Monthly Archives: November 2009

American Cancer Society, ENT and Allergy Associates once again partner to fight smoking, especially among teens

Source: www.earthtimes.org
Author: press release

The American Cancer Society and ENT and Allergy Associates, LLP (ENTA) are once again teaming up to bring a strong and relevant anti-smoking message to teens and ENTA patients through a strategic partnership that includes outreach to local high schools and patient education.

“The most effective way for us to fight cancer is to partner with systems in our communities to reach the largest number of people possible,” said Dee McCabe, Executive Vice President, American Cancer Society. “ENTA has been a great partner, reaches thousands of people a day, and truly is committed to improving health of their patients.”

“At ENTA, we see far too many patients-each and every week-afflicted with cancer…so our partnership with the American Cancer Society allows us to educate people about the dangers of smoking, and point them toward smoking cessation and cancer prevention” said Dr. Wayne Eisman, President of ENT and Allergy Associates. “We are delighted to do everything we possibly can to help the ACS fight smoking, particularly among young people.”

A key part of the alliance is ENTA’s support of the American Cancer Society’s Great American Smokeout, held on November 19th. Throughout the month of November, ENTA will offer patients materials on how to quit smoking in its 30 offices throughout the Greater New York and New Jersey area. Also, several ENTA doctors will speak at local high schools to teens about the dangers of smoking, how to deal with peer pressure, and how the tobacco industry targets its advertising to teens.

As part of the Great American Smokeout, ENTA is challenging students to create their own anti-smoking song and compete for a prize of $2,000. The contest is open to all public high school students throughout New York and New Jersey. The American Cancer Society Web site also includes financial benefits of quitting smoking, a cigarette calculator, and directions on how to become an advocate in the fight against the tobacco industry.

ENT and Allergy Associates has a clinical alliance with the Mount Sinai Medical Center for the treatment of patients with head and neck disorders, and has established a first-of-its kind program for head and neck cancer screening.

November, 2009|Oral Cancer News|

Early PET-CT predicts treatment response of head and neck cancer

Source: www.curetoday.com
Author: staff

In patients with advanced squamous cell carcinoma of the head and neck, negative findings on post-treatment positron emission tomography/computed tomography (PET-CT) predict a good treatment response, researchers say.

In 31 patients with clinical stage III and IV tumors treated with cisplatin and concurrent external beam radiotherapy, PET-CT was performed 6 to 8 weeks after therapy was completed, along with a comprehensive physical examination of the head and neck, as reported by Dr. James P. Malone, from the Southern Illinois School of Medicine, Springfield, and colleagues in the November Archives of Otolaryngology — Head and Neck Surgery.

Seventeen patients had evidence of persistent disease on physical exam, CT, and/or PET-CT, and these individuals had surgery for further evaluation. Fourteen patients had complete clinical responses, including no evidence of FDG uptake on PET-CT; these subjects were observed with routine follow-up.

According to the researchers, all but one of these 14 patients remained disease free at the primary tumor site during a median follow-up of 26 months.

Thus, the authors point out, the sensitivity of PET-CT was 83%, and its negative predictive value was “excellent” at 92% for detection of persistent disease at the primary tumor site. Because of a high false-positive rate, specificity was low at 54%, with a positive predictive value of 31%.

Dr. Malone’s group attributes the high false-positive rate to inflammation related to recent treatment.

The investigators also note that 5 of 16 patients with abnormal FDG update developed local disease. “For patients with abnormal FDG uptake at the primary site on early PET-CT and no evidence of local disease on physical examination, we recommend close outpatient follow-up with consideration of repeating PET-CT in 6 to 8 weeks or evaluation under anesthesia and biopsy of the primary tumor site,” they said.

“On the basis of this study, PET-CT performed 6 to 8 weeks after the completion of (chemoradiotherapy) for advanced squamous cell carcinoma of the head and neck is a valuable tool for measuring treatment response and facilitating clinical decision making,” the research team concludes.

November, 2009|Oral Cancer News|

Distinct population of highly malignant cells in a head and neck squamous cell carcinoma cell line established by xenograft model

Source: Journal of Biomedical Science
Author: Staff

The progression and metastasis of solid tumors, including head and neck squamous cell carcinoma (HNSCC), have been related to the behavior of a small subpopulation of cancer stem cells. Here, we have established a highly malignant HNSCC cell line, SASVO3, from primary tumors using three sequential rounds of xenotransplantation.

SASVO3 possesses enhanced tumorigenic ability both in vitro and in vivo. Moreover, SASVO3 exhibits properties of cancer stem cells, including that increased the abilities of sphere-forming, the number of side population cells, the potential of transplanted tumor growth and elevated expression of the stem cell marker Bmi1.

Injection of SASVO3 into the tail vein of nude mice resulted in lung metastases. These results are consistent with the postulate that the malignant and/or metastasis potential of HNSCC cells may reside in a stem-like subpopulation.

Authors:
Chi-Yuan ChenShih-Hwa ChiouChih-Yang HuangChia-Ing JanShu-Chun LinMing-Long TsaiJeng-Fan Lo

Source:
Journal of Biomedical Science 2009, 16:100

November, 2009|Oral Cancer News|

Presence of rash associated with improved survival in patients receiving adjuvant Erbitux® for locally advanced head and neck cancer

Source: professional.cancerconsultants.com
Author: staff

A multicenter randomized trial has shown that patients with locoregionally advanced head and neck cancer receiving adjuvant Erbitux® (cetuximab) and radiotherapy who develop a rash have a better survival than patients receiving this therapy who don’t develop a rash. The details of this five-year follow-up of a Phase III randomized study were published early online in the Lancet Oncology on November 7, 2009.[1]

Standard treatment for head and neck cancer is largely determined by the stage and by the specific locations within the head or neck area where the cancer has spread. The patient’s overall medical condition is also a deciding factor. Treatment typically consists of radiation therapy, chemotherapy with surgery, or surgery alone.

Erbitux is a monoclonal antibody that binds to the epithelial growth factory receptor (EGFR) and inhibits the receptor’s effects on cellular replication. Erbitux is currently FDA-approved for treatment of head and neck cancer. Researchers involved in an international study have previously reported that the addition of Erbitux to radiation therapy improves survival over radiation therapy alone in the treatment of head and neck cancer. The results of this randomized trial with a 54-month follow-up were published in the February 9, 2006, issue of the New England Journal of Medicine. This trial included 424 patients; approximately half were treated with Erbitux plus high-dose radiation therapy, and the other half received high-dose radiation therapy alone. This study now has a follow-up of more than five years.

The Following table summarizes some of the findings of this trial.

Table 1: Effect of the Addition of Erbitux to Radiotherapy in Head and Neck Cancer

table

Rash and reactions at the site of infusions were the most common side effects experienced by patients treated with Erbitux. Patients receiving Erbitux who experience a rash had 51% improvement in overall survival compared with patients receiving Erbitux without a rash.

The researchers concluded that the addition of cetuximab to radiation therapy is well tolerated and improves overall survival compared with radiation therapy alone in the treatment of patients with head and neck cancer.

Comments: This study with a longer follow-up demonstrates the lasting effect of adding Erbitux to radiotherapy for treatment of head and neck cancer. The association of rash with an increased response is of major interest.

Reference:
[1] Bonner JA, Harari PM, Giralt J, et al. Radiotherapy plus cetuximab for locoregionally advanced head and neck cancer: 5-year survival data from a phase 3 randomised trial, and relation between cetuximab-induced rash and survival. Lancet Oncology [early online publication]. November 7, 2009.

November, 2009|Oral Cancer News|

Neck response to chemoradiotherapy

Source: Arch Otolaryngol Head Neck Surg. 2009;135(11):1133-1136
Author: Alexander Langerman, MD et al.

Complete Radiographic Response Correlates With Pathologic Complete Response in Locoregionally Advanced Head and Neck Cancer

Objective:
The role of neck dissection following chemoradiotherapy (CRT) for locoregionally advanced head and neck cancer is an area of active debate. Patients who have a complete radiographic response may not need dissection, and the extent of neck dissection necessary for those patients with residual disease is unclear.

Design:
Retrospective review of data from a prospectively collected database of patients with locoregionally advanced head and neck cancer treated as part of a phase 2 study of induction chemotherapy followed by concurrent CRT. The results of post-CRT neck computed tomography (CT) imaging and pathologic analysis of the neck dissection specimens were compared to evaluate correlation between radiographic and pathologic response.

Results:
Forty-nine patients underwent 61 hemineck dissections. Overall, 209 neck levels were dissected. Radiologic complete response in the neck was achieved in 39 patients, all of whom had pathologic specimens negative for tumor cells. Ten patients (20%) had a total of 14 neck levels with residual disease on CT imaging. Five (50%) of these 10 patients were found to have residual tumor cells on pathologic analysis. Tumor cells were contained only to those levels found positive on CT imaging; they were present in 7 (50%) of the 14 positive levels.

Conclusions:
Neck levels with residual disease on post-CRT CT imaging warrant removal. However, neck levels without evidence of disease on post-CRT CT imaging are unlikely to harbor cancer, which lends further support to the concept of basing neck dissection on post-CRT staging and performance of limited neck dissections for patients with limited residual disease.

Introduction:
The role of neck dissection following chemoradiotherapy (CRT) for locoregionally advanced head and neck cancer is an area of active debate. Traditionally, many centers recommended a planned neck dissection for all patients based on the extent of pretreatment neck adenopathy. This was supported by studies that demonstrate improved survival in patients who undergo posttreatment neck dissection.1-2 Proponents argue that post-CRT neck dissection may remove subclinical residual nodal disease within treated lymph nodes, even in the setting of a complete radiographic response. However, other studies demonstrated no survival advantage of neck dissection for those patients with complete radiographic response,3-4 and, in a pooled Radiation Therapy Oncology Group analysis, post-CRT neck dissection was associated with long-term toxicity.5

Throughout this debate, few studies have correlated radiographic and pathologic response to determine potential response to therapy. Therefore, we analyzed a population of patients with locoregionally advanced head and neck cancer uniformly treated with induction chemotherapy and concurrent CRT and post-CRT neck dissection, to correlate posttherapy radiographic findings to pathologic response.

Methods:
From November 1, 1998, to August 31, 2002, 222 patients with locoregionally advanced head and neck cancer (American Joint Committee on Cancer stage IV, except stage III base of tongue and hypopharynx cancers) were treated as part of a University of Chicago multi-institutional phase 2 study of induction chemotherapy followed by concurrent CRT. Patients with N2 or greater neck disease were recommended to undergo post-CRT neck dissection regardless of response to therapy. From the entire patient cohort, we restricted this analysis to patients treated at the University of Chicago (n = 130).

Treatment methods and outcomes for all patients have been previously reported.6 Briefly, all patients were treated with 2 cycles of induction carboplatin/paclitaxel followed by 5 cycles of concomitant hydroxyurea/fluorouracil/paclitaxel and 72 to 75 Gy of radiation. Patients underwent a post-CRT panendoscopy and biopsy of the primary site with frozen section analysis. Neck dissections were performed at the time of panendoscopy for patients with a complete response at the primary site.

Following CRT, all patients were restaged clinically and radiologically in a multidisciplinary conference with a contrast-enhanced computed tomography (CT) imaging of the head and neck. Patients with pretreatment N2 or greater neck disease or residual posttreatment disease underwent selective neck dissection. The extent of dissection was dictated by primary site and extent of prechemoradiation neck disease rather than postchemoradiation neck staging. At the time of the trial, a single, dedicated head and neck pathologist interpreted all neck dissection specimens.

Correlation of radiographic and pathologic response was performed in the following manner: post-CRT radiographic response for each patient was identified from study records. For completeness, CT imaging of patients with any evidence of lymphadenopathy was reviewed on a standard picture archiving and communication system workstation (Koninklijke Philips Electronics NV, Eindhoven, the Netherlands) that uses soft tissue windows. The location of pre-CRT and post-CRT lymphadenopathy was recorded for each patient. Lymphadenopathy was evaluated by means of criteria reviewed by Som.7 Nodes greater than 1 cm, with ill-defined or enhanced borders, or with areas of low attenuation suggestive of necrosis were considered pathologic. A complete response was defined as resolution of all evidence of radiographic disease. A partial response was defined as at least a 30% decrease in the sum of the longest diameter of the involved lymph node.

Detailed pathology reports of neck dissection specimens were reviewed for evidence of viable tumor cells. The location of the viable tumor cells was recorded for each patient and compared to the location of pre-CRT and post-CRT lymphadenopathy.

Data were entered onto an Excel spreadsheet (Microsoft Corporation, Redmond, Washington). The 2-tailed t test was used to determine statistical significance with a threshold of P.05. This study was conducted with the approval of the institutional review board of the parent trial.6

Results:
Of the 130 patients treated at the University of Chicago, 94 (72.3%) were initially staged with N2 or greater disease. Sixty-five of these 94 patients (69.1%) had complete response at the primary site. Of these 65 patients, 13 (20.0%) had neck dissections performed before referral to our institution for CRT and received no further neck treatment. The remaining 52 (80.0%) underwent planned neck dissection at a median of 10 weeks after CRT. Of these, 3 patients had incomplete neck level data on pathologic records and were excluded from further study. The remaining 49 patients underwent 61 hemi-neck dissections of 209 neck levels. The prechemoradiation neck stage was N2a in 2 (4.1%), N2b in 23 (46.9%), N2c in 10 (20.4%), and N3 in 14 (28.6%). No eligible patients refused neck dissection.

Radiographic Response to CRT
Radiologic complete response in the neck was achieved in 39 of 49 patients (79.6%), and 10 patients had radiographic residual disease. Radiographic residual neck disease was identified in 14 neck levels, most commonly in level II: 1 (7.0%) in level I, 9 (64.0%) in level II, 1 (7.0%) in level III, 1 (7.0%) in level IV, and 2 (14.0%) in level V.

Pathologic Response to CRT:
All patients with a radiographic complete response also had a pathologic complete response. Five (50.0%) of the 10 patients with radiographic residual disease were found to have residual tumor cells on pathologic analysis. Tumor cells were contained only to those levels found positive on CT imaging, being present in 7 (50.0%) of the 14 positive levels but none of the 26 negative levels in these patients. Tumor cells were found only in level I in 1 patient, only in level II in 3 patients, and in level II/III/IV in 1 patient (Figure). Pathologic positivity was not related to pre-CRT N stage (P = .24).

nrtc_ocf
Figure. Distribution of suspicious-appearing lymph nodes on postchemoradiation computed tomography imaging and positive pathologic diagnosis in 10 patients who underwent neck dissection. Gray areas represent extent of neck dissection. P indicates pathologically positive; N pathologically negative.

Comment:
The necessity and extent of neck dissection following chemoradiation is controversial. At our institution and many others, the traditional method has been to perform a selective neck dissection appropriate for the primary site unless more extensive disease mandates more extensive dissection. For instance, an oral cavity tumor would warrant a supraomohyoid (levels I-III) neck dissection in the absence of disease beyond these levels. These criteria have been further refined by limitation of the neck dissection to only those patients with pre-CRT N2 or greater disease or residual disease post-CRT. In other words, in the majority of cases, the extent of dissection was dictated by primary site and extent of pre-CRT neck disease rather than post-CRT neck staging.

In the present study, all patients with a radiographic complete response also had a pathologic complete response. In those with a radiographic partial response, pathologically viable tumor cells were found in 50.0% of patients. Furthermore, pathologic residual disease was limited to levels restaged as positive on CT imaging.

Other series have reported a correlation of radiographic and pathologic complete response. Robbins et al8 analyzed 54 patients with advanced head and neck cancer who underwent neck dissection for evidence of persistent neck disease limited to a single level after combined intra-arterial chemotherapy and radiation. Their data demonstrated pathologically positive neck disease limited only to those neck levels that remained clinically positive by CT imaging in 52 of 54 patients (96.3%).

The above data, plus those included in this current report, suggest that radiographic residual neck disease should be dissected and that radiographically negative neck levels are unlikely to harbor disease. Although both the present data set and that of Robbins et al8 used CT imaging for restaging, considerable evidence has emerged in favor of positron-emission tomography (PET)9 or PET-CT.10-11 To the contrary, some have argued that PET adds little to CT.12 The relative merits of these modalities are beyond the scope of this article, but based on our and those of others, it appears that in centers where PET is unavailable or not used routinely, CT may be adequate to help surgeons decide whether or not to perform a post-CRT neck dissection.

Our data also suggest that a neck dissection limited to levels of radiographic involvement (ie, superselective neck dissection) constitutes adequate therapy following CRT. This concept was first suggested by Robbins et al.8 In their series, of the 2 patients whose CT scans failed to predict residual neck disease, 1 had neck disease in a contiguous level, which prompted the argument that it would have been discovered at the time of surgery, and which leaves only 1 patient for whom superselective neck dissection would have been inadequate. Robbins et al also reported that 100% of the radiographically positive neck disease was pathologically positive. Our data support this assertion because no patient was found to have disease other than at radiographically evident levels.

In a review article on management of the neck following radiation, Medina et al13 summarized what has remained otherwise unpublished data on 55 patients who underwent neck dissection for clinically or radiologically residual disease in the neck following radiation with or without chemotherapy. The full details with regard to neck level positivity were not reported, but all 5 patients with disease limited to level II on restaging had no pathologically positive disease beyond level II. Data were less convincing for patients with disease in multiple levels on posttherapy restaging, with 2 of those 10 patients having disease beyond that predicted by restaging. However, it is possible that not all of these patients were restaged radiographically. Overall, the yield of pathologically viable-appearing disease in the neck dissection specimens was 27%. Based on this data, Medina et al argued that disease limited to level II may be appropriate for superselective neck dissection.

The reliability of research into the response of the neck (and primary site) to CRT ultimately hinges on the pathologic interpretation in tissue from post-CRT surgical extirpation and two of us (A.L. and K.M.S.) are currently preparing a forthcoming formal review of the pathology of tumor response to CRT. We believe markers that indicate the progression of host response (eg, inflammatory markers and degree of fibrosis) as well as aspects of the tumor nidus (eg, nuclear changes and necrosis) can and should be incorporated into guidelines to standardize the interpretation of these specimens. Further careful study of radiographic partial responders without pathologic residual disease is warranted to identify characteristics that could limit surgery to those with higher risk of pathologic positivity.

This study is limited by its retrospective nature. Additionally, because the patients in this study all underwent neck dissections, the natural history of the neck disease cannot be determined, and it is unknown how the tumor detected in the neck pathologic specimens would have behaved in vivo. Furthermore, although a thorough pathologic analysis was conducted at the time of surgical extirpation, it is always possible that microscopic disease was undetected. Finally, it should be noted that, by protocol, only those patients who had a complete response at their primary site underwent the planned neck dissections analyzed in this study, and these results may not be applicable to patients who failed CRT at the primary site.

Conclusions:
The high percentage of tumor cells in radiographically positive neck specimens suggests that neck levels with residual disease on post-CRT CT imaging warrant removal. Furthermore, neck levels without evidence of disease on post-CRT CT are unlikely to harbor cancer, which lends further support to the concept of basing neck dissection on post-CRT neck staging and performing superselective neck dissections for patients with limited residual disease.

References:
1. Brizel DM, Prosnitz RG, Hunter S; et al. Necessity for adjuvant neck dissection in setting of concurrent chemoradiation for advanced head-and-neck cancer. Int J Radiat Oncol Biol Phys. 2004;58(5):1418-1423. FULL TEXT | ISI | PUBMED
2. McHam SA, Adelstein DJ, Rybicki LA; et al. Who merits a neck dissection after definitive chemoradiotherapy for N2-N3 squamous cell head and neck cancer? Head Neck. 2003;25(10):791-798. FULL TEXT | ISI | PUBMED
3. Liauw SL, Mancuso AA, Amdur RJ; et al. Postradiotherapy neck dissection for lymph node–positive head and neck cancer: the use of computed tomography to manage the neck. J Clin Oncol. 2006;24(9):1421-1427. FREE FULL TEXT
4. Clayman GL, Johnson CJ II, Morrison W, Ginsberg L, Lippman SM. The role of neck dissection after chemoradiotherapy for oropharyngeal cancer with advanced nodal disease. Arch Otolaryngol Head Neck Surg. 2001;127(2):135-139. FREE FULL TEXT
5. Machtay M, Moughan J, Trotti A; et al. Factors associated with severe late toxicity after concurrent chemoradiation for locally advanced head and neck cancer. J Clin Oncol. 2008;26(21):3582-3589. FREE FULL TEXT
6. Salama JK, Stenson KM, Kistner EO; et al. Induction chemotherapy and concurrent chemoradiotherapy for locoregionally advanced head and neck cancer: a multi-institutional phase II trial investigating three radiotherapy dose levels. Ann Oncol. 2008;19(10):1787-1794. FREE FULL TEXT
7. Som PM. Detection of metastasis in cervical lymph nodes: CT and MR criteria and differential diagnosis. AJR Am J Roentgenol. 1992;158(5):961-969. FREE FULL TEXT
8. Robbins KT, Shannon K, Vieira F. Superselective neck dissection after chemoradiation: feasibility based on clinical and pathologic comparisons. Arch Otolaryngol Head Neck Surg. 2007;133(5):486-489. FREE FULL TEXT
9. Isles MG, McConkey C, Mehanna HM. A systematic review and meta-analysis of the role of positron-emission tomography in the follow up of head and neck squamous cell carcinoma following radiotherapy or chemoradiotherapy. Clin Otolaryngol. 2008;33(3):210-222. FULL TEXT | ISI | PUBMED
10. Rabalais AG, Walvekar R, Nuss D; et al. Positron emission tomography-computed tomography surveillance for the node-positive neck after chemoradiotherapy. Laryngoscope. 2009;119(6):1120-1124. FULL TEXT | ISI | PUBMED
11. Nayak JV, Walvekar RR, Andrade RS; et al. Deferring planned neck dissection following chemoradiation for stage IV head and neck cancer: the utility of PET-CT. Laryngoscope. 2007;117(12):2129-2134. FULL TEXT | ISI | PUBMED
12. Tan A, Adelstein DJ, Rybicki LA; et al. Ability of positron-emission tomography to detect residual neck node disease in patients with head and neck squamous cell carcinoma after definitive chemoradiotherapy. Arch Otolaryngol Head Neck Surg. 2007;133(5):435-440. FREE FULL TEXT
13. Medina JE, Vasan NR, Krempl GA. Management of the neck after treatment with radiation with or without chemotherapy. Curr Treat Options Oncol. 2007;8(3):261-264. FULL TEXT | PUBMED

Authors:
Alexander Langerman, MD; Colleen Plein, BA; Everett E. Vokes, MD; Joseph K. Salama, MD; Daniel J. Haraf, MD; Elizabeth A. Blair, MD; Kerstin M. Stenson, MD

Authors’ affiliations:
Author Affiliations: Sections of Otolaryngology–Head and Neck Surgery (Drs Langerman, Blair, and Stenson and Ms Plein) and Hematology–Oncology (Dr Vokes), Department of Radiation and Cellular Oncology (Drs Vokes, Salama, and Haraf), and Department of Surgery, Cancer Research Center (Drs Vokes, Salama, and Haraf), University of Chicago, Chicago, Illinois.

Author Contributions:
Dr Langerman had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Langerman, Vokes, Haraf, Blair, and Stenson. Acquisition of data: Langerman, Plein, and Haraf. Analysis and interpretation of data: Langerman, Plein, Salama, and Stenson. Drafting of the manuscript: Langerman. Critical revision of the manuscript for important intellectual content: Plein, Vokes, Salama, Haraf, Blair, and Stenson.

November, 2009|Oral Cancer News|

Erbitux recognized by ASCO as a 2009 major cancer advance as first SCCHN treatment to improve survival in 30 years

Source: www.vwd.de
Author: press release

The American Society of Clinical Oncology (ASCO) has once again recognized Erbitux® (cetuximab) as one of the major clinical cancer advances of 2009. This year Erbitux was selected by ASCO for providing the first significant increase in survival for 30 years in the treatment of patients with first-line recurrent and/or metastatic squamous cell carcinoma of the head and neck(SCCHN).1

ASCO Clinical Advances Report1
The ASCO report, ‘Clinical Cancer Advances 2009: Major Research Advances in Cancer Treatment, Prevention and Screening’, published this week in the Journal of Clinical Oncology, is an independent assessment of the most significant clinical cancer research studies of the past year.

Erbitux was singled out for the pivotal first-line SCCHN study, the first randomized trial in 30 years to identify a regimen that increases survival for patients with recurrent and/or metastatic SCCHN. The report commented that, “The ability to improve overall survival with chemotherapy has proven elusive over the last 30 years in several randomized trials comparing different chemotherapy regimens in this setting. Thus, the results of this trial are particularly noteworthy and are changing clinical practice.”

This is the second consecutive year that Erbitux has featured in the ASCO ‘Advances’ list.3 In 2008 it was recognized for extending survival in the first-line treatment of NSCLC and for the role of KRAS tumor status in predicting whether patients with newly diagnosed metastatic colorectal cancer will respond to Erbitux.2

“Merck Serono is honored that Erbitux is recognized by ASCO two years in a row, and across three different disease areas – colorectal cancer, lung cancer and now head and neck cancer, as a major clinical advance,” commented Dr. Wolfgang Wein, Executive Vice President, Oncology, Merck Serono, a division of Merck KGaA, Darmstadt, Germany. “This latest acknowledgement from ASCO is a tribute to the role Erbitux now plays as a gold standard therapy in first-line recurrent and/or metastatic SCCHN”.

The study demonstrated that SCCHN patients treated with Erbitux plus chemotherapy experienced the following improvements, compared to chemotherapy alone:3
– Median overall survival (OS) increased by nearly 3 months (10.1 vs. 7.4 months; p=0.04), equating to a 20% reduction in the risk of death (Hazard Ratio [HR] 0.80) during the study period
– 46% increase in median progression-free survival (5.6 vs. 3.3 months; p <0.001)
– Almost doubling of response rate (36% vs. 20%; p<0.001)
– Based on the EXTREME study, the ESMO Guidelines Working Group earlier this year recommended Erbitux as the only treatment with a grade of recommendation ‘A’ and level of evidence ’I’^4

Long-Term Survival Results in Locally Advanced SCCHN
Also this week, the 5-year survival data from the Bonner trial for Erbitux in locally advanced (LA) SCCHN were published in the Lancet Oncology. The Phase III Bonner trial formed the basis for the initial Erbitux LA SCCHN license, granted in Europe in 2006. This new long-term analysis provides further support for the combination of Erbitux and radiotherapy in the treatment of LA SCCHN, demonstrating:^5
– Almost half of patients receiving Erbitux plus radiotherapy are still alive at 5 years – in contrast to only one third of patients receiving  radiotherapy alone (45.6% vs. 36.4%; p=0.018)
– Adding Erbitux to radiotherapy leads to a sustained survival benefit (OS
49.0 vs. 29.3 months; HR 0.725; p=0.018)
– The development of prominent skin rash is associated with an additional survival benefit leading to a reduction in the risk of death of 51%

Head and Neck Cancer
Head and neck cancer includes cancers of the tongue, mouth, salivary glands, pharynx, larynx, sinuses and other sites located in the head and neck area. It is estimated that there are around 143,000 new cases of head and neck cancer and more than 68,000 deaths due to the disease in Europe each year.^6 About 90% of head and neck cancers are of the squamous cell variety^7 and nearly all express the epidermal growth factor receptor which is critical for tumor growth.8 About 40% of patients with head and neck cancer have recurrent and/or metastatic SCCHN.9 At least 75% of all head and neck cancers are attributed to two major risk factors, smoking and alcohol consumption.10

References
1 . Petrelli NJ, et al. J Clin Oncol 2009;ePub ahead of print November 6, 2009.
2 . Winer E, et al. J Clin Oncol 2009;27(5):812-26.
3 . Vermorken JB, et al. N Engl J Med 2008;359:1116-27.
4 . Licitra L, & Felip E. Ann Oncol 2009;20(Suppl 4):iv121–iv122.
5 . Bonner J, et al. Lancet Oncol 2009;ePub ahead of print November 7, 2009.
6 . GLOBOCAN 2002 (www-dep.iarc.fr), accessed November 2009.
7 . Vermorken J. Ann Oncol 2005;16(Suppl 2):ii258-ii264.
8 . Grandis JR & Tweardy DJ. Cancer Res 1993;53(15):3579-84.
9 . Lefebvre J-L. Ann Oncol 2005;16(Suppl 6):vi7-vi12.
10 . Hashibe M, et al. J Natl Inst 2007;99:777-89

November, 2009|Oral Cancer News|

Terminal cancer patient is given the all clear

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

A mouth cancer patient who was told he had only a year to live is celebrating after being given the all clear from doctors.

In May this year, Brian Barford was given the awful news after he had been referred by a dentist to Northampton General Hospital where he was told he had mouth cancer.

The 66-year-old said: “My mouth had been bleeding but I had no other signs. I had no idea – there had been no swelling or anything.

“I saw the consultant who said the tumour was too near the vital organs to operate on and there was nothing they could do. It was just a matter of time.

“They told me I had around a year to live.

“It hit me like a ton of bricks.

“I accepted it, though I was never going to give up, but I thought, ‘I’m 66, and I’ve had a good life.'”

Mr Barford, from Kings Heath, Northampton, decided to enjoy the time he had left and spend his days with loved ones. He went running, drank beer and, following a two-week course of radiotherapy, took a well-earned holiday with family and friends.

On hearing the news Mr Barford had been diagnosed with cancer, colleagues at his former workplace, Phoenix Paving LTD, in Kettering, took their old workmate for a day to remember, watching the cricket at Lord’s.

With the onslaught of cancer, his weight plummeted from 14 to 11 stone. His wife Susan, aged 56, gave up her job as an assistant carer to look after him.

But last week, during a routine check-up, he requested another scan … with miraculous results.

Brian simply wanted to know if the tumour had grown, but the consultant had other news.

Mr Barford said: “The doctor came over and couldn’t stop smiling. He said to me ‘It’s gone. There’s no trace of it.'”

He added: “I’m dumbfounded. I’m so pleased. I don’t think it’s sunk in yet.

“There are lots of people who aren’t so lucky, but you can never give up hope.

“I want to enjoy life and hopefully me and Susan will have a few more years together.

“I’d like to get back to work if I can too. I like to keep busy.”

November, 2009|Oral Cancer News|

Smokeless, not safe

Source: www.sltrib.com
Author: Tribune editorial

Tobacco-product marketers face an uncommon business problem: They have to lure new customers to replace the nearly half-million Americans who are killed by their products each year.

These folks are smart or, should we say, devious. They know that some people never start smoking simply because they don’t like the smell on their clothing and their breath, or because laws prevent them smoking indoors and they don’t want to face the social stigma associated with lighting up outdoors or chewing and spitting. And some smart and determined smokers are able to quit for the same reasons.

So, these clever marketers have come up with new tobacco products that smell minty, produce no smoke or need to spit, and can be used discreetly. They claim the new smokeless tobacco isn’t aimed at teenagers, but the evidence clearly indicates otherwise. They have catchy names like Snus, Orbs and Stride and come packaged in brightly colored, cell-phone-size containers. Some look and taste like candy. They can be carried and used without parents or teachers catching on.

And they contain so much highly addictive nicotine — triple the amount in cigarettes — and they’re so easy to use, that once a kid gets hooked, he or she usually stays hooked. Even better for tobacco pushers, they often move on to cigarettes once they’re addicted, and studies show the younger people are when they start smoking, the harder it is to quit.

For tobacco companies, it looks like problem solved.

But these new killers, being test-marketed in Columbus, Ohio; Portland, Ore.; and Indianapolis, Ind., are creating a new set of health problems for users and for taxpayers who will have to help pay their medical bills. Because these innocent-looking products can cause disfiguring and sometimes fatal mouth and throat cancers. And, since their toxins are carried throughout the body, they contribute to heart disease, stroke and cancers afflicting other organs, including liver cancer, which has an overall five-year survival rate of only 10 percent.

Unintended victims of the new smokeless products are children and toddlers who could find an open container and ingest a dangerous number of the candy lookalikes. The companies tout their containers as child-proof, but as parents can attest, that doesn’t mean children won’t find a way into them. A 1-year-old could become seriously ill or even die from ingesting as few as 10 of the mint-like Camel Orbs.

These dangerous products have passed no clinical trials for safety, nor do manufacturers have to reveal their ingredients. Altogether, they are a recipe for public-health disaster and should be banned.

November, 2009|Oral Cancer News|

Medicines to deter some cancers are not taken

Source: www.nytimes.com
Author: Gina Kolata

Many Americans do not think twice about taking medicines to prevent heart disease and stroke. But cancer is different. Much of what Americans do in the name of warding off cancer has not been shown to matter, and some things are actually harmful. Yet the few medicines proved to deter cancer are widely ignored.

Take prostate cancer, the second-most commonly diagnosed cancer in the United States, surpassed only by easily treated skin cancers. More than 192,000 cases of it will be diagnosed this year, and more than 27,000 men will die from it.

And, it turns out, there is a way to prevent many cases of prostate cancer. A large and rigorous study found that a generic drug, finasteride, costing about $2 a day, could prevent as many as 50,000 cases each year. Another study found that finasteride’s close cousin, dutasteride, about $3.50 a day, has the same effect.

Nevertheless, researchers say, the drugs that work are largely ignored. And supplements that have been shown to be not just ineffective but possibly harmful are taken by men hoping to protect themselves from prostate cancer.

As the nation’s war on cancer continues, with little change in the overall cancer mortality rate, many experts on cancer and public health say more attention should be paid to prevention.

But prevention has proved more difficult than many imagined. It has been devilishly difficult to show conclusively that something simple like eating more fruits and vegetables or exercising regularly helps. And, as the response to the prostate drugs shows, people are not enthusiastic about taking anticancer pills, or are worried about side effects or not really convinced the drugs work. Others are just unaware of them.

And prostate cancer is not unique. Scientists have what they consider definitive evidence that two drugs can cut the risk of breast cancer in half. Women and doctors have pretty much ignored the findings.

Companies have taken note, saying that it makes little economic sense to spend decades developing drugs to prevent cancer. The better business plan seems to be looking for drugs to treat cancer. That is a sobering lesson, said Dr. Ian M. Thompson Jr., chairman of the urology department at the University of Texas Health Science Center in San Antonio.

“A scientific discovery that is very clear cut and that is not implemented by the public is a tragedy,” he said.

Few Sure Things
A few ways are known for sure to prevent cancer; the biggest is to avoid cigarette smoking. That alone would drop the cancer death rate by a third. No other measure comes close.

Another huge success, for breast cancer, is to avoid taking estrogen and progestin at menopause. Sales of those drugs plummeted in 2002 after a federal study, the Women’s Health Initiative, concluded that they did not prevent heart disease and might increase breast cancer. The next year, the breast cancer rate dropped by 15 percent after having steadily increased since 1945.

The vaccine for human papilloma virus, protects against most strains of the virus, which causes cervical cancer.

But other measures that are often assumed — and marketed — as ways to prevent cancer may not make much difference, researchers say.

For example, public health experts for years recommended eating five servings of fruits and vegetables a day to prevent cancer, but the evidence is conflicting, at best suggestive, and far from definitive.

Low-fat diets were long thought to prevent breast cancer. But a large federal study randomizing women to a low-fat or normal diet and looking for an effect in breast cancer found nothing, said its director, Ross L. Prentice of the Fred Hutchinson Cancer Research Center in Seattle.

Fiber, found in fruits, vegetables and grains, is often thought to prevent colon cancer, even though two large studies found no effect.

“We thought we would show relationships that were strong and true,” said Dr. Tim Byers, professor of epidemiology at the Colorado School of Public Health, “particularly for dietary choices and food and vegetable intake. Now we have settled into thinking they are important but it’s not like saying you can cut your risk in half or three-quarters.” Others wonder whether even such qualified support is misplaced.

There has to be a reason the research disappointed, said Colin B. Begg, chairman of the department of epidemiology and biostatistics at Memorial Sloan-Kettering Cancer Center. Perhaps the crucial time to intervene is early in life.

“That’s one possibility,” Dr. Begg said. “The other is that it’s all sort of nonsense to begin with.”

Many hold out hope for exercise or weight loss. Studies have associated strenuous exercise with less cancer. But that is the same sort of evidence that misled scientists about aspects of diet.

“I think it’s wishful thinking,” said Dr. Susan Love, a breast surgeon and president of the Dr. Susan Love Research Foundation. “We would like things to be more in our control. I think that’s part of it. And in the absence of anything else, what do we tell women about how to prevent breast cancer? We tell them to exercise and eat a good diet.”

As for obesity, researchers differ. Studies that observed large numbers of people often found that fatter people have more cancer. But many of the correlations are weak, and different studies have pointed to different cancers, raising questions about whether some of the effects are real.

Dr. Otis W. Brawley, chief medical officer of the American Cancer Society, said he was convinced. The strongest link, he and others say, is with obesity and breast cancer. But there, Dr. Brawley says, the crucial period may occur early in life — girls who gain weight when they are young, he said, tend to start menstruating earlier, which increases their breast cancer risk because it adds years of exposure to the body’s estrogen. It may be that weight loss in adulthood does not help.

“We have very little evidence that losing weight or changing diet reduces risk of cancer,” he said. “It is likely that it takes years to effect a change in risk. We do have data that the change in diet decreases cardiovascular disease risk, so it’s easier to advocate diet change.”

Others, like Donald A. Berry, head of the division of quantitative sciences at the University of Texas M. D. Anderson Cancer Center, are dubious about blaming obesity for cancer rates. If there is a risk, Dr. Berry said, he suspects it is small. The studies are relying on correlations — they cannot assess cause and effect. And studies that come up with such associations are likely to be published, even though often the associations turn out to be spurious. That means, Dr. Berry said, that “the false-positive rate skyrockets.”

Still, Dr. Prentice said, disheartening as the findings have been, it would be a mistake to give up on lifestyle changes. Instead, he said, perhaps it is time to rethink the way studies are done.

“This should be a stimulus to our research community to say, How can we conduct observational studies in a way to reveal more reliable information?” Dr. Prentice said.

Diet and exercise, he added, “are likely quite important, but we just aren’t getting the answers.”

Great Hopes Dashed
Dr. Peter Greenwald knows the dashed hopes of cancer prevention research firsthand. As far back as 1981, when he arrived at the National Cancer Institute to direct “cancer prevention and control,” Dr. Greenwald began thinking about testing whether simple measures, like vitamin supplements, could prevent common cancers.

He focused on what looked like it could be a sure thing — beta carotene, found in orange fruits and vegetables as well as in green leafy vegetables.

The body converts beta carotene to vitamin A, which can prevent cancer in rats. People eating the most fruits and vegetables had less cancer. And the more beta carotene in a person’s blood, the lower the cancer risk. Lung cancer seemed particularly vulnerable to beta carotene’s effects, particularly in smokers and former smokers.

What was needed was cause-and-effect evidence, studies showing that if people bolstered their beta carotene and vitamin A levels, they would be protected from cancer. The cancer institute decided to take it on with two large studies.

But not only did the supplements not work, but there was evidence that beta carotene might actually increase cancer risk in smokers.

Dr. Greenwald and his colleagues still held out hope for vitamins and minerals as cancer preventatives. So his group proposed the largest cancer prevention clinical trial ever tried, involving 35,000 men 50 and older. This time, the idea was that vitamin E and selenium might prevent prostate cancer.

Once again, there was presumptive evidence. But this time it was harder to persuade scientists to go ahead. After the beta carotene and vitamin A studies, several other studies had also failed to find evidence that food components or special diets could prevent cancer.

“By this time, a lot of people were very concerned,” said Dr. Scott M. Lippman, an oncologist at M. D. Anderson. He argued that the huge study had to be done. The supplements were being promoted for “prostate health,” and the evidence that they might actually work was tantalizing.

The selenium and vitamin E study ended early. Once again, there was no protection from cancer, and there were hints the supplements might be causing cancer. Once again, the great hope turned into a stunning disappointment.

Prevention researchers say they are left sadder but wiser.

“Over the years, I’ve grown more skeptical and more cautious,” said Dr. Meir J. Stampfer, a professor of nutrition and epidemiology at the Harvard School of Public Health. “Findings get reported in the literature, and the more extreme findings tend to excite the imagination. Then, as evidence accumulates, those findings are not confirmed.”

Dr. Stampfer remains optimistic, though, pointing to the story of heart disease, where softer evidence eventually led to discoveries that measures like lowering blood pressure and cholesterol could prevent disease. An amazing decline in illness and death resulted. “Cancer is harder,” Dr. Stampfer said, but he added that it is too soon to give up. Dr. Greenwald, too, has not given up. He still hopes a diet with fruits and vegetables, along with exercise and weight control, might help prevent cancer. But he knows the evidence is not definitive and scientists have been fooled before. As for Dr. Lippman, he said the field had suffered from an excess of premature enthusiasm, especially before the beta carotene studies.

“We were pulled into this,” he said. “People said, We’ve got it! There were incredibly high expectations that were, in retrospect, unrealistic.”

Claims That Go Too Far
David G. Schardt, a senior nutritionist with the Center for Science in the Public Interest, an advocacy group, likes to relax in front of his television set at night. But what he was seeing last winter made his blood boil.

“I would sit there watching network news and the ads would come on,” Mr. Schardt said. Bayer, advertising its One A Day vitamins, was saying the selenium in the pills might improve “prostate health.” And as he drove to his office in Washington, Mr. Schardt heard Bayer advertisements on the radio that actually mentioned prostate cancer.

“I couldn’t believe it,” he said. After all, the federal study had already shown that selenium was useless and might be harmful. Finally, on Oct. 1, Mr. Schardt and the Center for Science in the Public Interest filed a lawsuit.

Tricia McKernan, a Bayer spokeswoman, says the advertisements relied on the Food and Drug Administration’s “permitted qualified health claim that ‘selenium may reduce the risk of certain cancers,’ ” especially prostate cancer. The F.D.A. no longer permits that claim, Ms. McKernan noted. She said Bayer was revising its packaging and promotional materials for its One A Day Men’s and One A Day Men’s 50+ vitamins, removing references to selenium reducing prostate cancer risk.

But a subtle promotion of selenium and vitamin E by supplement makers goes on, with claims that the pills improve “prostate health” by increasing the body’s “antioxidant defenses.”

Dr. Thompson said he sees the lure of supplements when he counsels patients. “I can’t tell you how many times I talked to somebody about prostate cancer prevention,” he said. He gives the high-risk men a prescription for one of the drugs that work. But the men do not fill it.

Instead, he said, they are taking “prostate health” vitamins.

In 1990, Dr. Victor G. Vogel was at M. D. Anderson and had high hopes of changing the world. It just may be possible, he thought, to prevent many cases of breast cancer in women at high risk, a group that includes every woman over age 60, the time when the risk takes a sharp turn upward.

Dr. Vogel was to be an investigator in a huge study of 13,000 women that seemed to have everything going for it. It would test a drug, tamoxifen, an estrogen-blocker widely used to treat women with breast cancer. The studies showing the drug’s effects in breast cancer patients, though, had an unexpected bonus. It looked as if tamoxifen was also preventing new cancers in the opposite breast.

“By the time we got to 1990, there was just a huge amount of data,” Dr. Vogel said. The drug’s risks were well established and seemed well worth taking if the benefit was cutting cancer in half among women at high risk. Most side effects, like hot flashes, were temporary. But there also was a risk of blood clots similar to that conferred by birth control pills or estrogen used to relieve symptoms of menopause. And there were about two additional cases of uterine cancer per 1,000 women per year.

By 1998, the results were in. Tamoxifen cut the breast cancer rate in half. Similar studies in Britain and Italy, also involving high-risk women who had not had breast cancer, came to similar conclusions. And women did not have to take the drug for a lifetime — they needed just five years of therapy.

Dr. Vogel was ecstatic.

“If I had told you in 1990 that in 10 years I would have a pill that would cut the risk of breast cancer in half, you wouldn’t have believed me,” he said.

But, he said, to his shock, “The world said, So what?”

“We were met with shoulder shrugs and harrumphs,” Dr. Vogel said. Sales of tamoxifen, worldwide, “didn’t budge.”

Maybe, Dr. Vogel thought, the problem was that internists and gynecologists were not comfortable prescribing a drug used to treat cancer patients. Then, in 1999, he had a chance to do another breast cancer prevention trial, this time of an osteoporosis drug, raloxifene, or Evista, which did not have the cancer drug taint. It was to be compared with tamoxifen.

The $110 million study, involving 19,000 women, ended in 2006. The two drugs were found to be equally effective in preventing breast cancer, but with raloxifene there was no excess uterine cancer and the clotting risk was 30 percent less.

“It was a spectacular clinical trial,” Dr. Vogel said. But, he added, “Once again, the world met the result with a shrug and a harrumph.”

“Those were your tax dollars and mine,” he added. “You can’t do too many $110 million studies.”

He cannot understand why no one cares, but some doctors say they see a number of problems. It is usually not the cost; tamoxifen is about 30 cents a day and raloxifene $3.30 a day. It is doctors’ practices and women’s concerns.

Most doctors, said Dr. Therese B. Bevers, medical director of the Cancer Prevention Center at M. D. Anderson, do not take the first step — calculating a woman’s lifetime risk of getting breast cancer — in part because that can lead to the next step, spending an hour or so discussing cancer risk and drug risks and benefits.

Dr. Bevers suggests the drugs for women whose lifetime odds exceeds 20 percent. That could include, for example, a 55-year-old woman who began menstruating early (increasing the risk), had her first child late (again increasing the risk), and whose mother and sister got breast cancer. About half the time, though, women with that kind of risk turn down the drugs, Dr. Bevers said. “The No. 1 reason I hear is, ‘Oh, I just don’t like to take medications,’ ” she added.

Others, like Cecilia Anderson, who is 57 and lives in Houston, worry about side effects. “I felt like my quality of life was in question,” she said. “I am busy, I am out there. I totally love my life and don’t want it to be compromised.” Her lifetime risk of breast cancer is 20.5 percent, compared with an average risk of 9.8 percent for a woman her age. Ms. Anderson declined the drugs. “I live a different lifestyle,” she said. “I eat organic foods, I exercise. Through all of that comes a spiritual element as well. Mind, body, and spirit are all connected.”

Studies’ Complications
Then came the studies of finasteride and dutasteride for prostate cancer. The drugs block the conversion of testosterone to dihydrotestosterone, a hormone that prostate cancers need to grow. They are on the market to shrink the prostate in older men, whose prostates often enlarge. (Finasteride is also sold to grow hair — but the dose is one-fifth the dose that shrinks prostates and that dose has not been tested for cancer prevention.) Doctors can prescribe the drugs for cancer prevention but, at this point, that is not on their label.

The prostate cancer studies were complicated by other another factor; at first, researchers thought, erroneously, that finasteride was actually spurring the growth of aggressive prostate cancers. The drug’s side effects can include impotence or decreased ejaculate. But the Food and Drug Administration concluded that these effects, if they occur at all, are gone after a year.

Now, even though the F.D.A. deemed the drug’s adverse reactions to be “usually mild and transient.” The American Urological Association and the American Society for Clinical Oncology recommend that men 50 and older consider taking it. But there appears to be little interest even among high-risk men.

Dr. Vogel wonders what message the indifference to the breast cancer and prostate cancer drugs is sending. Why would a company want to develop drugs for cancer prevention?

That is a lesson that hits home, said Dr. Gregory Curt, an oncologist who directs emerging products at AstraZeneca, a drug company.

He hopes companies will take more interest when researchers find biomarkers — cancer risk indicators that are the equivalent of blood pressure or cholesterol. That way people taking the drugs can see that they are reducing their risk. And studies can be smaller and quicker because companies can follow these markers rather than waiting for people to develop cancer.

But risk assessment is not easy, and biomarkers are still more of a dream than a reality. There are other problems, too. If each cancer requires a different drug for prevention, how many drugs can a person take? For now, Dr. Curt said, the very idea of cancer prevention is daunting. And since cancer can take decades to develop, by the time a study concludes, a drug’s patent life may be over.

It is not a pretty picture, Dr. Vogel said.

“You have to think that in boardrooms they are saying, Man, did we learn a lesson,” he said. “We will stay as far away as possible from cancer prevention.”

November, 2009|Oral Cancer News|

Mouth is indicator of overall health, says dental school professor

Source: www.sciencedaily.com
Author: staff

One day in medical clinics, the big picture of a patient’s state of health may be found in little pictures from the mouth, says Li Mao, MD, a new professor at the University of Maryland Dental School.

The mouth or oral cavity area is an excellent indicator of the whole body’s health, says Mao, who is the chair of the new Department of Oncology and Diagnostic Sciences at the School. Mao recently joined the Dental School to be at the forefront of a movement to retool dental education, he says, to make dentists practice more within the bigger health care community.

Future lung cancer prevention trials, for example, could soon be designed so that surface tissues inside the cheek could be checked to detect tobacco-induced damage in the lungs, according to a study led by Mao last year published in the journal Cancer Prevention Research.

“We hypothesized that tobacco-induced molecular alterations in the oral epithelium are similar to those in the lungs,” says Mao. “This might have broader implications for using the mouth as a diagnostic indicator for general health.”

University of Maryland Dental School Dean Christian S. Stohler, DMD, DrMedDent, a leader in the movement to retool dental education, says, “I feel that dentists should play a major role in prevention of cancer and Dr. Mao is the leading oral cancer researcher in the country. He crosses the bridge between medicine and dentistry. Being a physician helps expand dental health care and he wants to change how patients are being treated because his background is in head and neck cancer.”

Mao believes that system biology-based approaches — the pinpointing of molecular changes in living tissue — is becoming an important technology in cancer studies and biomarker discovery. He says that 50 percent of oral cancer patients get diagnosed too late.

Note:
1. adapted from materials provided by University of Maryland Baltimore, via Newswise.

November, 2009|Oral Cancer News|