radiotherapy

Leaders in Dentistry: Dr. Ezra Cohen

Source: Dr. Bicuspid
By: Donna Domino, Features Editor
Date: July 17, 2013

Ezra Cohen, MD, University of Chicago.
May 21, 2013 — DrBicuspid.com is pleased to present the next installment of Leaders in Dentistry, a series of interviews with researchers, practitioners, and opinion leaders who are influencing the practice of dentistry.

We spoke with Ezra Cohen, MD, an associate professor of medicine and the co-director of the head and neck cancer program at the University of Chicago, and the associate director for education at the university’s Comprehensive Cancer Center. Dr. Cohen specializes in head and neck, thyroid, and salivary gland cancers, and is an expert in novel cancer therapies who has conducted extensive research in molecularly targeted agents in the treatment of these cancers.

His research interests include discovering how cancers become resistant to existing treatments and overcoming these mechanisms and ways to combine radiotherapy with novel agents. Here Dr. Cohen discusses trends in the incidence, detection, and treatment of oral and head and neck cancers.

DrBicuspid.com: What’s the significance of your recent finding that there may be five distinct subgroups of the human papillomavirus (HPV)?

Dr. Cohen: The purpose of the research was trying to define molecular subgroups of head and neck cancer (HNC) to inform therapy and outcomes a lot more than we do now as defined by stage and anatomic site. We were taking advantage of a cohort of patients that we treated in a similar fashion at the University of Chicago with a chemotherapy regimen that we commonly use here. The patients had tumors banked and the specimens were carefully clinically annotated, so we had information on response, outcome, and toxicity.

Because many of these patients had participated in clinical trials, we could draw upon all this clinical data and begin to coordinate the data with molecular profiling. We noticed that five subgroups served the classification best. If we went to more subgroups, it did not help to differentiate the patients with respect to outcome; if we went to fewer subgroups, we were leaving out important categories.

What really made us stop and realize that this was real was that HPV-positive patients and HPV-negative patients segregated into their own groups quite nicely. We of course validated the entire algorithm on different datasets, and we showed that, indeed, on other datasets the five subgroups still held and the outcomes were still different between those subgroups. So we felt reassured that this wasn’t just a spurious finding based on a limited number of samples and limited datasets, that these subgroups are real.

When we looked at specific genes or groups of genes that made up the subgroups, we were then able to see some very important patterns. The predominantly HPV-negative subgroup looked like they classified into one that was driven by hypoxia, one that was driven by stem cell or mesenchymal type of features that we are calling basal, and one that was driven by cell cycle or epidermal growth factor receptor (EGFR)-related genes that we are calling the classical HNC.

HPV positives segregated primarily into two subgroups: one that appeared to express a lot of immune-related genes and one that was actually similar to the basal HPV-negative group. What is interesting is that the latter HPV group actually did worse and was closer in terms of outcome to the basal subgroup in the predominantly HPV-negative group. We have known that obviously not all HPV-positive patients do well. So maybe here is a classifier that we can apply prospectively to begin to segregate patients into groups of those that will do well and those that may be amenable to specific therapies such as EGFR inhibitions, hypoxia modulations, or immune modulation, depending on the subgroup.

A report published in January in the Journal of the National Cancer Institute noted that the rate of HPV-related oropharyngeal cancers is rising, but there is no etiological data on what’s causing the increase. What do you think is causing the increase?

We are still trying to figure that out, but there are some things we can be confident about and some things we have to surmise. We can be confident that the number of HPV-positive and tobacco-unrelated cancer patients are definitely increasing. Also, no doubt these are sexually transmitted entities and that HPV oropharynx cancer is a sexually transmitted disease. The epidemiology strongly favors that and there likely is an immune-host component to this — the ability to eliminate the virus completely versus allowing the virus to integrate into DNA. What we do not know is why. Why are we seeing an increase in the incidence? Why do people not clear the virus? And in the subgroup of those patients, do they eventually develop cancer?

There is a parallel with oral herpes infections and the rise of HPV oropharynx cancer. There is a parallel with a change in sexual practices to more oral sexual activity versus other forms of sexual activity. And there is a parallel to a younger age of sexual activity where, because of concerns about contraception and sexually transmitted diseases, oral sexual activity may be preferred in younger individuals versus older people who are having sex to conceive.

Those may be demographic factors that are beginning to favor the emergence of HPV-positive cases. And, of course, these are things that have been going on for decades, not just now, because the virus takes 20 to 30 years to produce cancer. These are exposures that happened 20 years ago. They are trends that would parallel what we are seeing in terms of hosts that are not clearing the virus.

There may be modulating factors. We know that males are more likely to harbor the infection than females and that males have a much higher incidence — a 3-to-1 ratio — of HPV-related oropharynx cancer than females. There may be something hormone-related or differences in the immune systems that somehow protects females from developing oropharynx cancer. There may be an interaction with smoking, and some have cited an interaction with marijuana and the development of this cancer. How those may play a role in the ability of the immune system to clear this virus we still have to elucidate. But clearly there are host factors that in some individuals do not allow clearance of this virus, and we do not understand those completely.

Are you seeing more HNC and oral cancer cases in your facility? If so, why?

We are definitely seeing more oropharynx cancers. It could be a combination of factors. We are a tertiary care center that has an interest in HNC and the numbers are truly rising. We are seeing more young patients with tongue cancer who do not have the typical risk factors. That is a disease that worries us quite a bit, not only because we really cannot explain the biology, but our data indicate these patients have worse outcomes.

Researchers have found that parts of the genome are missing in cancer patients. Has there been any information related to oral cancer patients? A recent study of head and neck cancer patients showed that in one patient, 5,000 genes had at least one mutation, and 1,300 had at least two. But the researchers said most were “passengers” — that is, mutations alongside another mutation that acts as a “driver.” What do you think is the significance of these findings?

Without doubt it is true. When we sequence cancers, including oral and HNC, we can see a lot of mutations. The challenge is trying to figure out which ones are important. We call those drivers because they affect the biology of the cancer. So the presumption is if you inhibit a driver, you will have a therapeutic effect on the cancer. If you modify a passenger, you are unlikely to see a therapeutic benefit.

It is certainly true in oral and HNC. We think one gene that is commonly mutated in tobacco-related HNC is p53. We think that is an important gene in the biology of these cancers because it is a common mutation in 50% to 60% of these cancers, and because it is a gene that affects so many critical pathways in the carcinogenic process. It tends to happen very early; even before cancers develop, we see evidence of p53 mutations. That is an example of a gene we think is indeed a driver. On the other hand, there are mutations in many other genes, but we are just not sure how important they are.

What is the greatest challenge in successfully treating head and neck cancers?

Head and neck cancer is an important disease in the way we view cancer and our approaches to it because of two factors. It is a disease in which in a majority of patients we are at least going to consider curative therapy. That does not apply to lung, pancreatic, esophageal cancer, and most cancers that we treat.

The other thing is if you think about what defines us as human beings, especially social animals, so much of it occurs above the clavicle. They involve structures that are profoundly affected not only by the disease but by the treatment. So when you think about it in that context, HNC becomes a cancer that most affects quality of life and that has the greatest financial and social implications of any cancer we know of. So choosing the appropriate therapy on an individual basis for HNC really becomes critical. I cannot overemphasize that. This is a cancer in which the patient has to be cognizant of where they are going for treatment, what type of treatment they will get, and the experience of the center because cure and function are at stake.

A study compared outcomes in patients treated in multidisciplinary centers and with collaboration prior to therapy, and the differences were dramatic. There is evidence that outcomes are better. I think it is a critical component. Not just having multidisciplinary conferences — the content of the conference is important, but one surrogate of that is likely the experience of the center. A radiation oncologist, medical oncologist, and surgeon who treat five of these a year is likely to be much different than somebody who treats hundreds of these a year.

Where do you think we will see the next big breakthrough for oral cancer, in treatment or prevention?

I think the next wave of breakthroughs will be predicated on what we are learning in the molecular biology of this disease. That will lead to the development of agents specifically for HNC and the molecular alterations, which will lead to better patient selection for therapies and, ultimately, better outcomes. But screening and prevention are critical, especially for oral cancer because this is a disease we should be able to screen for quite readily. For cancers of the oropharynx, hypopharynx, and larynx, those are a little bit more difficult to screen for, but for oral cancer, screening and prevention are very important.

There are also ongoing efforts for different compounds that hopefully try to prevent a second cancer from developing or a preneoplastic lesion from turning into a cancer. Nothing has been approved yet, but there are a lot of efforts going on around the country.

What role can dental professionals play in improving the detection of oral cancer?

It is the hygienist who often spends more time with patients, so we have to train those individuals, as well as primary care physicians, to implement oral cancer screening. But clearly the dental office is a key component, and it really should be the individual that spends the most time with a patient, and for most practices that is probably the hygienist.

What kinds of research are you doing now?

Research naturally flows out of the classification. We are developing protocols specifically for HP- positive versus HPV-negative patients. We will look at this classification in a prospective manner to see if it is validated. We are of course integrating novel agents based on what we understand about the molecular biology. We feel very strongly that the PI3 kinase is an important pathway in many cancers, and we think it is a very important pathway in HPV-positive cancers. We are developing and have ongoing clinical trials that specifically target that pathway to see if indeed these agents will be effective.

We also have a large chemoprevention effort using an approach that was developed at the University of Chicago to inhibit early blood vessel growth in preneoplastic lesions using the drug vandetanib, which is commercially available. We are very encouraged by the preclinical data, and hopefully we’ll have something to offer patients to actually prevent the cancer from occurring in the first place.
* This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

July, 2013|Oral Cancer News|

SSRI Prevents Depression in Head, Neck Cancer

Source: MedPage Today
By Salynn Boyles, Contributing Writer
Published: June 21, 2013

 

Prophylactic escitalopram cut the incidence of depression in head and neck cancer patients by more than 50% and improved quality of life, a clinical trial showed.

Significantly fewer patients taking the antidepressant developed depression, when compared with those on placebo (10% vs 24.6%; stratified log-rank test, P=.04), according to a study in the June 20 issue of JAMA Otolaryngology Head and Neck Surgery.

“Depression is very common among patients with this disease, but it is not easy to predict who will become depressed at the beginning of treatment,” University of Nebraska Medical Center professor of head and neck oncology William Lydiatt, MD, told MedPage Today. “That’s why the prevention paradigm may offer considerable benefit at an acceptable risk.”

As many as half of head and neck cancer patients develop clinical depression within months of their diagnosis and suicide rates are among the highest in patients with a medical illness, Lydiatt noted.

“The burden of treatment is extensive and frequently includes dysphagia, disfigurement, voice alterations, mucositis, need for tracheostomy and feeding tubes, fatigue and depression,” the researchers wrote.

They chose the generic version of the popular SSRI Lexapro for the trial to give patients an affordable treatment option that’s well tolerated in the elderly.

The randomized, double-blind trial included 148 newly diagnosed head and neck cancer patients entering treatment who did not yet have a diagnosis of depression. The patients were stratified by sex, site of disease, stage, and primary modality of treatment (surgery versus radiation).

Half were treated with escitalopram at a dosage of 10 mg/d for the first week (one tablet) followed by 20 mg/d (two tablets) until week 16, followed by an additional week of 10 mg/d. During the acute phase of the study, dosage was reduced to 10 mg/d when adverse events occurred. Patients not treated with the antidepressant received matching placebo pills.

Among the study’s major findings:

  • Patients undergoing radiation as their initial therapy were significantly more likely than those who had surgery to develop depression (hazard ratio, 3.6; 95% CI ,1.38-9.40; P=.009).
  • A Cox progression hazards regression model comparing the two groups, after controlling for age, smoking status, and other variables, demonstrated an advantage for escitalopram (hazard ratio, 0.37; 95% CI, 0.14-0.96: P=.04).
  • Patients who took escitalopram and who completed the study without developing depression rated their overall quality of life as significantly better than those in the placebo group for 3 consecutive months after ending treatment with the antidepressant (overall quality of life, good or outstanding at weeks 20, 24 and 28 – escitalopram group = 96%, 100%, 96%, respectively; placebo group = 77%, 86%, 85%).

 

Lydiatt said the finding that radiotherapy patients had a higher risk for depression than surgery patients is a big surprise with important potential clinical implications.

“The higher incidence of depression in the cohort receiving radiation suggests that radiation represents a greater and longer duration stress event than surgery,” the researchers wrote. “Radiation may also generate greater inflammatory cytokines during treatment, which could contribute to the higher rate (of depression).”

Although overall treatment success and survival were not study endpoints, Lydiatt said he hopes to conduct further research with these outcomes in mind.

“I would not be surprised to see a survival advantage associated with this approach,” he said. “Depression is associated with so many negative manifestations in these patients. Depressed patients don’t comply with their treatments to the same degree as patients who aren’t depressed and they don’t take care of themselves as well. They often lose their spark to live.

*This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

 

June, 2013|Oral Cancer News|

‘Dentist should have spotted my cancer’

Source: menmedia.co.uk
Author: staff

An NHS dentist who advised a patient to treat what turned out to be a life-threatening oral cancer with mouthwash is being sued for tens of thousands of pounds in damages.

Paula Drabble, 58, went to Pinfold Dental Practice, in Hattersley, Hyde, in June 2008 with concerns about a white lesion on her gum.

She was told by her dentist, Ian Hughes, it was nothing serious, a court heard.

Mrs Drabble of Mottram Moor, Mottram, Hyde, had five further appointments with Mr Hughes and was advised to ‘manage’ her complaint with mouthwash. She was eventually referred to hospital in April 2009, and ‘seriously invasive cancer’ diagnosed.

She had surgery, including removal of affected bone, followed by radiotherapy and chemotherapy.

She has now made a good recovery and has begun a High Court fight for damages, claiming Mr Hughes was negligent to have not spotted the cancer and referred her to hospital earlier. Timothy Briden, for Mrs Drabble, told the court his client had developed the patch on her gum some years earlier. The lesion was found to be benign by medics at the University Dental Hospital in Manchester and she was discharged in 2004 with a letter being sent to Mr Hughes, warning him to ‘re-refer if you notice or indeed Mrs Drabble notices any changes’.

Marcus Dignum, for Mr Hughes, denied that his client was at fault in failing to spot the cancer. He said: “Plainly the court will have every sympathy with Mrs Drabble in respect of her ordeal, as does Mr Hughes, but the allegations made against him are extremely serious from both a personal and professional standpoint. They are vigorously denied.

“In June 2008 the presence of the cancer would not have been detectable with the human eye, as its presence would have been at a cellular level only.”

January, 2013|Oral Cancer News|

Neoadjuvant chemo does not improve oral cancer survival rates

Source: www.drbicuspid.com
Author: DrBicuspid Staff

Patients with advanced resectable oral squamous cell carcinoma (OSCC) who undergo surgery do not benefit from improved survival after induction with docetaxel, cisplatin, and fluorouracil (TPF), according to a new study (Journal of Clinical Oncology, November 5, 2012). Study author Zhi-yuan Zhang, MD, PhD, from Shanghai Jiao Tong University School of Medicine, and colleagues assessed 256 patients with resectable locally advanced OSCC.

A total of 222 patients completed the full treatment protocol. They received two cycles of TPF induction chemotherapy (75 mg/m2 of docetaxel on day 1, 75 mg/m2 of cisplatin on day 1, and 750 mg/m2 of fluorouracil on days 1 to 5) followed by radical surgery and postoperative radiotherapy versus upfront radical surgery and postoperative radiotherapy.

The primary end point was overall survival. Secondary end points included local control and safety.

After a median follow-up of 30 months, there was no significant difference in overall survival or disease-free survival between patients treated with or without TPF induction, the study authors noted. Patients in the induction chemotherapy arm with a clinical response or favorable pathologic response had superior overall survival and locoregional and distant control.

“Our study failed to demonstrate that TPF induction chemotherapy improves survival compared with upfront surgery in patients with resectable stage III or IVA OSCC,” the authors concluded.

The lack of survival benefit indicates that TPF induction chemotherapy without selection could not benefit OSCC patients in general, Dr. Zhang told Reuters Health in a news story.

“On the other hand, superior outcomes are seen in responders, as assessed both by clinical and pathologic responses,” he said. “Therefore, induction chemotherapy is likely to be effective for biologically distinct subgroups, and biomarker development might lead to identification of patients whose tumors are likely to respond to a particular treatment.”

November, 2012|Oral Cancer News|

DNA alone inadequate to identify HPV-related cancers

Source: www.oncologypractice.com
Author: Mary Ann Moon

Testing for the presence of human papillomavirus DNA alone, especially using polymerase chain reaction methods, is not adequate to identify which head and neck squamous cell carcinomas are caused by the virus, according to two studies published online Sept. 18 in Cancer Research.

Identifying HPV-driven malignancies is important because they respond better to treatment and have better outcomes than those unrelated to HPV infection. Indeed, treatment of head and neck squamous cell carcinoma (HNSCC) may soon be guided by the tumor’s HPV status, since trials are now underway to determine whether de-escalation of chemo- and radiotherapy is safe and effective in such patients.

At present, however, the biomarkers that are best suited to making this identification are unclear.

Case Series Assesses Biomarkers
In the first study, researchers assessed the usefulness of four biomarkers in determining which HNSCCs in a case series were driven by HPV. They began by examining fresh-frozen tumor biopsy samples from 199 German adults diagnosed as having oropharyngeal squamous cell cancer between 1990 and 2008.

The four biomarkers were HPV-16 viral load, viral oncogene RNA (E6 and E7), p16INK4a, and RNA patterns similar to those characteristic of cervical carcinomas (CxCa RNA), said Dr. Dana Holzinger of the German Cancer Research Center at Heidelberg (Germany) University and her associates.

The simple presence of HPV DNA in a tumor sample was found to be a poor indicator of prognosis, likely because it often signaled past HPV infections or recent oral exposure, rather than active HPV infection that progressed to malignancy, the investigators said (Cancer Res. 2012 Sept. 18).

Instead, “we showed that high viral load and a cancer-specific pattern of viral gene expression are most suited to identify patients with HPV-driven tumors among patients with oropharyngeal cancer. Viral expression pattern is a completely new marker in this field, and viral load has hardly been analyzed before,” Dr. Holzinger said in a press statement accompanying the publication of these findings.

“Once standardized assays for these markers, applicable in routine clinical laboratories, are established, they will allow precise identification” of cancers that are or are not HPV-driven, which will in turn influence prognosis and treatment, she added.

Results Back Combination Approach
In the second study, Dr. Caihua Liang of Brown University, Providence, R.I., and her associates examined 488 HNSCC samples as well as serum samples collected in a population-based study in the Boston area during 1999-2003.

As in the first study, these investigators found that the mere presence of HPV-16 DNA in these tumors, particularly when detected by PCR analysis, did not accurately predict overall survival or progression-free survival.

Instead, “our study strongly suggests that the combination of detection of HPV-16 DNA in HNSCC tumors [plus] p16 immunostaining with E6/E7 antibodies represents the most clinically valuable surrogate marker for the identification of patients . . . who have a better prognosis,” they said (Cancer Res. 2012 Sept. 28).

“Assessment of HPV DNA using polymerase chain reaction methods as a biomarker in individual head and neck cancers is a poor predictor of outcome, and is also poorly associated with antibody response indicative of exposure and/or infection by HPV,” senior author Dr. Karl T. Kelsey added in the press statement.

“We may not be diagnosing these tumors as accurately and precisely as we need to for adjusting treatments,” said Dr. Kelsey, a professor in the department of epidemiology and the department of pathology and laboratory medicine at Brown University.

Dr. Holzinger’s study was funded in part by the European Commission, BMBG/HGAF-Canceropole Grand-Est, and the German Research Foundation. Her associates reported ties to Qiagen and Roche. Dr. Liang’s study was supported by the National Institutes of Health and the Flight Attendant Medical Research Institute, and one associate reported ties to Bristol-Myers Squibb.

September, 2012|Oral Cancer News|

Study will evaluate Panitumumab regimen in advanced SCCHN

Source: http://www.onclive.com/
Author: staff

Canadian researchers are investigating standard fractionation radiotherapy with concurrent high-dose cisplatin versus accelerated fractionation radiotherapy with panitumumab in patients with locally advanced stage III and IV squamous cell carcinoma of the head and neck (SCCHN).

The NCIC Clinical Trials Group has completed accrual for the randomized phase III study, which has a planned sample size of 320 patients with SCC of the oral cavity, oropharynx, larynx, or hypopharynx. The trial was launched in December 2008, and the Data Safety and Monitoring Committee recommended continuing the trial in October 2011.

Patients assigned to arm I will undergo standard fractionation radiotherapy once daily, five days a week, for seven weeks; they will also receive cisplatin intravenously over one hour on days 1, 22, and 43 of radiotherapy.

Participants assigned to arm II will undergo accelerated fractionation radiotherapy once or twice daily, five days a week, for six weeks; they will also receive panitumumab intravenously over 30-90 minutes one week prior to and on days 15 and 36 of radiotherapy.

The primary endpoint is progression-free survival (PFS), while secondary endpoints include overall survival, local and regional PFS, distant metastases, adverse events, swallowing-related quality of life, functional swallowing outcomes, and economic assessments.

The FDA has approved panitumumab under the brand name Vectibix for the treatment of patients with metastatic colorectal carcinoma with disease progression on or following chemotherapy regimens containing fluoropyrimidine, oxaliplatin, and irinotecan. Panitumumab is a human IgG2 kappa monoclonal antibody that binds specifically to human epidermal growth factor receptor (EGFR).

Amgen, which markets Vectibix, has joined the Canadian Cancer Research Society Institute in supporting the trial (NCT00820248).

Source:
Waldron JN, Parulekar W, O’Sullivan B, et al. A phase III study of standard fractionation radiotherapy with concurrent high-dose cisplatin versus accelerated fractionation radiotherapy (RT) with panitumumab in patients with locally advanced stage III and IV squamous cell carcinoma of the head and neck (SCCHN) (NCIC Clinical Trials Group HN.6). J Clin Oncol. 2012;30(suppl; abstr TPS5600)

September, 2012|Oral Cancer News|

The Impact of Timing of EGFR and IGF-1R Inhibition for Sensitizing Head and Neck Cancer to Radiation

Source: AntiCancer Research

Abstract

Background: Targeting the epidermal growth factor receptor (EGFR) improved radiotherapy outcome by 10-15% in head and neck tumors (HNSCC). We tested the therapeutic benefits of co-targeting EGFR and insulin-like growth factor-1 receptor (IGF-1R) to further enhance tumor response to radiation. Materials and Methods: Mice bearing FaDu tumor xenografts were treated with ganitumab (previously known as AMG479, an anti-IGF-1R antibody), panitumumab (an anti-EGFR antibody), or both in combination with fractionated doses of radiation. Tumor growth delay and tumor cure/recurrence served as end-points. Results: The best tumor growth delay was achieved when ganitumab and panitumumab were given concurrently with radiation. Tumor cure/recurrence studies showed that combining ganitumab, panitumumab and radiation resulted in significantly higher radiocurability rates than use of either of the agents given with radiation. Conclusion: These findings provide the rationale for clinical testing of the combination of ganitumab and panitumumab for the treatment of HNSCC.

This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

July, 2012|Oral Cancer News|

Tobacco Smoking and Increased Risk of Death and Progression for Patients With p16-Positive and p16-Negative Oropharyngeal Cancer

Source: Journal of Clinical Oncology

Purpose Tobacco smoking is associated with oropharynx cancer survival, but to what extent cancer progression or death increases with increasing tobacco exposure is unknown.

Patients and Methods Patients with oropharynx cancer enrolled onto a phase III trial of radiotherapy from 1991 to 1997 (Radiation Therapy Oncology Group [RTOG] 9003) or of chemoradiotherapy from 2002 to 2005 (RTOG 0129) were evaluated for tumor human papillomavirus status by a surrogate, p16 immunohistochemistry, and for tobacco exposure by a standardized questionnaire. Associations between tobacco exposure and overall survival (OS) and progression-free survival (PFS) were estimated by Cox proportional hazards models.

Results Prevalence of p16-positive cancer was 39.5% among patients in RTOG 9003 and 68.0% in RTOG 0129. Median pack-years of tobacco smoking were lower among p16-positive than p16-negative patients in both trials (RTOG 9003: 29 v 45.9 pack-years; P = .02; RTOG 0129: 10 v 40 pack-years; P < .001). After adjustment for p16 and other factors, risk of progression (PFS) or death (OS) increased by 1% per pack-year (for both, hazard ratio [HR], 1.01; 95% CI, 1.00 to 1.01; P = .002) or 2% per year of smoking (for both, HR, 1.02; 95% CI, 1.01 to 1.03; P < .001) in both trials. In RTOG 9003, risk of death doubled (HR, 2.19; 95% CI, 1.46 to 3.28) among those who smoked during radiotherapy after accounting for pack-years and other factors, and risk of second primary tumors increased by 1.5% per pack-year (HR, 1.015; 95% CI, 1.005 to 1.026).

Conclusion Risk of oropharyngeal cancer progression and death increases directly as a function of tobacco exposure at diagnosis and during therapy and is independent of tumor p16 status and treatment.

This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

June, 2012|Oral Cancer News|

The UK’s first robotic mouth cancer operation

Source: www.privatehealth.co.uk
Author: staff

Pioneering surgery which allows doctors to remove cancer in the mouth using a minimally invasive technique is now available at the Wellington Hospital.

Traditionally, the only way to remove Squamous Cell Carcinoma – cancer of the oropharynx which encompasses the tonsils and base of the tongue – has been to split the jaw, take out the cancer and repair the neck with tissue from the forearm.

This 10-hour procedure requires two surgical teams and often has complications. Patients are in hospital for at least three weeks and need months of rehabilitation to help them swallow and speak again.

Because the treatment is so invasive, many doctors try to avoid it using chemotherapy and radiotherapy instead. However, surgery is often the best chance of a cure.

The new one-hour technique called Transoral Robotic Surgery allows the cancer to be removed without splitting the jaw or taking tissue from other parts of the body. Instead, the tonsils are accessed through the mouth using a specially designed robotic machine.

Developed in the US in 2009 and now approved by the American Food and Drug Administration and licensed for use in the UK, it uses the Da Vinci robot to access this difficult to reach area.

It gives the surgeon greater precision, dexterity and accuracy while carrying out the procedure and the patient has no stitches. Infection rates are reduced which speeds up recovery rates, patients are in hospital for just a week and are able to swallow normally soon afterwards and require no long-term feeding tubes.

Neil Tolley, a Consultant Head and Neck Surgeon at the Wellington Hospital, who is now carrying out the new technique, says: “The mouth is a small place. The da Vinci robot allows access to anatomical sites and permits surgery to be performed which would otherwise be technically very difficult or impossible to perform conventionally.

“On the patients treated so far, the swallowing outcomes have been excellent with no need for a gastrostomy tube to feed them, yet the same cure rates have been achieved.”

Keith Hern – Battling throat cancer, chemotherapy, radiotherapy and NLP

Source: www.youtube.com

Keith Hern was diagnosed with throat cancer and his story is captured in the book Bangers and Mash. In this video Keith talks frankly and honestly about the moment that changed his life forever – when he found he had cancer.