 patients with HPV-unrelated HNSCC (median age, 66 years; interquartile range [IQR], 58-70; 71% men) into two groups: those who were platinum-resistant (group 1; n = 30) and those who were resistant to cetuximab (group 2; n = 32). Primary tumor sites included the oral cavity (42%) and larynx (29%), and 81% of patients had received one or two prior lines of treatment for metastatic or recurrent disease.

All participants received oral palbociclib (125 mg daily on days 1-21) and IV cetuximab (400 mg/m2 on day 1 of cycle one, followed by 250 mg/m2 once weekly) in 28-day cycles. Objective response, defined as complete and partial responses per RECIST 1.1 criteria, served as the primary endpoint.

Researchers followed patients in group 1 for a median 5.4 months (IQR, 4.4-12.1) and those in group 2 for a median 5.5 months (IQR, 4.3-8.3).

Among 28 evaluable group 1 patients, 11 (39%; 95% CI, 22-59) attained an objective response, including three complete responses. Repeat scans confirmed all but one of the responses. Half of the group 1 patients (n = 14) had stable disease and three (11%) demonstrated progressive disease. Median duration of response was 4 months (IQR, 1.8-5.6), median PFS was 5.4 months (95% CI, 3.4-7) and median OS was 9.5 months (95% CI, 5.3-16.5).

Palbociclib plus cetuximab shows antitumor activity among head and neck cancer subsetAmong 27 evaluable group 2 patients, five (19%; 95% CI, 6-38) achieved an objective response, including one complete response. Four of the responses were later confirmed. Thirteen of the group 2 patients (48%) had stable disease and nine (33%) demonstrated progressive disease. Median duration of response was 6 months (IQR, 2-15.5), median PFS was 3.7 months (95% CI, 2.9-4.3) and median OS was 6.3 months (95% CI, 4.9-10).

In each group, only one patient with a tumor response previously had received immunotherapy.

The most prevalent grade 3 to grade 4 adverse event associated with palbociclib was neutropenia, which occurred in 34% (n = 21) of all patients. The researchers did not document any treatment-related deaths.

The researchers cited various limitations to their study, including its single-group design, and noted that the results will need to be confirmed in a controlled trial with a larger sample size. They acknowledged that immunotherapy might have affected OS outcomes, and that the study design did not permit the evaluation of whether palbocilib’s antitumor activity occurred directly or by reversal of primary cetuximab resistance.

These data suggest a need for further study of palbociclib in patients with recurring or metastatic HNSCC, according to a related editorial by Garth W. Strohbehn, MD, hematology/oncology fellow at University of Chicago, and Everett E. Vokes, MD, professor of medicine and radiation oncology physician-in-chief at University of Chicago Medicine.

“However, we should be circumspect about the prospect of CDK 4/6 inhibitors as standardized, cost-effective therapies in recurrent and metastatic HNSCC,” the authors wrote. “Bringing this class of drugs to head and neck oncology clinics, as either monotherapies or immunotherapy partners, will require appropriately controlled studies linked to biomarker evaluation with both survival and cost-effectiveness endpoints.” – by Jennifer Byrne

Source:
Adkins D, et al. Lancet Oncol. 2019;doi:10.1016/S1470-2045(19)30405-X.
Strohbehn GW and Vokes EE. Lancet Oncol. 2019;doi:10.1016/S1470-2045(19)30484-X.

Disclosures: Adkins reports research funding from Pfizer as part of the work presented in the study; personal fees for advisory/consultant roles from Celgene, Cue Biopharma, Eli Lilly, Loxo Oncology, Merck and Pfizer; and research funding from AstraZeneca, Atara, Blueprint Medicine, Bristol-Myers Squibb, Celgene, CellCeutix, Celldex, Eli Lilly, Enzychem, Exelixis, Gliknik, Kura, Matrix Biomed, Medimmune Innate, Novartis, Pfizer and Polaris outside the submitted work. Please see the study for all other authors’ relevant financial disclosures. Vokes reports consultant/advisory roles with AbbVie, Amgen, AstraZeneca, Bristol-Myers, Celgene, EMD Serono, Genentech, Merck, Novartis and Regeneron. Strohbehn reports no relevant financial disclosures.

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August, 2019|Oral Cancer News|

Israeli researchers find new way to eliminate drug-resistant cancerous tumors

Source: www.xinhuanet.com
Author: Wu Qin

Israeli researchers have found a way to deal with cancerous tumors that have developed drug resistance, Israel’s Ben-Gurion University (BGU) reported on Tuesday. The study was conducted by researchers from BGU and the Soroka Medical Center – both located in the southern city of Beer Sheva – and published in the journal JCI Insight.

The researchers were able to suppress a drug-resistant protein found on the wall of head and neck cancer cells, resulting in shrinkage and even disappearance of the tumors.

Head and neck cancer is considered deadly, with low survival rates, while the efficacy of existing treatments is inadequate.

One of the new treatments currently being given to patients is a drug called BYL719, which inhibits a signal transmission pathway in the cells. This pathway, called phosphoinositide 3-kinases (PI3K), is increased in head and neck cancer patients and leads to the rapid progression of the disease.

The first clinical study using the drug indicated an improvement in patients’ condition; however, many of the cancer cells developed drug resistance.

Previous research has shown that resistance to the treatment is caused by the rise of the AXL protein, which is located on the cancer cell’s wall and causes the growth and survival of the cancer cells.

The new study found that suppressing AXL expression through genetic engineering or drug inhibition restored the cancer cells’ susceptibility to the drug and significantly stopped the disease, to the extent of tumor shrinkage and disappearance.

This suppression was also effective in mice with tumors taken from head and neck patients who underwent surgeries at Soroka Medical Center.

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August, 2019|Oral Cancer News|

cole Gibbs on the dental visit that led to a cancer diagnosis and how it reaffirmed her love for tennis

Source: ESPN
Date: August 1st, 2019
Author: Nicole Gibbs, as told to D’Arcy Maine

 

Nicole Gibbs is a 26-year-old professional tennis player, currently ranked No. 137 in the world and playing for the Orange County Breakers of World TeamTennis. The former NCAA singles and doubles champion was diagnosed with cancer in the spring after a routine dentist appointment. She shared her story with us amid her comeback to the court.

Shortly before Caroline Wozniacki’s bachelorette party festivities in April, I received a promotional email for a free teeth-whitening from my new dentist. “Oh, sweet!” I remember thinking. Naturally, I wanted to look good for the weekend (knowing how much of it was going to end up on Instagram and all), and for at least two years I was slacking on getting a regular cleaning.

So I went. And it changed everything.

It was my first time seeing this dentist, and he instantly noticed a small growth on the roof of my mouth. I mentioned this to my primary doctor at least five years ago; she told me it was nothing to worry about, a common bone growth that didn’t seem to be growing rapidly or doing anything of concern. My dentist at the time felt the same. It was about a centimeter in diameter and not causing me any pain or discomfort. However, my new dentist felt differently — the growth set off major alarm bells for him, and he encouraged me to get it biopsied. He felt certain it was not a bone growth.

I went to an oral surgeon the very next day. He thought it would be benign, based on its history, how long it had been in my mouth and how slowly it was growing. But the biopsied sample was sent to a pathology lab for an official diagnosis. I then, happy to at least not have that hanging over my head, went to the Bahamas to celebrate Wozniacki.

Shortly after getting back home, about a week after the initial dentist appointment, I got the call with the results.

It was cancer.

As soon as the doctor said the word, I glazed over. I didn’t hear much else, but I am pretty sure I cracked an awkward joke. It wasn’t until I called my fiancé, Jack Brody, that it really hit me. I started to fall apart and panic. It felt like my biggest fear come true. Since a very young age, I had been terrified about getting cancer. I almost started to question myself, like, had I manifested this with my anxiety about it? Did I bring this upon myself somehow by being so concerned about it?

Then my thoughts went to the tennis court. Would I ever be able to play again?

I made the mistake of going to WebMD and doing a Google search for oral cancer because I didn’t have any more specifics at that point, and the first thing that popped up was “17 percent five-year survival rate.” I thought, “Oh cool, I’m going to die.” It was terrifying, but I thankfully discovered soon after I had mucoepidermoid carcinoma, which is more of a subset and much less scary. I didn’t let myself play internet doctor after that and told Jack he was the only one allowed to Google anything from that point forward.

Everyone was hopeful we could treat the cancer with surgery alone, but radiation was also a possibility if the surgeons weren’t able to remove it all. While that is worrisome enough on its own, someone mentioned to me I could potentially lose all my teeth as a consequence of radiation. Leading up to the procedure, I kept thinking, “Please just be a surgery, please just be a surgery.” I didn’t want my teeth to fall out.

I had the surgery on May 17. The typical recovery period is four to six weeks, but my surgeon believed that, as a professional athlete, I could be on the low end of the timetable. My goal was to be back in time for Wimbledon qualifying, which started on June 24, and that felt possible.

However, there were a number of complications that made us throw that dream right out of the window, starting with the procedure being significantly more invasive than they initially planned. Too much of the tumor was taken out during the biopsy, and as a result, they didn’t have a clear idea of where it was. They needed to cut in further and wider to ensure they got it all out.

Not only that, but the prosthetic — really just a glorified retainer — I needed to wear on the roof of my mouth to protect it after the surgery didn’t fit properly. So they had to screw it in. Do you know what happens when you have a screwed-in retainer that doesn’t get to be taken out and cleaned? It causes an infection. So instead of the two days I had expected to stay in the hospital, I was there for seven long, agonizing days.

During my extended stay, I also got some unexpected news: Turns out I didn’t have mucoepidermoid carcinoma, but instead microcystic adnexal carcinoma. Don’t worry if you’ve never heard of it. My doctors told me they had only ever seen 12 recorded cases of it.

That’s right — 12. I was lucky No. 13.

While that didn’t change the treatment much, it did mean the cancer had a greater risk of being elsewhere in the body. It has the potential to travel aggressively along nerve pathways. When I asked what exactly that meant, my doctor said, “In layman’s terms, that means it can jump tissue.” How frightening is that? Thankfully, I already had a full-body PET (positron emission tomography) scan, and there were no signs of cancer anywhere else. But still, it was alarming. (I still haven’t quite determined if the rarity and odds of this type of cancer mean I should now engage in every risk-taking activity or become a bubble kid and never go outside, but I’ll let you know when I figure that out.)

We thought I would be on a feeding tube for two days, as I couldn’t ingest food orally, and then I would graduate to soft foods once I got home. However, one of the stitches in my mouth blew open (another fun setback!), and every time I would try to eat or drink, it would come out of my nose. Sure, it’s sort of a great party trick, but not really what I was going for. In the end, I had to go home with the feeding tube — and use it for 3½ weeks in total.

It was tough. I definitely gained a new appreciation for how brutal medical trauma can be. I found it really dehumanizing. It’s so challenging to have a tube hanging out of you and looking visibly ill. You can’t hide from it. And then losing the ability to socialize around food, which is so much of our lives. I didn’t want to go out to dinner while I had a feeding tube and couldn’t eat anything.

I made sure to get out of the house, just to get some sunshine, at least once a day. I took long walks and tried to find small things to do, to give me a little purpose. But it brought me to my breaking point on several occasions. I remember looking at Jack and saying, “I really can’t do this anymore.” But I quickly realized that I didn’t have a choice. I knew I just had to tough it out.

The worst moments were when I was getting off the pain medication after 2½ weeks of strong dosages. I don’t know the mechanics of it, but I ended up feeling very depressed once I stopped taking it for about 48 hours. It was right around the time I started to go back to the gym to slowly train. On the first morning off the medication, I said to my trainer, Daniel Ciccolini, “I just can’t do this today.” I don’t think I had said a word other than that or smiled at all, and I was just in the worst mood. I was incapable physically of much of anything, but he was so patient. He took me through all of these easy core and mobility exercises. Whatever we could accomplish that day, we did, even though it was such a brutal day.

Because I was able to accomplish something that day, anything really, it gave me hope. If I hadn’t had that, it would have been devastating.

And every day after that, I felt a little bit better and made a little bit more progress. I did more with my trainer and my incredible support system. I could feel myself gaining in physical strength, and I was like, “OK, I’m getting somewhere!”

I returned to competitive tennis in early July at a tournament in Hawaii. I went in with no expectations whatsoever. I still can’t even drink too much water during changeovers without it going out my nose. (The doctors are hoping the hole in my mouth will fully close up on its own in the next few months, but otherwise, I will need another surgery.) I surfed every day in Hawaii and even had a glass of wine with dinner some nights — things I would have never done while competing. I shocked even myself and ended up making it to the final.

I ended up losing in the championship match to Usue Maitane Arconada, but when I thought about where I had been less than two months before, I certainly felt like a winner.

Before this experience, I was constantly wondering, “Is tennis something that I really love? Would I miss it in my life if it was gone?” And I’m blessed in so many ways to have been forced into that answer. I wasn’t ready for tennis to be taken away from me.

It may sound weird, but I’m thankful that this happened for a number of reasons, one of which is because it reconfirmed my love of sports and tennis. It reminded me that I’m not done. It’s given me such a fresh perspective, and I’m grateful for that.

I’ve been playing for the Orange County Breakers for the World TeamTennis season. It’s been a little bit of a whirlwind — I went from playing in the final in Honolulu on Sunday to playing in our opener the very next day in Orlando — but it’s been great, and I’m making up for lost time in terms of getting match experience this summer. My teammates have been so sweet. Every time I say, “Guys, I’m so sorry, I’ve been playing terribly,” they’re like, “Remember where you were five weeks ago?” The support has been so incredible.

I’m still finalizing my upcoming schedule, but I’ll be playing in several tournaments over the next few weeks before going to New York for US Open qualifying in the middle of August. My newfound semi-relaxed attitude worked in Hawaii, so I’m going to try and maintain that going forward. I was so disciplined before. I would never have surfed during a tournament; I would have been concerned about getting hurt or being too tired. But ultimately, that’s just no way to live. And I would never tell my best friend to live their life that way, in fear of bad things happening or being so worried about results. Ironically, I think it’s going to free me up to play much better tennis. And if it does, it does. If it doesn’t, then I’m at least having fun and enjoying my life.

At the end of the day, I feel so lucky. Yes, I’m lucky because the cancer could have been so much worse, but really, I’m lucky because I think I needed this experience in my life. I am genuinely thankful that it happened.

I know that sounds nuts, but early on when we were getting the diagnosis, Jack said, “I think if this isn’t the worst thing that ever happens to us, it’ll be the best thing that ever happens to us.” And so far, that’s been really, really true.

I want to hold on to all of these lessons and remember that tennis is not everything. It’s a lot of fun, and it should be. But it’s put my life into a new sense of balance I didn’t have, and I think I’m going to be a much happier person for the rest of my life as a result if I can keep this perspective. You have to enjoy the time you have because you’re not guaranteed to always be here. I knew that in theory, but to actually feel like my life might be taken away, it was such a powerful reminder to enjoy every day and every moment.

Cancer was initially my nightmare, but it weirdly turned into a dream-come-true diagnosis because it made me confront so many things in my life. It was debilitating and scary at times, but look at me — I’m back up on my feet so soon after and appreciating every second. It’s a win in my book.

 

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August, 2019|Oral Cancer News|

Which HPV vaccination schedule is best: 1, 2 or 3 doses?

Source: www.precisionvaccinations.com
Author: Don Ward Hackett

A new cervical cancer prevention study of women first offered Human Papillomavirus (HPV) vaccine found that 1-dose of quadrivalent HPV vaccine was as effective as 3-doses at preventing histologically confirmed, high–grade cervical lesions.

This Australian study’s finding published online on July 15, 2019, supports the hypothesis that the 1-dose HPV vaccination schedule may be a viable strategy when working towards the global elimination of cervical cancer.

These researchers said ‘If one dose could prevent precancerous cervical lesions, then global cervical cancer prevention would be greatly facilitated.’

This is an important goal since about 90 percent of cervical cancer cases are caused by HPV. This study included 250,648 women in Australia with 19.5 percent unvaccinated, 69.8 percent had received 3-doses, 7.3 percent 2-doses, and 3.4 percent just 1-dose of the HPV vaccine.

This study’s limitations include some degree of under–linkage and inaccurate data linkage because Australia does not have a unique national identifier, which impacts the classifications of vaccinated women as unvaccinated.

Additionally, these researchers said ‘we believe that these data support decision-makers to consider how a 1-dose HPV vaccination schedule, or a planned schedule with a 3–5 year interval between doses, could reduce vaccine demand globally, which currently exceeds vaccine supply.’

But the Gardasil 9 vaccine manufacturer appears to be resolving this supply/demand imbalance. During July 2019, Merck said it is spending $1.68 billion, opening 2 new Gardasil production plants, and adding 525 related jobs.

To clarify the Gardasil 9 vaccine dosing schedule, the Centers for Disease Control and Prevention (CDC) publish the following information:

Who should still receive a 3-dose schedule?
The CDC continues to recommend a 3-dose schedule for persons starting the HPV vaccination series on or after the 15th birthday, and for persons with certain immunocompromising conditions. The 2nd vaccine dose should be given 1–2 months after the 1st dose, and the 3rd dose, should be given 6 months after the first dose.

Who should receive just 2-doses?
Two doses of the HPV vaccine are recommended for all boys and girls at ages 11-12; the vaccine can be given as early as age 9. If you wait until they’re older, they may need three doses instead of two.

In the USA, HPV vaccines have been licensed for use among women since 2006 and among men since 2010.

HPV infections are so common that nearly all men and women will get at least one type of HPV at some point in their lives. Nearly 80 million Americans are currently infected with some type of HPV, says the CDC. About 14 million Americans, including teens, become infected each year. HPV is spread through intimate skin-to-skin contact. You can get HPV by having vaginal, anal, or oral sex with someone who has the virus.

Cervical cancer is the only type of HPV cancer with a recommended screening test. The other types of HPV cancer may not be detected until they cause health problems. HPV vaccination helps prevent these cancers by preventing infections that cause these cancers, says the CDC. HPV vaccines, like any medicine, can cause side effects, which you are encouraged to report to the CDC or a healthcare provider.

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August, 2019|Oral Cancer News|

How clean is your toothbrush?

Source: versionweekly.com
Author: rajathe

Dental care has become increasingly difficult in this fast-paced era and due to the scarcity of time. Therefore, following minute steps or procedures could be highly effective to evade colossal dental problems and save time in the long run. And an effective measure towards this, is to sanitize your toothbrush. The mouth contains bacteria and so does the bathroom. So, it is impossible for the toothbrush to stay sanitized with just a water wash after cleansing the teeth.

Toothbrush sanitizing ¡s not synonymous to sterilizing. Sanitation helps in getting rid of almost 99.9 percent of bacteria whereas sterilization kills living organisms. Brushing our teeth is quite vital ¡n our day-to-day life in order to keep and maintain personal oral hygiene and for the removal of plaque. And for this, certain appropriate measures need to be taken.

As a result of a recent research, scientists have found that toothbrushes engulf microorganisms that can result in an oral, dental or infection of some kind. We are acquainted with the fact that an oral cavity is an umbrella to hundreds of different types of microorganisms, which in a way gets transferred to the toothbrush. There is also a probability that the microorganisms in the environment make room for itself on the toothbrush on its own. Also, toothbrushes may even have bacteria on them right out of the box since they are not required to be sold in a sterile package.

Toothbrush Hygiene
Our schedules are so busy that we have time for nothing and that leads to the negligence of petty issues like washing toothbrush properly, which in turn contributes to dental problems. The majority of us simply clean or scrub the head of the toothbrush only once after we complete the brushing process. It would be more hygienic if the toothbrush could be rinsed in lukewarm water to get rid of food debris and leftover toothpaste in the bristles.

Clinically there is no evidence that if a toothbrush is soaked in antibacterial mouthwash ¡t would deliver positive results but it won’t disrupt the toothbrush in any way either.

The proper procedures for sanitizing the toothbrush is as follows:

  • Keep the toothbrush immersed in the mouthwash and warm water mix
  • Take the brush out of the solution after 15 minutes
  • Don’t keep it immersed for too long, or it will destroy the bristles
  • Don’t reuse the mixed solution as it defeats the cleansing or sanitizing process

Gum disease (periodontal) and health complications share a strong alliance and result in hazardous diseases such as stroke, heart disease, etc. It also affects pregnant women in terms of low birth weight and pre-term babies. Research shows that 90 per cent of diseases and health hazards are likely to have oral manifestations like swollen mouth ulcers, gums, excessive gum problems, and dry mouth. Other diseases include diabetes, leukaemia, pancreatic cancer, oral cancer, kidney disease and heart disease.

A dentist may be a saviour if a proper diagnosis can be conducted from the roots in its infant stages. Routine visits to a dentist can also help in keeping one’s smile attractive. This would also enable dentists to foretell a lot more about one’s health which includes whether or not one may develop a disease like diabetes in the near future.

Research has proven that our mouth acts like a mirror that reflects the condition of the body. On the contrary, poor oral health, heralds a plethora of health problems. And, good oral health keeps diseases from occurring.

Recommendations
According to dentists, the growth and abundance of bacteria on toothbrushes requires dark, warm and humid conditions. Veiling a toothbrush in a dosed area can invite problems. One should always keep the toothbrush dry, airy and in a holder that does not come in contact with the bristles or other toothbrushes. The toothbrush should be replaced every three to four months. Also, keep in mind that the sharing of toothbrushes contribute to the problem on a massive scale.

Precautions
If anyone in the family gets infected because of a contagious agent, following some preventive measures can help. Replacing toothbrushes every three to four months, purchasing expendable toothbrushes and using an antibacterial mouthwash for rinsing and soaking is beneficial. Also, you need to know that a UV sanitizer will not result in a maximum removal of germs. Another flaw in the usage of UV sanitizer is that the ultraviolet light may destroy the bristles.

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August, 2019|Oral Cancer News|

Psychological impact of head and neck cancers

Source: pharmafield.co.uk
Author: Emma Morriss

Bristol-Myers Squibb (BMS), in partnership with patient groups The Swallows and the Mouth Cancer Foundation, have announced the results from a patient survey into the psychological impact of head and neck cancers. The research explored the long-term burden of treatment on head and neck cancer patients.

After undergoing treatment for head and neck cancer, which can include surgery, chemotherapy or radiotherapy, many patients report an ongoing impact on their day-to-day life. However, 55% of the 118 patients surveyed indicated they did not receive the right level of information in preparation for the complications encountered from treatment.

There are around 11,900 new head and neck cancer cases in the UK every year and the incidence of head and neck cancer has increased by 32% since the early 1990s.

Following treatment, the survey showed 56% of patients had problems with simple things like swallowing, often experiencing severe pain, while two-thirds of patients experienced changes in their voice or speech. The survey also showed self-reported change from pre- to post- treatment in vital areas including a drop in the ability to communicate (37%), memory loss (21%), and trouble sleeping (20%).

As well as physical symptoms, treatment can have severe implications on mental health too. 52% of patients reported feelings of anxiety before treatment, which only reduced to 48% following treatment. However, emotional and psychological support was only offered to 46% of patients.

A majority of patients did receive access to a clinical nurse specialist, however there was still 23% who were not offered this service. Clinical nurse specialists use their skills and expertise in cancer care to provide physical and emotional support, coordinate care services and inform and advise patients on clinical as well as practical issues, which have been shown to lead to more positive patient outcomes.

“These results show the impact treatment may have on head and neck cancer patients. The continued problems and symptoms experienced by patients after treatment significantly impacts patients’ daily life. We also know physical disfigurement can increase social anxiety. It is important that we raise the awareness of this and work together to provide solutions to improve and support patient outcomes.” said Mouth Cancer Foundation, Clinical Ambassador, Mr Mahesh Kumar.

“With the incidence of head and neck cancers increasing, it is vital we understand what we can do to help patients. We are so pleased to have worked in collaboration with BMS and the Mouth Cancer Foundation to help raise awareness of this disease and understand where patients might need more help to reduce the impact on their lives. We know head and neck cancers, and the associated complications, do not get a lot of attention so it’s crucial for awareness days such as World Head and Neck Cancer Day to be used to shine a light on the disease. By doing so, it will help to improve detection, treatment and outcomes for patients.” commented Chris Curtis, Chairman of The Swallows.

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Aggressive radiotherapy dose de-escalation confers benefits in HPV-associated oropharyngeal squamous cell carcinoma

Aggressively de-escalated adjuvant radiotherapy for patients with HPV-associated oropharynx squamous cell carcinoma produced local tumor control rates comparable to those of historical controls, according to results of a single-arm phase 2 study published in Journal of Clinical Oncology.

The de-escalated treatment also was associated with decreased toxicity and slight improvement in swallowing function.

“HPV-associated oropharyngeal squamous cell carcinoma represents a demographically and biologically distinct disease compared with historical head and neck squamous cell carcinomas,” Daniel J. Ma, MD, radiation oncologist at Mayo Clinic in Rochester, Minnesota, and colleagues wrote. “Patients are more likely to be younger and nonsmokers and have fewer medical comorbidities. Furthermore, in vitro and in vivo experiments have demonstrated that these tumors are more sensitive to radiotherapy and chemotherapy compared with historical head and neck squamous cell carcinomas.”

The current standard treatment for HPV-associated oropharyngeal squamous cell carcinoma is 7 weeks of radiotherapy at 70 Gy in combination with cisplatin or surgery followed by a 6-week regimen of adjuvant radiotherapy at 60 Gy to 66 Gy with or without cisplatin.

However, these approaches result in significant toxicities.

The two-cohort study by Ma and colleagues included 79 patients (mean age, 58.7 years; 89.9% men) with p16-positive oropharyngeal squamous cell carcinoma who had a smoking history of 10 years or less and negative margins.

Patients in cohort A (n = 36) received 30 Gy delivered in 1.5-Gy fractions twice daily for 2 weeks in combination with 15 mg/m2 docetaxel once per week. Cohort B (n = 43), which included patients with extranodal extension, received the same treatment plus a simultaneous boost to nodal levels with extranodal extension to 36 Gy delivered twice-daily in 1.8 Gy fractions.

Locoregional tumor control at 2 years served as the study’s primary endpoint. Two-year PFS, OS, toxicity, swallow function and patient-reported quality of life served as secondary endpoints.

Median follow-up was 35.7 months (range, 25.2-61.8).

Results showed 2-year rates of 96.2% for locoregional tumor control (100% cohort A vs. 93% cohort B), 91.1% for PFS and 98.7% for OS, outcomes comparable to those observed with standard adjuvant treatment.

One patient in cohort A and nine patients in cohort B experienced disease recurrence.

Rates of grade 3 of higher toxicities were 2.5% before radiotherapy de-escalation and 0% at 1 year and 2 years after de-escalation.

Researchers observed a slight improvement in swallowing function from before radiotherapy to 1 year after completion of treatment.

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July, 2019|Oral Cancer News|

UB center helps bring local dental products to market

Source: www.buffalo.edu
Author: Marcene Robinson

Stocked on the shelves of Western New York pharmacies is a bottle of dry mouth spray Lubricity, a product developed and manufactured locally by You First Services, Inc. with the support of the University at Buffalo Center for Dental Studies.

Through the partnership, the UB Center for Dental Studies verified the effectiveness of Lubricity through clinical trials, helping bring the product to market and contribute to the growth of You First Services as a budding employer in the region.

Since its establishment in 1988, the UB Center for Dental Studies has built an extensive history of performing scientific and clinical studies for new products by major companies around the world, including Johnson & Johnson and Colgate-Palmolive.

However, the center also works with local manufacturers, providing access to cutting-edge technology, state-of-the-art facilities and guidance from experienced researchers. Since its inception, the center has completed more than $15 million in research projects with contracts ranging from $10,000 to $450,000.

“Ease of accessibility to university scholars is one of the major benefits of having a research university like UB in our community, said Sebastian Ciancio, DDS, director of the Center for Dental Studies and Distinguished Service Professor in the UB School of Dental Medicine.

“Our Center for Dental Studies has helped manufacturers bring a number of useful products to the marketplace to improve oral health of consumers.”

Approved by the U.S. Food and Drug Administration in 2018, Lubricity, works as a saliva substitute for those who suffer from dry mouth. A side effect of more than 500 medications, dry mouth doubles the rate of dental decay compared to people without the condition, and increases the risk of pathogenic and fungal infections, says Ciancio.

The mouth spray, which contains hyaluronic acid, commonly known as “nature’s lubricant,” says Ciancio, is the commercialization of research concepts developed by late UB Distinguished Professor Robert Baier.

Lubricity, which can also be found online at Walmart, Walgreens and Amazon, and in independent pharmacies and hospitals pharmacies, is the flagship product and one of the early successes of You First Services. Formed in 2013, the company has grown from a fledgling startup housed in the UB Technology Incubator at Baird Research Park to a multimillion-dollar manufacturer of oral health care and sterilization products.

The company has received multiple peer-reviewed grants for programs in its disinfection and sterilization and infectious diseases control divisions, and earned the 2018 Bright Buffalo Niagara Industry Partner Award.

In addition to retaining space at Baird Research Park, in 2017, You First Services constructed a $2.6 million pharmaceutical manufacturing facility in Buffalo with the goal of creating 28 full-time jobs in the region.

The company also employs 12 UB alumni, and has provided paid internships to nearly a dozen UB students from fields that include engineering, biological sciences, business, communications and architecture.

“We are very proud of our long-standing relationship and for the incredible quality of the research programs here at the University at Buffalo, said Satish Sharma, MD, executive chairman and chief executive officer of You First Services Group of Companies and research associate professor of urology in the Jacobs School of Medicine and Biomedical Sciences at UB.

“The Center for Dental Studies’ scientific performance in terms of productivity, impact and excellence has remained outstanding. We at YFS will continue to work together with the University at Buffalo to continue to develop our programs to make a significant impact on the overall economy of the state and region.”

The UB Center for Dental Studies recently performed clinical trials for You First Services’ second product MetaQil, a mouth rinse that treats dysgeusia, a metallic taste disorder that occurs due to a number of causes, including damage to oral tissues by chemotherapy. The condition causes patients to experience a loss of taste or an overwhelming metallic taste.

The center performed a clinical trial of more than 50 local participants, who were treated with either MetaQil or a placebo. The study found that nearly 85% of participants reported a significant reduction in metallic taste while using the product.

MetaQil is available in local pharmacies and online.

The Center for Dental Studies and You First Services will continue to explore opportunities for research collaboration and clinical trials. To learn more about the UB Center for Dental Studies, visit the center’s website.

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Examining the potential of preoperative CT lymphography with ICG in oral cancer

Source: www.cancernetwork.com
Author: Leah Lawrence

The majority of patients with localized squamous cell carcinoma of the tongue had at least one sentinel lymph node (SLN) successfully identified and removed using preoperative computed tomography (CT) lymphography and intraoperative indocyanine green (ICG) fluorescence, according to a small study published in JAMA Otolaryngology-Head & Neck Surgery.

According to Kohei Honda, MD, of Hiigata University Graduate School of Medical and Dental Sciences, in Akita, Japan, and colleagues, this combined method “has the potential to provide clear visualization with high sensitivity, even if the SLN is located close to the primary injection site”.

Traditionally, SLN detection is performed using preoperative lymphoscintigraphy with radioisotopes and intraoperative γ-probe detection with or without blue dye mapping. However, the use of radioisotopes has its disadvantages, including exposure to radiation, high cost, and masking of SLN because of shine-through radioactivity when close to the injection site.

Honda and colleagues tested the usefulness of SLN biopsy with preoperative CT lymphography and intraoperative ICG. The study included 18 patients with previously untreated cN0 tongue cancer. All patients underwent CT lymphography prior to SLN biopsy. During biopsy, a minimum skin incision was made according to a predetermined location of SLN and SLN were excised under ICG guidance.

Of the 18 patients, SLN could be mapped using preoperative CT lymphography in 16 patients (89%), in whom at least one SLN was identified and removed using intraoperative ICG.

Metastases to SLN were found in 5 of the 16 patients (31%). There were two patients with T1N0 and three with advanced T2N0.

Of the 30 SLNs removed, 80% were identified by preoperative CT lymphography and intraoperative ICG methods, 17% by ICG methods alone, and 3% by CT lymphography alone.

“In a previous study, we performed preoperative SLN mapping using CT lymphography and an intraoperative blue dye method for early tongue cancer. The identification ratio in finding the SLN using the intraoperative blue dye method was 67%,” the researchers wrote. “We could therefore improve the intraoperative detection rate from 67% to 100% using ICG instead of blue dye.”

Furthermore, a method free of radioisotopes could offer patients a lower cost, freedom from radiation, and no need for facility approval.

In an editorial published with the study, Remco de Bree, MD, PhD, Jan Willem Dankbaar, MD, PhD, and Bart de Keizer, MD, PhD, of University Medical Center, Utrecht, Netherlands, wrote that although this new technique seems promising, more studies are needed to improve its accuracy and to evaluate its usefulness.

“Use of CT lymphography may have a future in lymphatic drainage mapping of localized oral cancer and might become a high-resolution alternative for standard lymphoscintigraphy using radioisotopes if specific nuclear medicine facilities are not available, use of radioisotopes is not wanted or needed, or the shine-through phenomenon must be avoided,” they wrote. “However, intraoperative localization of the SLNs by matching CT lymphography with other nonradioactive techniques, such as ICG fluorescence imaging is challenging.”

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Precision Medicine Is Crushing Once-Untreatable Cancers

Source: Newsweek
Date: June 16th, 2019
Author: David H. freedman

 

For tens of thousands of patients, precision medicine is rewriting their cancer stories.

Linda Boyed, for example, an energetic 52-year-old occupational therapist, was thrilled to be on vacation with her family in Hawaii, hitting the beaches and taking long walks. But she couldn’t shake a constant feeling of fatigue. By the time she returned home, near Columbus, Ohio, her skin had yellowed. Her doctor passed her to an oncologist, who delivered the bad news: Cancer of the bile ducts in her liver had already spread too far for chemotherapy or surgery to do any good. He offered to help keep her comfortable for her final few months.

Boyed’s husband refused to accept that prognosis. He found a doctor at Ohio State’s cancer center who was running studies of experimental drugs for gastrointestinal cancers. Boyed signed herself up. Genetic tests on her tumors revealed a mutation in a gene called FGFR (short for “fibroblast growth factor receptor”), which was likely spurring the cancer’s growth. The doctor gave her an experimental drug, called BGJ398, to inhibit the action of the FGFR mutation. Boyed’s symptoms cleared up, the tumors stopped growing, and she regained the weight she had lost.

That was three years ago.

These days Boyed gets downright bubbly when she tells the story. “I basically lead a normal life now,” she says. “I just watched my son graduate from high school. I think I actually did more in the past year than I did before the cancer.”

Stories like Boyed’s are playing out across the U.S., as new cancer drugs emerge from labs and enter trials. The days when cancer patients received one-size-fits-all regimens of chemotherapy and radiation may soon be a thing of the past. Instead, doctors are taking a far more nuanced view of what drugs and treatments will work on which patients and on what different kinds of cancers. The idea of this so-called precision medicine, or personalized medicine, is that ultimately doctors will use genetic tests—of both the patient and the cancer tumor—to determine the exact drugs or treatments that have the best chance of working.

Although precision-medicine techniques are now being trained on many diseases, their impact is being felt most strongly in cancer treatment. Researchers are building a growing list of genes and genetic mutations that show up in tumors and matching them to drugs that can stop them. The cancer genes that drugs can target now number in the dozens, and researchers are hot on the trail of hundreds more. For some cancers once considered virtual death sentences, the outlook is already much improved: About half of lung-cancer patients respond well to one of the new gene-matched therapies, and in half of those cases, the cancer doesn’t come back. FGFR inhibitors, the drug that saved Boyed, have shown promise not only in bile duct cancer but also for some types of bladder, lung, breast and uterine cancers. “We have six trials open now for FGFR inhibitor drugs alone,” says Sameek Roychowdhury, the oncologist who saved Boyed’s life. “By the end of this year there should be 20.”

After decades of fits and starts in the field of cancer research, the progress made in precision medicine is welcome news indeed. But make no mistake: There is no “cure.” Medicine is not even close to bringing cancer to its knees. For patients diagnosed with advanced cancers—those that have already metastasized, or spread—only one in 10 turn out to have genes currently known to make the cancer susceptible to a new drug. “Our goal is to give 100 percent of patients a new therapy based on genomic testing,” says Roychowdhury. “But today we don’t know how to provide a special treatment for the results of nine of 10 genomic tests we do.”

Most patients don’t even get that one-in-ten chance. Many doctors still lack expertise in the area and fail to administer the genetic tests that could open the door to a precision medicine treatment. Expense is also an obstacle: Insurance companies don’t reimburse adequately for the tests. For these reasons, only 10 percent of cancer patients undergo genetic testing. Precision medicine is helping, at best, only a few percent of the nearly 2 million people who are diagnosed with cancer in the U.S. each year, and the fraction is much smaller among the 17 million cancer patients worldwide.

To increase the number of patients eligible for treatment, doctors are turning to artificial intelligence for help. Genetic testing is churning out so much data that even an army of Ph.Ds couldn’t make sense of it all. Artificial intelligence turns that volume of data from a liability to an advantage. Scientists are now delegating the task of finding the weaknesses in cancer tumors to “deep learning” software that can churn through millions of genetic test results and patient outcomes to find new relationships between tumor genes, cancer growth and specific drugs.

Teasing Out Patterns

To increase the odds that a cancer patient who walks through their doors is given a treatment option, City of Hope National Medical Center outside of Los Angeles plans within two years to be the first major hospital in the U.S. to do genomic testing on the tumors of every single one of its 9,000 cancer patients a year. “Tumors that look identical under the microscope look vastly different under from a genomic point of view,” says Michael Caligiuri, a physician and president of City of Hope National Medical Center outside of Los Angeles. “They need to be treated differently.”

As other hospitals follow suit, they will generate a vast volume of data—grist for the AI mill. The 20,000 genes of a typical human genome include three billion DNA nucleotides, or bits of information, any of which can be mutated, repeated or moved in any number of ways to cause cancer. Each of the human body’s billions of cells has its own copy of the genome, subject to its own mutations.

But DNA is only part of the picture: Whereas DNA is a blueprint, the real work in our cells is carried out by proteins—complex molecules that control almost everything in our biology. Proteins govern both the growth of a cancer tumor and the work of the immune system in fighting it. There are as many as 6 million basic proteins and variations on them, and researchers are now measuring thousands of them directly in cancer-tissue samples and feeding that information to the deep-learning programs.

“Drugs don’t target genes, they target proteins,” says David Spetzler, chief scientific officer of Caris Life Sciences in Irving, Texas. “That’s where we’re seeing the most progress in understanding cancer, and it’s what’s going to be the most useful information we gather in the next five years.” Says Jeffrey Balser, a physician who heads the Vanderbilt University Medical Center: “That’s a lot of incredibly deep knowledge coming to the table.”

Deep-learning algorithms don’t work the way scientists do—they never “understand” the biology behind the cancer they’re analyzing. Instead, they digest reams of information from tissue samples of patients that had certain kinds of cancer, and correlate that information with the ultimate fate of those patients—who responded to which treatments and who didn’t. It’s a kind of hit-or-miss association exercise, but one that’s conducted thousands of times, using vast amounts of data. Computers can tease out patterns in the data that a human could never see—linking, say, the presence of the FGFR gene to a particular cancer of the bile duct.

Spetzler’s company, for instance, is working to crunch protein-fortified data with deep-learning software. To wring useful insights out of the data from 170,000 cancer patients that Caris has access to, the company enlists hundreds of different deep-learning algorithms. The programs essentially compete with one another to find patterns in the data that indicate which drugs will work best with which patients. “Different algorithms will miss different patients, but together they can do a better job,” says Spetzler.

AI is helping provide yet another critical set of clues to how to match patients to new drugs by learning to read slides of tissue samples taken in biopsies. Those slides have always been read under a microscope by pathologists, who come up with a cancer diagnosis based on the cells’ appearance. So-called “machine learning” programs are starting to step in. An Israeli company called Nucleai has trained its software with 20 million digitized biopsy slides to recognize cancer, and it already performs with 97 percent accuracy.

Diagnosing cancer is just the start, says Nucleai CEO Avi Veidman. The goal now is to use AI to extract more information from slides than pathologists can—information that can help match patients to new drugs. “Most of the information in that tissue isn’t being used when doctors or software are trying to predict the treatments that will work,” says Veidman, who spent two decades with Israel’s intelligence forces developing AI software to recognize missile bases and terrorist activity in satellite images before turning his attention to cancer three years ago. “AI can analyze the different types of features in the image much more efficiently and find hidden patterns.” He notes, for example, that subtle signs of the battle between the patient’s cancer cells and immune-system cells can be spotted by the software, and those signs can provide essential clues to whether or not the cancer might be vulnerable to one of several new immunotherapy drugs—that is, drugs that work not by fighting the cancer directly, but by boosting a patient’s immune system so it can attack the tumor.

South-Korean firm Lunit has developed AI software that can analyze pathology slides to predict, for example, which patients will respond to a relatively new type of cancer drug called checkpoint inhibitors, which can prevent cancer cells from blocking a patient’s immune cells. Lunit claims that the software is 50 percent more accurate than tests that use genetic data alone. “That’s going way beyond what human eyes can do,” says CEO and physician Beomseok Brandon Suh. “The software is finding patterns that are too complex for people to recognize, but that have biological meaning.”

Similar advances are taking place with AI-based systems that are reading X-rays, MRIs and other image data. “There are already algorithms that are as good at reading a mammogram as a highly trained radiologist, or at recognizing skin cancer as a dermatologist,” says Chi Young Ok, a pathologist at the MD Anderson Cancer Center in Houston. “The progress is astounding.” Eventually those images, too, are likely to help AI systems go beyond diagnosing cancer to spotting hints of the vulnerability of a patient’s unique cancer.

Data Dilemma

Deep-learning algorithms look at more data and analyze it more thoroughly than machine learning programs do. They are a bit like Seymour, the ravenous plant in Little Shop of Horrors, whose appetite never stopped growing. Although researchers and clinicians now have access to databases that contain information from as many as 250,000 cancer patients, it’s not nearly enough.

Thousands of different mutations in a patient’s genome can shape the development of cancers and determine which treatments are effective. Each cancer cell is a moving target, continually developing new mutations that can help it evade immune cells and survive powerful cancer drugs. Since AI software needs thousands of examples of a particular pattern before it can begin to recognize it, and since a particular pattern of mutations may come up in only a few thousand patients altogether, the software may well need access to the data of millions of patients to make faster progress. “We can make predictions now about how tumors will evolve and what treatments will work, but right now a significant fraction of those predictions are wrong,” says UCLA’s Paul Boutros, a physician who heads up cancer data science for the UCLA Jonsson Comprehensive Cancer Center.

A number of collaborations—with names like the International Cancer Genome Consortium, the Oncology Research Information Exchange Network, and the Actionable Genome Consortium—have sprung up among research centers and hospitals to share patient data. Gathered with patients’ permission and with personally identifiable information stripped out, that data could eventually help researchers reach the needed critical mass of information. “We need to get to the point where all these different data networks are tied together into a network of networks,” says City of Hope’s Caligiuri. Clinicians need access to that data, too, to find patients like the ones they’re treating to see what might work. “We should be able to go to a computer, type in information about a patient’s cancer, and up will pop 50 cases around the world that are similar at the molecular level,” he says.

Easing the Bottleneck

Medicine is of no use if patients don’t have access to it. To get new drugs out faster, researchers are using AI to speed the process of drug development. One of the biggest causes of delay in testing new drugs is recruiting enough patients for a trial. Researchers not only need a group to try the new drug, but another “control” group to get the standard treatment, for purposes of comparison. Even when a new precision drug is promising, it can take years to run the trials that demonstrate the drug actually works for an identifiable group of patients.

To speed things along, researchers are starting to use high-powered statistics and computer models to avoid having to recruit a control group at all. Instead, they use a mashup of data from past studies to predict how a real control group would fare. “The results you get from a synthetic control arm are as reliable as if you had actually enrolled control-group patients in the trial with the same physicians and protocols,” says Glen de Vries, president of Medidata Solutions, which has designed the statistical tools.

That won’t be enough to ease the trial bottleneck for clinicians and researchers hoping to come up with precision treatments for the deadliest, most aggressive cancers. For instance, glioblastoma, the brain cancer, has the lowest median survival time from diagnosis—15 months—of any major cancer. It’s challenging enough to design a drug that can make it through the blood-brain barrier to get at a glioblastoma tumor. The disease works so quickly that there’s barely time to give an experimental drug a chance to show whether or not it is effective.

To give more experimental precision drugs a better shot at glioblastomas, the newly created Ivy Brain Tumor Center at the Barrow Neurological Institute in Phoenix has developed “accelerated trials” for its brain-cancer patients. A newly diagnosed patient is first given a dose of an experimental precision drug. The dose is too small to harm the patient (in case it turns out to be toxic, always a risk with new drugs) but big enough to reach the tumor. After surgery, doctors test the tumor to see if the drug had any effect. If it did, the patient continues with an increased dose. If not, the patient and doctor find out in time to take another course of treatment. “Speed is the key to finding drugs that work,” says Ivy director Nader Sanai. The approach has already turned up a personalized treatment that in one patient’s case beat back a form of brain cancer called malignant meningioma.

While all these approaches together are likely to bring us closer to the day when most cancers succumb to precision treatments, no one thinks that day will be here soon. Still, the move to personalized treatments is benefitting almost all cancer patients by sparing them the ordeal of a treatment that has little chance of working. “If you can look at a genomic or other test and know ahead of time whether or not a patient’s tumor will respond to a treatment, then even if only one out of 100 patients responds you’ve saved 99 patients from unnecessary complications and expense,” says Stanley Robboy, vice-chair for diagnostic pathology at the Duke University Cancer Center. “These drugs can cost $100,000, and can bankrupt families.”

Even that modest benefit, however, is being denied to most advanced cancer patients today. Health insurance companies frequently balk at paying for the genetic tests, which can cost as much as $10,000. “Medicare and some companies are starting to provide some coverage,” says Roychowdhury. “But it’s an arduous process to get reimbursed for the testing, and it’s hard to get the cutting-edge tests covered at all.” That’s one reason most of the top cancer centers in the country don’t routinely provide the testing to all their patients, even though virtually all experts agree that should be the standard of care everywhere for cancer.

When a patient does get a tumor tested and the test shows a match to a promising precision drug, insurers often refuse to pay for the drug too, says Roychowdhury. The insurers cover only drugs that have already gotten FDA approval as a standard treatment, after a long period of trials. FGFR inhibitors of the sort that rescued Linda Boyed and many others are still usually not reimbursable. Patients who become part of formal drug trial, as Boyed did, usually get the drug for free. But in some cases patients with the most advanced cancers—the ones who need experimental drugs the most—are excluded from trials. Drug companies and even academic researchers often want to avoid including very sick patients out of fear they’ll skew the results toward failure.

Payment isn’t the only obstacle to treatment. About 85 percent of U.S. cancer patients get treated at a community hospital, where they see an oncologist who treats many different types of cancers. Those generalists are typically not up on the latest tests and treatments, says Caligiuri. The hospitals who employ them don’t expect them to go through the time and expense of figuring it out. While highly regarded cancer centers place as many as a quarter of their patients on newer precision drugs, the percentage at most community hospitals is nearly zero.

What should patients do? “The first and most important thing I would say to anyone who has just received a diagnosis of cancer is that you need to get a second opinion from an oncologist who is a specialist in your type of cancer before you start any treatment,” says Caligiuri. “If your first treatment isn’t the optimal one, the tumor develops multiple resistances not only to that treatment but to other treatments that might have worked if you got them first.” When asked about other treatment options, community oncologists often insist that patients are best off starting treatment first. Some play on patients’ fears that even a short delay might hurt their chances of recovery—when in fact, it might save their lives.

Vanderbilt’s cancer center is trying to fix this problem by boosting the participation of community-hospital oncologists in precision-medicine initiatives. Its My Cancer Genome website helps doctors and patients find out what new treatments and trials might be available for any particular cancer—the site lists 4,000 trials. “It pains me when patients come to us and they’ve already been given a treatment that wasn’t going to help them,” says Vanderbilt’s Balser. “At that point the patient is behind the eight ball, and all we can do is try to pick up the pieces.” Like many other top cancer centers, Vanderbilt is also creating affiliations with community hospitals in its region to support those hospitals in gaining access to precision-medicine expertise, genetic testing and trials of the newest drugs. Vanderbilt already has forged such ties to nearly 70 hospitals in five states.

A growing roster of precision-medicine approaches will also help in preventing cancers from taking hold in the first place. Some imaging techniques, such as PET scans, are approaching the needed sensitivity and resolution to pick up a cluster of newly formed cancer cells so tiny that it can be blasted away on the spot with a beam of focused radiation. Such treatments would be convenient and come with fewer complications.

And why wait until someone gets cancer to look at genetic information? If everyone routinely got genetic screening to see which cancers they’re at high risk for, tests like PET scans, which can cost $7,000 or more, could be given selectively. Unfortunately, genetic screening itself is currently either too expensive or, in the case of consumer-focused genetic-testing companies like 23andMe, too unrefined to justify being rolled out to the entire population. But researchers and biotech companies are working on cutting the costs and raising the accuracy of genetic tests. “If we can know the cancer you’re at risk for, the right image every three years can change your life,” says Caligiuri.

Of course, it would be good to know that if a cancer does slip through, precision medicine will have just the right drug for it. That way cancer patients will have more to look forward to than just being made comfortable in their final days—the fate that was Linda Boyed’s, until it wasn’t.

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July, 2019|Oral Cancer News|