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An updated analysis of the phase III EMILIA trial showed that the antibody-drug conjugate T-DM1 significantly extended survival compared with the combination of lapatinib/capecitabine in women with HER2-positive, unresectable, locally advanced or metastatic breast cancer. The data were presented at the European Society for Medical Oncology (ESMO) 2012 Congress.

At a median follow-up of about 20 months, T-DM1 reduced the mortality risk by 32% (hazard ratio [HR] = 0.68; 95% CI, 0.55-0.85; 

 <.001), with a 6-month difference favoring T-DM1. Median overall survival (OS; death from any cause) was 30.9 months for T-DM1 versus 25.1 months for lapatinib/capecitabine, which experts called “unprecedented” in metastatic breast cancer.

“The significant improvement in progression-free survival and overall survival as well as the favorable safety suggest that T-DM1 should be an important therapeutic option in the treatment of metastatic HER2-positive breast cancer,” said lead author Sunil Verma, MD, Sunnybrook Odette Cancer Center, Toronto, Ontario, Canada. The results of the EMILIA trial were simultaneously published online in the 

to coincide with Verma’s presentation (

The OS data presented at ESMO were from the second EMILIA interim analysis, with a data cutoff of July 31, 2012, when more than 50% of targeted survival events had occurred. Final OS data are expected in 2014.

T-DM1 is an antibody-drug conjugate linking trastuzumab to the potent chemotherapy (DM1), allowing intracellular delivery of chemotherapy that is said to be 500 times more cytotoxic than paclitaxel.

The EMILIA trial was conducted at 213 sites in 26 countries. Investigators randomized 991 patients with HER2-positive advanced breast cancer previously treated with trastuzumab and a taxane in a 1:1 ratio to T-DM1 or lapatinib/capecitabine. Pre-specified stratification factors included world region, number of prior chemotherapy regimens for metastatic breast cancer or unresectable locally advanced breast cancer, and presence of visceral disease.

Final progression-free survival (PFS) data, presented earlier at the 2012 ASCO Annual Meeting, showed a median PFS of 9.6 months with T-DM1 versus 6.4 months with lapatinib/capecitabine, a 35% reduction in the risk of progression favoring T-DM1 (HR = 0.65; 95% CI, 0.55-0.77; 

Objective response rates were 43.6% for T-DM1 versus 30.8% for lapatinib/capecitabine (

Subgroup analysis showed favorable results for T-DM1 in most subgroups. Verma said that regional differences were probably due to different post-progression treatment in various countries.

Grade 3 or higher adverse events occurred more frequently with lapatinib/capecitabine: 57% versus 41% for T-DM1. Patients in the T-DM1 arm had a higher incidence of thrombocytopenia and increased serum aminotransferase levels, whereas those treated with lapatinib/capecitabine had higher rates of diarrhea, nausea, vomiting, and hand-foot syndrome. The rates of cardiac dysfunction were very low and similar in both treatment arms.

Formal discussant of this trial, Javier Cortes, MD, Vall d’Hebron University Hospital and Institute of Oncology, Barcelona, Spain, was quite impressed with the nearly 6-month improvement in survival. “I do not remember any paper in metastatic breast cancer with an improvement of 6 months. T-DM1 is clearly better than previous drugs for survival. This will benefit thousands of women.”

He also said that the cardiac safety data suggest that T-DM1 may be a good option for patients who cannot receive trastuzumab due to cardiac problems.

Genentech announced in August that it had submitted an application to the FDA for T-DM1 in HER2-positive metastatic breast cancer.

	Verma S, Miles D, Gianni L. Updated overall survival results from EMILIA, a phase 3 study of trastuzumab emtansine (T-DM1) vs capecitabine (X) and lapatinib (L) in HER2-positive locally advanced or metastatic breast cancer (MBC). Paper presented at: 37th European Society for Medical Oncology Congress; September 28-October 2, 2012; Vienna, Austria. Abstract LBA12.

An updated analysis of the phase III EMILIA trial showed that T-DM1 significantly extended survival in women with HER2-positive, unresectable, locally advanced or metastatic breast cancer.

Updated Data Show T-DM1 Improves Overall Survival in HER2-Positive Breast Cancer

Crizotinib, the first-in-class ALK inhibitor, extended progression-free survival (PFS) and improved response rates compared with single-agent chemotherapy with pemetrexed or docetaxel in patients with advanced, previously treated, ALK-positive, non-small cell lung cancer (NSCLC), according to the results of the phase III PROFILE 1007 trial presented September 30 at the ESMO 2012 Congress in Vienna. Crizotinib achieved a greater improvement in lung cancer symptoms and quality of life (QOL) compared with chemotherapy.

“This is the first head-to-head study comparing crizotinib with standard chemotherapy in NSCLC. These results establish crizotinib as the standard of care [in the US] for patients with advanced previously treated ALK-positive (ALK+) NSCLC,” stated lead author Alice T.  Shaw, MD, PhD, Dana-Farber/Harvard Cancer Center, Boston. Crizotinib (Xalkori, Pfizer) is FDA-approved for the treatment of ALK+ NSCLC.

ALK rearrangement, occurring in 3% to 5% of lung cancers, is one of several genetic changes that can drive lung cancer. Because of the high prevalence of lung cancer cases, ALK+ cases account for more than 50,000 new cases of NSCLC each year, Shaw said.

Several studies have identified distinct clinical features associated with ALK abnormality, she continued. These factors include younger age (10 to 15 years younger); no smoking history; and adenocarcinoma.

PROFILE 1007 was a global study conducted at more than 100 sites in 20 countries. The study randomized 347 patients with ALK+, stage IIIb or IV NSCLC to crizotinib 250 mg/bid; pemetrexed 500 mg/m

; or docetaxel 75 mg/m2 on a 21-day cycle. Median number of cycles of treatment was 11 for crizotinib and 4 for chemotherapy.

The study met its primary endpoint of progression-free survival (PFS): median PFS was 7.7 months with crizotinib versus 3.0 months with chemotherapy, representing a 51% reduction in risk of progression for the ALK inhibitor (

 < .0001).  Looking at the two chemotherapy drugs separately, median PFS was 7.7 months with crizotinib versus 4.2 months with pemetrexed (

= .0004 compared with crizotinib) versus 2.6 months with docetaxel (

According to independent radiologic review, crizotinib tripled the overall response rate compared with chemotherapy: 65.3% versus 19.3%, respectively (

An interim analysis showed no difference in overall survival between the two arms, but Shaw said the data are immature and also confounded by crossover to crizotinib from the chemotherapy arms.

Toxicities of crizotinib were mild and manageable, she continued. The rate of grade 3/4 toxicities was under 5% with the exception of elevated transaminases reported in 16% of patients and pulmonary embolism in 5%. The rate of myelosuppression was higher with chemotherapy compared with crizotinib.

QOL was superior for crizotinib-treated patients, based on patient reported outcomes regarding time to deterioration in lung cancer symptoms: median of 5.6 months with crizotinib versus 1.4 months with chemotherapy (

Fortunato Ciardiello , MD, PhD, Seconda UniversitaÌ€ di Napoli in Naples, Italy, emphasized the importance of this study. “This shows that a selective specific inhibitor of a molecular target makes a big difference in treatment outcome. We need to define the underlying genetics and then select therapy accordingly.”

The availability of genetic testing and reimbursement depends on the country. “In the US, genetic testing is available at major cancer centers, which follow the NCCN guidelines to offer EGFR and ALK testing upfront to lung cancer patients,” Shaw said. “I don’t know if community oncologists do this testing,” she added.

With a median PFS of 7 months, patients will develop resistance to this targeted therapy. Two next-generation ALK inhibitors are in phase II studies—LBK 178 and AB6 273&mdash;and heat shock protein inhibitors are also under study. These new agents may prove useful in patients who become resistant to crizotinib, she said.

	Shaw AT, et al. Phase 3 randomized study of crizotinib versus pemetrexed or docetaxel chemotherapy in advanced, ALK-positive NSCLC (PROFILE 1007). Vienna, Austria: European Society for Medical Oncology; September 30, 2012.  Abstract LBA1.

Crizotinib extended PFS and improved response rates compared with single-agent chemotherapy with pemetrexed or docetaxel in patients with advanced, previously treated, ALK-positive, NSCLC.

Positive Results in ALK-Positive NSCLC With First ALK Inhibitor

Patients with heavily pretreated metastatic colorectal cancer (mCRC) who received the recently approved drug regorafenib experienced a sustained survival benefit, and the benefit of this multitargeted tyrosine kinase inhibitor (TKI) was observed across all prespecified subgroups, according to updated findings from the CORRECT clinical trial presented at the European Society for Medical Oncology (ESMO) 2012 congress in Vienna, Austria.

No new or unexpected safety findings emerged with longer-term follow-up.

At the first preplanned interim analysis of overall survival (OS), the study met the primary endpoint with a clear difference in favor of regorafenib. Median OS was 6.4 months for regorafenib versus 5 months for placebo (

 <.0052), and the study was halted early. These results were reported at the 2012 American Society of Clinical Oncology (ASCO) meeting earlier this year.

At the 2012 ESMO congress, the final updated analysis of OS confirmed the benefit of regorafenib. At 6 months, median overall survival was 6.4 months for regorafenib (95% CI, 5.8-7.0) versus 5 months for placebo (95% CI, 4.4-5.9), resulting in a 21% reduced risk of death for the newly approved agent (HR=0.79; 95% CI, 0.66-0.94; 

=.0038). At 6 months, 52.2% of the regorafenib-treated group were alive versus 43.1% of placebo patients; at 1 year, 24.1% and 17%, respectively, were alive.

“Regorafenib is the first oral multitargeted TKI with proven activity in metastatic colorectal cancer, improving overall survival in patients who progress on standard therapies,” said lead author Eric van Cutsem, MD, University Hospitals Gasthuisberg/Leuven, Leuven, Belgium. “The benefit is sustained over time, with manageable side effects. Regorafenib represents a new potential standard of care for patients with chemo refractory metastatic disease.”

Additionally, van Cutsem pointed out that the patients in this trial had good performance status despite disease progression and said that regorafenib was an option “as long as patients are in good condition.” He emphasized that many patients with mCRC fail standard treatments, and in this setting, there has been no salvage therapy available, “although many patients remain in good condition.”

Regorafenib recently gained FDA approval for mCRC in the salvage setting. The drug interferes with cell proliferation, inhibits the tumor microenvironment, cell signaling, and neoangiogenesis.

The phase III, randomized, placebo-controlled CORRECT trial was conducted at 114 centers in 16 countries in 760 patients with mCRC who progressed despite being treated with several lines of standard therapies. Patients were randomized in a 2:1 ratio to oral regorafenib 160 mg/day or placebo for 3 weeks on and 1 week off; both groups received best supportive care and were treated until disease progression, unacceptable toxicity, or investigator’s decision to withdraw treatment.

At baseline, demographics in both arms were well balanced. Median age was about 61 years and approximately 78% were Caucasian; 52.5% of patients who received regorafenib were ECOG Performance Status (PS) 0, and 47.5% were ECOG PS 1. The primary site of the cancer was the colon in 64%, the rectum in 29.9%, and a combination of the two sites in 5.9% of patients who received regorafenib. Slightly more patients with wild type KRAS were observed in the regorafenib group. Adenocarcinoma was observed in 98% of patients, and 100% received prior bevacizumab. No difference between treatment arms was observed for prior lines of chemotherapy for metastatic disease.

Dose reductions were initiated in 20% of regorafenib-treated patients. Although no difference in partial response was seen between groups, regorafenib was superior to placebo in achieving disease control (i.e., response plus stable disease): 41% versus 15% for placebo patients.

In the regorafenib group, drug-related adverse events included hand-foot syndrome in 46.6% (all grades, Grade 3, 16.6%); fatigue 47.4% (all grades; grade 3, 9.2%), hypertension 27.8% (all grades; grade 3, 7.2%); diarrhea 33.8% (all grades; grade 3, 7%); and rash or skin desquamation in 26% (all grades; grade 3, 5.8%). Rates for these events were considerably lower in the placebo group. Subgroup analysis of safety showed no difference in adverse events compared with the overall analysis, except slightly more hand-foot syndrome occurred in Asians than Caucasians and rash/desquamation was slightly more frequent in females than males.

At present, there is no biomarker to identify which subgroups have the most benefit from regorafenib. Translational research on serum and tissue samples from patients in the trial is planned.

Regorafenib is marketed by Bayer HealthCare Pharmaceuticals as Stivarga in the United States.

	Van Cutsem E, Grothey A, Sobrero A, et al. Phase 3 CORRECT trial of regorafenib in metastatic colorectal cancer (mCRC): overall survival update. Presented at: European Society of Medical Oncology 2012 Congress; September 28—October 2, 2012; Vienna, Austria. Abstract LBA18.

Patients with heavily pretreated metastatic colorectal cancer who received regorafenib experienced a sustained survival benefit across all prespecified subgroups.

Updated Regorafenib Survival Results Confirm Effectiveness

Ezra E.W. Cohen, MD, Associate Professor, Section of Hematology/Oncology, Department of Medicine, Co-Director, Head and Neck Cancer Program, Director, Hematology/Oncology Fellowship Program, University of Chicago Medical Center, discusses an analysis of the phase III EXAM trial that examined the efficacy and pharmacokinetics of cabozantinib (XL184) for patients with advanced medullary thyroid cancer (MTC).

Cohen explains that one of the aspects of the study was to examine if the presence of mutations in the proto-oncogene 

 effected the activity of cabozantinib, an active inhibitor of the RET tyrosine kinase, which is theorized to be one of the main drivers in MTC. Regardless of the presence of 

 mutations all patients benefited from treatment with cabozantinib and only a slight difference was observed between those with or without a 

The pharmacokinetics of cabozantinib are fairly well understood; however, the impact of dose size and drug exposure on efficacy was further examined in the EXAM trial. Cohen explains that evidence from this study seems to suggest that exposure levels did not alter the efficacy of cabozantinib. Overall, this agent demonstrates very robust activity across multiple patient groups.

Ezra E.W. Cohen, MD, from the University of Chicago Medical Center, on the pharmacokinetics and efficacy of cabozantinib for medullary thyroid cancer. 

Dr. Ezra Cohen on the Pharmacokinetics of Cabozantinib

In Asian patients with previously untreated advanced or recurrent gastric cancer, overall survival (OS) and progression-free survival (PFS) were significantly improved when docetaxel was added to S-1, an oral fluoropyrimidine that is a standard treatment for this malignancy in East Asia and parts of Europe.

At the European Society for Medical Oncology (ESMO) 2012 Congress, investigators from the START trial (S-1 plus Docetaxel versus S-1 for advanced gastric cancer) presented an update to the survival analysis previously reported at the 2011 Gastrointestinal Cancers Symposium.Â  Kazuhiro Yoshida, MD, of Gifu University Hospital, Gifu, Japan, presented the findings at ESMO for the Japan Clinical Cancer Research Organization and the Korean Cancer Study Group Intergroup trial.

In the previous analysis, no statistically significant difference in overall survival was observed with the combination (HR 0.88; 

“However, an independent biostatistician pointed out that there was a large number of censored cases, which led to an insufficient number of events for a proper [survival] analysis,” Yoshida said. “According to this recommendation, we performed further confirmation to resolve the censored cases to analyze the START trial properly.”

The current intention-to-treat analysis included 635 patients with advanced or relapsed gastric cancer randomly assigned to S-1 80 mg/m

 on days 1-28 every 6 weeks or S-1 80 mg/m

 on day 1 every 3 weeks. Patients received treatment until disease progression, for a median number of 5 cycles for the combination and 2 cycles for single-agent S-1. Patients were followed an average time of 11.4 months.

Median OS was 12.5 months in the docetaxel/S-1 group and 10.8 months in the S-1 group (HR = 0.837; 

 = 0.0319). PFS was 5.3 months versus 4.2 months, respectively (HR = 0.765; 

 = 0.001). The overall response rate in patients with measurable disease was 38.8% with the combination and 26.8% with S-1 alone (

Several subsets derived a particular survival benefit from the combination: the Japanese cohort (versus Korean) (HR = 0.810), patients with non-measurable (versus measurable) disease (HR = 0.649), patients with ECOG performance status of 0 (HR = 0.780), and patients with no lymph node metastasis (HR = 0.688).

“Adding docetaxel to S-1 significantly improved OS, PFS and response rates, nevertheless it resulted in some increase proportion of hematological toxicities,” he said. Neutropenia grade 3 and higher was observed in 29% of patients, and febrile neutropenia in 3%, compared to 4.2% and 0%, respectively, with S-1 alone.

The findings point to docetaxel plus S-1 as a new treatment option for patients with untreated advanced gastric cancer, Yoshida concluded.

Gunnar Folprecht, MD, of the University Cancer Center in Dresden, Germany, discussed the findings. He said that the findings presented at ESMO “would be taken as positive.” Folprecht concluded that docetaxel plus S-1 is more effective than S-1 alone “if there had not been the analysis presented at the Gastrointestinal Cancers Symposium.”

Folprecht emphasized that the primary analysis was negative. That analysis showed 1-year survival to be 52.5% with the combination versus 46.0% with the single agent. Two-year survival showed 23.7% versus 20.6%, respectively; and 3-year survival was 13.0% versus 12.3% (HR 0.88; 

S-1 is approved by the European Medicines Agency for advanced gastric cancer when given in combination with cisplatin, and the START trial suggests there may be a less toxic, platin-free way to give the drug, he added.

However, Folprecht stayed firm on his own views.

“My personal opinion is that docetaxel plus S-1 is not a new standard of care,” Folprecht said.

Two analyses, two different conclusions in Asian START trial when docetaxel was added to S-1 for patients with previously untreated advanced or recurrent gastric cancer.

Does Docetaxel Add Benefit to the Oral Fluoropyrimidine S-1 in Gastric Cancer?

Combining the new drugs dabrafenib and trametinib provided a clinically meaningful improvement in patients with melanoma that had 

 V600 mutations, according to results of a phase II study presented on Saturday at the 2012 ESMO Congress in Vienna, Austria.

Full-dose combination of a novel BRAF inhibitor (dabrafenib) and a novel MEK 1/2 inhibitor (trametinib) improved progression-free survival (PFS), response rate, and duration of response, said lead investigator Georgina V. Long, BSc, PhD, MBBS, clinical researcher at the Melanoma Institute Australia and Westmead Hospital in Sydney. In addition, the combination reduced the side effects associated with BRAF inhibitor monotherapy, which is highly unusual.

Both drugs act on the RAS kinase pathway, dabrafenib at an earlier point than trametinib. About 50% of patients with metastatic melanoma have a 

 mutation. “Dabrafenib attacks that abnormality and works for about 5 to 7 months, and patients develop resistance to the drug. The rationale for adding a MEK 1/2 inhibitor is that it blocks the ‘escape route’ for the BRAF inhibitor and allows continued response,” Long explained.

—positive metastatic melanoma to one of three treatment arms: monotherapy with dabrafenib 150 mg/bid; combination of dabrafenib 150 mg/bid with once-daily trametinib 1 mg; or full doses of both drugs (ie, dabrafenib 150 mg/bid; once-daily trametinib 2 mg).

Median time to follow-up was 14 months. Median PFS was 9.2 months for the full dose combination versus 5.8 months for the monotherapy arm (

 <.0001), representing a 61% reduction in risk of disease progression. Median PFS was 9.2 months for the arm using half-dose trametinib, which was also significantly better than monotherapy (

 = .005). At 12 months, 41% of the patients who received full-doses of both drugs had not progressed versus 9% of the monotherapy arm.

Analysis showed PFS benefit from full doses of both drugs for every category: age, sex, baseline disease stage, baseline LDH, or presence of brain metastasis

Looking at patients with the most common 

, PFS was 6.5 months with monotherapy, 7.3 months for the combination with half-dose trametinib, and 10 months for the full-dose combination (

Median overall survival (OS) had not been reached in any of the three arms at the time of the data were presented at ESMO. Twelve-month OS was 70% in the monotherapy arm, 68% in the combined therapy arm with half-dose trametinib, and 78% in the full-dose combination arm.

“This has never been seen before in metastatic melanoma,” Long noted.

Confirmed response rates were 54% for monotherapy, 50% for the combination of dabrafenib with half-dose trametinib, and 76% for the full-dose combination.

Median duration of response was 5.6 months for monotherapy, 9.5 months for the combination of full-dose dabrafenib and half-dose trametinib, and 10.5 months for the full dose combination of both drugs.

“Using one road block [ie, dabrafenib] and then adding an exit block [ie, trametinib] improves response and duration of response,” said Long.

Hyperproliferative skin toxicities (ie, alopecia hyperkeratosis, skin papilloma, and squamous cell carcinoma) associated with BRAF inhibition were reduced in both combination arms. Squamous cell carcinoma occurred in 10 patients on monotherapy, one patient in the combination arm that included half-dose trametinib, and four patients in the full-dose combination arm.

“This has never been seen before in the history of chemotherapy,” Long noted.

Pyrexia and nausea and vomiting were increased in the combination arm. The rate of pyrexia was 67% in the full-dose combination arm and 23% in the monotherapy arm. Long said that during the evolution of the study, it became clear that prophylaxis with corticosteroids was effective in preventing pyrexia, and going forward, that will be the practice. The median time to first episode of pyrexia was less than 6 weeks and only three patients in the full-dose combination arm developed grade 3 pyrexia. “The majority of patients develop only 1 episode of pyrexia,” explained Long.

The incidence of vomiting in the full-dose arm was 35%, but these were grades 1 and 2 and easily managed, said Long.

The distribution of other adverse events was similar in the three treatment arms.

Two phase III trials of this combination are now ongoing in metastatic melanoma: One comparing the full-dose combination versus dabrafenib alone and the other comparing the full-dose combination to trametinib alone.

Combining the new drugs dabrafenib and trametinib provided a clinically meaningful improvement in patients with melanoma that had BRAF V600 mutations.

BRAF Inhibitor Plus MEK Inhibitor Encouraging in Metastatic Melanoma

Gefitinib improved progression-free survival (PFS) and some quality of life measures when used as second-line therapy for esophageal cancer. However, the PFS benefit did not extend to improved overall survival (OS), the primary endpoint of the trial. These were the findings of the first randomized controlled trial to address a second-line treatment for esophageal cancer. The study was presented by David Ferry, MD, New Cross Hospital, Wolverhampton, UK, at the 2012 ESMO Congress in Vienna.

“At the moment, there is no therapy for esophageal cancer that has progressed on first-line therapy. The standard of care after progression is palliative therapy,” Ferry told listeners at an official ESMO press conference September 29.

The Phase III, multicenter, double-blind, study was conducted at 51 centers in the UK. Participants were 450 patients with esophageal cancer or cancer of the esophageal junction who progressed on first-line treatment with up to two previous chemotherapy regimens; they were randomized to the epidermal growth factor receptor (EGFR)-inhibitor gefitinib 500 mg/day versus placebo and treated until disease progression, as documented on regular CT scans.

At baseline, median age was 64 years and 83% were male; 76% had adenocarcinoma, and 78% had esophageal cancer. Twenty-five percent were performance status (PS) 0; 54% were PS 1, and 21% were PS 2.

A small but statistically significant difference in PFS was observed in favor of gefitinib: median PFS was 49 days on gefitinib versus 35 days for placebo (

“The improved PFS on gefitinib did not translate to an overall survival benefit. But these patients treated second-line have a very dire prognosis with an overall survival of 2 months,” Ferry said.  “We saw durable responses.”

At 8 weeks, disease control was observed in 25.5% of gefitinib-treated patients versus 16% of the placebo group (

The investigators found that PS was a prognostic marker for survival in this trial. Patients with PS 0 had a median OS of 6.03 months; those with PS 1 had median OS of 3.93 months; and those with PS 2 had a median OS of 1.97 months.

Both dysphagia (difficulty swallowing) and odynophagia (pain while swallowing) were significantly improved for patients taking gefitinib versus placebo (

 = .004). Ferry said that these two symptoms are important indicators of quality of life in patients with esophageal cancer.

The UK investigators are planning an associated study called TRANSCOG to analyze biopsies of more than 300 patients enrolled in the trial to identify molecular characteristics associated with enriched benefit of gefitinib.

When questioned as to why OS was selected as the primary endpoint of the trial, Ferry said, “A drug that doesn’t produce an overall survival benefit is unlikely to get approved. We need to put our new drugs through these tough tests [i.e., overall survival]. Otherwise, no new drugs will be approved for out patients for our patients.

At present, gefitinib should not be used outside of a clinical trial setting. Ferry said: “There is not sufficient benefit of gefitinib in unselected patients. That’s why will do the TRANSCOG translational study to identify biomarkers.”

He and his colleagues are planning a new placebo-controlled trial “with another active drug” using biomarkers for selection. Ferry did not name the new drug to be studied.

“That would be telling a secret,” he commented.

Gefitinib improved progression-free survival and some quality of life measures when used as second-line therapy for esophageal cancer.

Gefitinib: Small Benefit as Second-Line Therapy in Esophageal Cancer

OncLive presents live coverage from the 2012 European Society for Medical Oncology (ESMO) congress, held at the Austria Center Vienna from September 28 to October 2, in Vienna, Austria.

ESMO is a large European professional organization committed to furthering oncology care and treatment through the dissemination of research and data.The 2012 installment of the ESMO meeting highlights advances in multiple tumor types, including information on targeted agents for lung cancer, melanoma, and gastrointestinal cancers.

OncLive’s conference coverage features video interviews with leading oncologists and articles discussing the latest breaking news and clinical trial results presented at the meeting.

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View coverage from the 2012 ESMO Congress

Coverage from the 2012 European Society for Medical Oncology congress, held at the Austria Center Vienna from September 28 - October 2, in Vienna, Austria.


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