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Extending tamoxifen use improves breast cancer outcomes

CASE STUDY

NEWS

2012 in retrospective: Report highlights advances in oncology

CONFERENCE

Ponatinib active in drug-resistant CML and ALL, gets FDA nod

BRIEFS

Laparoscopic resection for colon cancer as good as open surgery

Capecitabine in metastatic breast cancer

June 2012January - February 2013

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Jan-Feb 20133

Naomi Rodrig

Treating women with estrogen recep-tor (ER)-positive breast cancer with tamoxifen for 10 years reduced the

rates of late recurrence and breast cancer mor-tality compared with the current standard of 5 years, according to the international ATLAS (Adjuvant Tamoxifen - Longer Against Short-er) study.

“Five years of adjuvant tamoxifen is already an excellent treatment that substan-tially reduces the 15-year risk for recurrence and death from ER-positive breast cancer. [Lancet 2011;378:771-784] ATLAS now shows that 10 years of tamoxifen is even more effec-tive,” said Dr. Christina Davies, Oxford University, UK, who presented the results at the 2012 CTRC-AACR* San Antonio Breast Cancer Symposium last month. The study was simultaneously published in The Lancet. [doi:10.1016/S0140-6736(12)61963-1]

The investigators enrolled 6,846 women with ER-positive breast cancer between 1996 and 2005. Half had node-positive disease. All the women had been using tamoxifen for 5 years, and were then randomly assigned to continue treatment for another 5 years or stop.

After about 8 years of follow-up, there were 1,328 breast cancer recurrences and 728 deaths after recurrence. Treatment alloca-tion had little effect on either recurrence or death rates during the period of 5 to 9 years after diagnosis.

However, during the second decade

following diagnosis, the women who continued tamoxifen had a significantly lower recurrence rate (617 recurrences in 3,428 women allocated to continue vs 711 in 3,418 controls; p=0.002) and a 29 percent lower breast cancer mortality rate (331 vs 397 deaths; p=0.01) than those who stopped after 5 years. Overall mortality rate was also reduced in the tamoxifen continuation arm (639 vs 722 deaths, p=0.01).

Risk of death from breast cancer 5 to 14 years after diagnosis was 12.2 percent among those who continued use vs 15 percent among those who stopped. The greatest benefit was observed during 10 to 14 years after diagnosis.

“The main additional benefit from continuing tamoxifen treatment is to reduce breast cancer mortality during the second decade after

Extending tamoxifen use improves breast cancer outcomes

Jan-Feb 20134diagnosis,” Davies said. “We already knew that 5 years of tamoxifen reduces breast cancer mortality in this late period by almost a third in comparison with no tamoxifen. The latest results suggest that 10 years of tamoxifen treatment can approximately halve breast cancer mortality during the second decade after diagnosis.”

She noted that continuing tamoxifen use can increase side effects, with endometrial cancer being the most life-threatening. The cumula-tive risk of endometrial cancer during years 5 to 14 was 3.1 percent (mortality 0.4 percent) for women randomized to continue vs 1.6 percent (mortality 0.2 percent) for controls. Because this risk is heavily outweighed by the reduction in breast cancer deaths, overall mortality was significantly reduced by longer treatment. In

premenopausal women, for whom tamoxifen is often the endocrine treatment of choice, there was no apparent excess of endometrial cancer.

The study data may be practice changing, offering potential benefits with extended use of tamoxifen. “The current recommendation is to stop tamoxifen or any other endocrine treatment after 5 years,” said Davies. “ATLAS showed that protection against breast cancer recurrence and death is greater with 10 years than with 5 years of tamoxifen use. Women and their doctors should be aware of this evidence when deciding how long to continue tamoxifen, or any other endocrine treatment.”

* CTRC: Cancer Therapy and Research Center; AACR: American Association for Cancer Research

The year 2012 concluded with two impor-tant conferences – the 35th Annual San

Antonio Breast Cancer Symposium and the 54th American Society of Hematology Annual Meeting and Exposition. As reported in this issue, key findings include the benefit of extending tamoxifen use to 10 years in patients with estrogen receptor-positive breast cancer and the efficacy of ponatinib in certain forms of drug-resis-tant leukemia, which led to its accelerated

approval by the US FDA recently.Also reported in this issue are the 19th

Hong Kong International Cancer Congress, and highlights from the American Society of Clinical Oncology’s 2012 annual report that summarizes major achievements in the field of cancer management.

We look forward to more exciting devel-opments in 2013. Happy New Year!

The Editor

Progress in 2012 and beyond

Br ie fsJan-Feb 20135

No OS advantage for eribulin

A phase III, head-to-head trial reported recently at the 2012 San Antonio Breast Cancer Symposium failed to demonstrate a statistically significant overall survival (OS) benefit

of eribulin vs capecitabine in heavily-pretreated patients with locally advanced or metastatic breast cancer (n=1,102). [Abstract S6-6]

Median OS was 15.9 months for eribulin vs 14.5 months for capecitabine (p=0.056), while median progression-free survival (PFS) was 4.1 vs 4.2 months (p=0.3050).

However, there was a trend towards longer OS with eribulin among patients with HER2-negative breast cancer (15.9 vs 13.5 months), those with estrogen receptor (ER)-negative disease (14.4 vs 10.5 months), and those with triple-negative disease (14.4 vs 9.4 months), suggesting that particular patient subgroups may benefit from eribulin therapy.

Eribulin was approved by the US FDA in 2010 for the treatment of metastatic breast cancer patients previously treated with anthracycline and a taxane in either the adjuvant or metastatic setting and at least two chemotherapeutic regimens for metastatic disease.

One look is worth a thousand words

A new study found that showing patients with advanced cancer a video of simulated cardiopulmonary resuscitation (CPR)

improved their understanding of the intervention and prompted more patients to opt against CPR. [DOI: 10.1200/JCO.2012.43.9570]

The investigators randomized 150 patients with advanced can-cer to listen to a verbal narrative describing CPR and the likelihood of successful resuscitation (control group, n=80) or listen to an iden-tical narrative and view a 3-minute video of a patient on ventila-tor and CPR being performed on a simulated patient (intervention arm, n=70).

Following the presentations, 79 percent of patients in the intervention group said they wanted no CPR, compared with 51 percent in the control group. Those in the intervention group also reported more knowledge about CPR after watching the video.

The innovative Advance Care Planning Decisions video used in the study was created by a nonprofit foundation led by physicians who aim to empower terminally ill and elderly patients and their families to make informed choices about end-of-life care.

Br ie fsJan-Feb 20136

Laparoscopic resection for colon cancer as good as open surgery

Long-term outcomes of laparoscopic-assisted colon resection (LCR) for colon cancer are comparable

with those of open colon resection (OCR), according to a study by the Australasian Laparoscopic Colon Cancer Study Group. [Ann Surgery 2012;256:915-919]

The trial investigated whether the short-term ben-efits associated with LCR [shorter hospitalization, less scarring, etc] could be achieved safely, without sur-vival disadvantages. A total of 601 patients with potentially curable colon cancer were random-ized to receive LCR or OCR. Primary endpoints were 5-year overall survival, recurrence-free survival, and freedom from recurrence.

At 5-year follow-up, there were no significant differences between the LCR and OCR groups in overall survival (77.7 vs 76.0 percent; p=0.64), recurrence-free survival (72.7 vs 71.2 percent; p=0.70), or freedom from recurrence (86.2 vs 85.6 percent; p=0.85).

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Conference CoverageJan-Feb 2013719th Hong Kong International Cancer Congress, University of Hong Kong, 8-9 November 2012 – Christina Lau reports

Recent understanding of the role of Epstein-Barr virus (EBV) infection in cancer pathogenesis has led research-

ers to develop EBV-targeted therapies for na-sopharyngeal carcinoma (NPC).

“Globally, around 2 million cancer cases per year are attributable to infections. Of these cases, 10.3 percent are EBV-associ-ated lymphomas and carcinomas,” said Professor Lawrence Young of the University of Birmingham, UK.

According to Young, EBV infects more than 90 percent of human population. The infection is predominantly asymp-tomatic with the virus establishing a life-long persistent infection in the memory B cell compartment.

“What EBV wants to do is to persist in a normal host and replicate. The development of EBV-associated cancer is an accident,” he said. “In normal differentiating epithe-lial cells, the virus is able to replicate after epithelial infection. If epithelial cells are unable to differentiate, however, EBV may remain latent, occasionally leading to the development of malignancies in the epithelium.”

As the EBV replication cycle is controlled by T cells, Young suggested that anything affecting T cell immune response could allow EBV to replicate more and infect more cells, increasing the chances of developing EBV-associated malignancies.

“Studies have shown that EBV adopts different forms of latent gene expres-sion in different malignancies. These include EBV nuclear antigens [EBNAs] and latent membrane proteins [LMPs],” Young noted. “Based on understanding of the impact of EBV latent gene expres-sion on the oncogenic process, researchers have started to develop EBV-targeted therapies that aim to activate the latent virus and then kill it when it replicates.”

A Dutch team, for example, has developed a cytolytic virus activation (CLVA) therapy for NPC. The therapy involves the use of gemcitabine and valproic acid to induce EBV lytic cycle, followed by the antiviral drug ganciclovir to block EBV replication and kill proliferating EBV-infected cells. In three patients with refractory NPC, CLVA therapy led to disease stabilization and was well toler-ated. [Clin Cancer Res 2012;18:5061-5070]

“Another approach of EBV-targeted therapy involves the infusion of EBV cytotoxic T lymphocytes [EBV-CTLs] generated from the patient’s own blood. Success has been shown in patients with relapsed or refractory NPC,” said Young. [Blood 2005;105:1898-1904; J Immunother 2010;33:983-990]

“Therapeutic vaccination represents a very exciting approach in NPC,” he continued. “Researchers have produced a therapeutic vaccine by inserting inactive EBV EBNA1 and LMP2 genes into a safe virus vector

Studies investigate EBV-targeted therapies for NPC

Conference CoverageJan-Feb 20138

Breakthroughs in targeted therapy for advanced gastric cancer have come to a

near standstill after the approval of trastu-zumab for HER2-positive disease. According to a Hong Kong expert, negative results of other targeted therapies can be explained by the highly heterogeneous nature of gastric cancer, which can be used to refine patient selection for potential benefit.

“There are multiple subtypes of gastric cancer based on histological, anatomical, epidemiological and molecular classifica-tions. Intratumoral heterogeneity adds another level of complexity,” said Dr. Hilda Wong of the Queen Mary Hospital.

According to Wong, this complex hetero-geneity may explain the negative results of targeted therapies in the AVAGAST (Avastin in Gastric Cancer), EXPAND (Xeloda and Cisplatin in Advanced Esophagogastric Cancer), REAL-3 (Randomized Trial of EOC ± Panitumumab for Advanced and Locally Advanced Esophagogastric Cancer) and GRANITE-1 (Gastric Antitumor Trial with Everolimus) trials, which were conducted in unselected patient populations. [J Clin Oncol 2011;29:3968-3976; Lordick F et al, ESMO 2012; J Clin Oncol 2012;30(suppl 15): abstract LBA4000; J Clin Oncol 2012;30(suppl 4): abstract LBA3]

“Efficacy shown in subgroup analyses of

the AVAGAST and REAL-3 trials suggests that it is possible to achieve significant benefit by refining patient selection,” she said. [J Clin Oncol 2012;30(suppl 4): abstract 5; Waddell TS et al, ESMO 2012]

There is currently little evidence on the predominant molecular aberrations in each histological, anatomical or epidemiological subtype of gastric cancer. In a review of the literature, Wong and colleagues found that HER2, EGFR and MET pathways are predom-inantly implicated in proximal non-diffuse tumors, while VEGF-related signaling is more common in the distal non-diffuse subtype. In contrast, loss of E-cadherin and FGFR2-, mTOR-, HER3- and MMP-related

Gastric cancer heterogeneity: Difficulty or opportunity?

[modified vaccinia Ankara, MVA]. This vaccine was shown to significantly boost T cell response in 15 of 18 NPC patients. A

single-arm phase II clinical trial is ongoing in Hong Kong in patients with persistent, recur-rent or metastatic EBV-positive NPC.”

pathways is more frequently involved in diffuse tumors. [Therap Adv Gastroenterol 2012, e-pub 9 July] “These clinical classifi-cations may contribute to the prospective selection of patients for targeted therapy, especially since we have no validated, acces-sible and predictive biomarker for direct patient selection to date except HER2,” she said.

“In addition, intratumoral heterogeneity of HER2 overexpression/amplification is of particular therapeutic relevance. Studies

have shown discordance within or between sections of the primary tumor in up to 79 percent of HER2-positive cases, while discor-dance between metastasis and primary tumor and between immunohistochemistry and FISH assays is also common,” she continued. “Clarification of the correlation between molecular profile, intratumoral heteroge-neity and clinicopathological characteristics will provide insights into tumor biology and facilitate clinical selection of patients for targeted therapy.”

Selective internal radiaton therapy (SIRT) in combination with sorafenib has demon-

strated encouraging results in a recent study of Asian patients with non-resectable hepato-cellular carcinoma (HCC), while data from Korea suggest that TomoTherapy is more effective than 3D conformal RT in locally advanced HCC.

“SIRT with yttrium-90 is indicated for inoperable larger or multifocal HCC, including HCC with portal vein involve-ment, as well as refractory colorectal cancer liver metastases and neuroendocrine tumor metastases. The disease control rate is approximately 80 percent, compared with 40 percent with transarterial chemoembolization [TACE],” said Professor Pierce Chow of the National University of Singapore and Singa-pore General Hospital.

The efficacy and safety of SIRT with yttrium-90 was demonstrated in several trials, including a multicenter European trial on HCC across all Barcelona Clinic Liver Cancer (BCLC) stages. In that trial, median survival was 12.8 months (BCLC A, 24.4 months;

BCLC B, 16.9 months; BCLC C, 10 months); the majority of patients (93.3 percent) had

SIRT and TomoTherapy for HCC: Asian perspective

Conference CoverageJan-Feb 20139only one SIRT session. [Hepatology 2011;54: 868-878]

“While yttrium-90 is efficacious in causing complete or partial destruction of the tumor, new lesions can arise from the liver or from metastasis. The Asia-Pacific HCC Trials Group tested yittrium-90 followed by sorafenib, to see if this can prevent or delay the develop-ment of new lesions and improve outcomes in advanced HCC,” said Chow.

The phase I/II trial, known as AHCC005, included 34 patients with BCLC B or C HCC. “Tumor response was encouraging, with 12 percent of patients achieving complete regres-sion, 23.5 percent achieving partial regres-sion, and 44 percent achieving stable disease. Tumor response rate was 33.5 percent, while disease control rate was 79.5 percent,” reported Chow. “The median time to progres-sion was 39 weeks. Median survival was 20.6 months for patients with BCLC B disease, and 8.2 months for those with BCLC C disease.”

“As there is currently no established first-

line therapy for inoperable HCC without metastasis, the HCC Trials Group has started a phase III randomized controlled trial to compare SIRT with sorafenib in patients with locally advanced HCC,” he continued. “Recruitment is ongoing, and patients previ-ously treated with surgery, TACE or radiofre-quency ablation are eligible.”

In another study (n=106), researchers from the Yonsei University, Korea have shown significantly longer overall survival (OS) (1-year, 81.1 vs 52.8 percent; 2-year, 42.2 vs 30.2 percent; 3-year, 31.6 vs 25.9 percent) with TomoTherapy vs 3D conformal RT in patients with locally advanced HCC. “While the two modalities showed similar progression-free survival [PFS] and OS in tumors ≤5 cm, significant benefits in PFS and OS were seen in tumors larger than 5 cm,” said investigator Professor Jinsil Seong. “We therefore strongly suggest TomoTherapy for locally advanced HCC patients with tumors larger than 5 cm.”

Conference CoverageJan-Feb 201310

Christina Lau

Ponatinib, a new oral tyrosine-kinase in-hibitor (TKI), has demonstrated activity in drug-resistant chronic myeloid leuke-

mia (CML) and Philadelphia chromosome-pos-itive acute lymphocytic leukemia (Ph+ ALL) in adults in a pivotal phase II trial. [Abstract 163]

The positive results have led to an accelerated approval by the US FDA 3 months ahead of its official deadline for a decision on the drug.

Ponatinib is a pan-BCR ABL TKI with potent activity against native and mutant forms of the BCR-ABL protein and other kinases. It targets cells with the “gatekeeper” T315I mutation, which confers resistance to currently approved TKIs for CML and Ph+ ALL and is found in 5-20 percent of patients.

In the PACE (Ponatinib Ph+ ALL and CML Evaluation) trial, researchers assessed ponatinib in 499 patients with CML and Ph+ ALL who were either resistant to or intolerant of dasat-inib or nilotinib (R/I patients) or had the T3151 mutation. Nearly all patients were previously treated with ≥2 available TKIs (imatinib, dasat-inib, and/or nilotinib). The primary endpoint was major cytogenetic response (MCyR) within 12 months of treatment for those with chronic-phase CML, and major hematologic response within 6 months after treatment for those with advanced-phase CML or Ph+ ALL.

“In chronic-phase CML patients, 55 percent achieved MCyR, including 50 percent of R/I

patients and 70 percent of those with T3151 mutation,” reported lead investigator Professor Jorge E Cortes of the University of Texas MD Anderson Cancer Center in Houston, USA. “At 1 year, 91 percent of these patients remained in MCyR.”

Major hematologic response was achieved in 58 percent of patients with accelerated-phase CML (57 percent of R/I patients and 50 percent

54th American Society of Hematology (ASH) Annual Meeting and Exposition, 8-11 December 2012, Atlanta, USA

Ponatinib active in drug-resistant CML and ALL, gets FDA nod

Conference CoverageJan-Feb 201311

Naomi Rodrig

A phase III, open-label trial demonstrated significant progression-free survival

(PFS) and overall survival (OS) advantage with a combination of pomalidomide and low-dose dexamethasone (POM + LoDEX) over high-dose dexamethasone (HiDEX) in patients with difficult-to-treat multiple myeloma (MM). [Abstract LBA 6]

Current MM treatments include combina-tions of steroids like DEX with targeted thera-pies such as bortezomib and lenalidomide. However, many patients eventually become resistant to these therapies and have a poor prognosis. Pomalidomide is a novel drug with immunomodulatory and anti-angio-genic properties, which has shown activity in relapsed and refractory MM.

In the trial, 455 MM patients with primary refractory or relapsed and refractory disease were randomized to receive either POM + LoDEX (n=302) or HiDEX (n=153) in a 28-day cycle until disease progression or severe toxicity. The primary endpoint was PFS; secondary endpoints included safety, OS, and quality of life.

“After a median follow-up of 18 weeks, PFS was significantly longer with POM + LoDEX vs HiDEX [median, 15.7 vs 8.0 weeks; hazard ratio (HR), 0.45; p<0.001],” reported lead author Professor Meletios Dimopoulos of the Alexandra Hospital in Athens, Greece. An interim analysis showed that OS was also significantly longer with POM + LoDEX vs HiDEX alone (median, not reached vs 34 weeks; HR, 0.53; p<0.001), crossing the prespecified superiority boundary. This

with T3151 mutation) and 34 percent of those with blast-phase CML or Ph+ ALL (35 percent of R/I patients and 33 percent with T3151 mutation).

“Complete cytogenetic response was achieved in 46 percent of patients with chronic-phase CML, with higher response rates in patients who were exposed to fewer prior TKIs and those with shorter disease duration,” he pointed out.

According to Cortes, the similar response rates observed in patients with and without the T3151 mutation imply that ponatinib may work across a wide range of mutations associated with TKI resistance as well as in cases where

mutations are not detected. “Ponatinib may be able to transform

highly fatal forms of leukemia into a curable disease. We have simply never had any treat-ment produce such high rates of durable response in such a heavily treated group of patients,” he suggested. “Our next step is to test ponatinib’s potential as an initial therapy to prevent relapse.”

Ponatinib was well tolerated with minimal toxicities. In the trial, the most common adverse events were skin toxicity, elevation of pancreatic enzymes and/or pancreatitis, and myelosuppression.

Pomalidomide/dexamethasone combo improves MM outcomes

Conference CoverageJan-Feb 201312included 45 patients who received POM after progressing on HiDEX. Median duration of treatment was 12.4 weeks in the combination arm and 8 weeks in the HiDEX arm.

“Once the OS advantage of the combina-tion regimen was confirmed, the DSMB [Data and Safety Monitoring Board] recommended an immediate crossover from HiDEX to POM + LoDEX,” he said. “We are excited about these results, as they show that a combina-tion approach with POM + LoDEX is superior to current treatment options for hard-to-treat myeloma patients.”

Overall, 25 percent of patients in the combination arm and 38 percent on HiDEX monotherapy died, mostly due to progressive disease and infections. The primary reason

for discontinuation was progressive disease. Frequent grade 3/4 hematologic toxicities included neutropenia (42 percent on POM + LoDEX vs 15 percent on HiDEX), throm-bocytopenia (21 vs 24 percent), and febrile neutropenia (7 vs 0 percent). Other grade 3/4 toxicities were predominantly infections (24 vs 23 percent), hemorrhage (3 vs 5 percent), and glucose intolerance.

“We believe that this study provides the basis to consider the POM + LoDEX combi-nation as a new standard of care for patients who have exhausted most standard treat-ments for refractory disease, and may even offer greater benefit among less heavily treated patients as a first-line therapy,” suggested Dimopoulos.

Anthracycline can be safely omitted from B-cell ALL induction therapyElvira Manzano

The anthracycline daunorubicin can be safely omitted during induction therapy

for patients with standard-risk B-cell acute lymphoblastic leukemia (ALL), results of a randomized controlled phase III trial suggest. [Abstract 135]

Patients with standard-risk ALL are commonly treated with regimens that include initial infusions of daunorubicin. While the therapy is effective, prolonged use is associ-ated with cardiomyopathy and heart failure.

To determine whether daunorubicin can be safely left out of an initial 1-month induc-tion regimen, researchers evaluated 1,128 children (age 1-9 years) with ALL admitted

Conference CoverageJan-Feb 201313at 21 centers in France and Belgium. All were initially treated with prednisone prephase plus methotrexate, dexamethasone, vincris-tine and L-asparaginase 6,000 IU/m2 for nine infusions and had a good response. They were then randomized to receive a standard dose of daunorubicin (40 mg/m2 on days 22 and 29), or no daunorubicin.

After randomization, all patients received doxorubicin-based delayed intensification therapy, followed by 24 months of mainte-nance therapy. No leukemic induction failure was observed, resulting in a 99.7 percent complete response rate.

In the study, outcomes were similar whether or not patients received daunorubicin. Over a 5-year period, the event-free survival (EFS) rate was 92.9 percent with daunorubicin vs 93.3 percent without daunorubicin (p=0.89), while overall survival (OS) rate was 97.2 vs 98.2 percent [p=0.85]. There was also no differ-ence in complete remission rates or minimal residual disease (MRD) between groups.

“We now have strong evidence that reducing the amount of chemotherapy initially

administered to these children, who consti-tute the majority of ALL patients, does not negatively affect their immediate outcome,” said study author Dr. Andre Baruchel of the Robert Debré University Hospital in Paris, France. “Perhaps more importantly, we now know that eliminating harmful chemotherapy from their treatment can help minimize their risk of heart damage later in life.”

“There is no difference in complete remis-sion rate, MRD levels, EFS, OS, cumulative incidence of relapse [or] secondary malig-nancy in the randomized population,” Baruchel said. “We conclude that daunoru-bicin is dispensable during induction therapy in children with standard-risk B-cell ALL with good early response to vincristine, dexameth-asone and asparaginase.”

Commenting on the study, ASH Presi-dent Dr. Armaud Keating of the University of Toronto, Canada, said the study is impor-tant as the complication can be devastating in some patients. “Some eventually succumb to heart failure and may even become candi-dates for a heart transplant.”

Case StudyJan-Feb 201314

Capecitabine treatment in metastatic breast cancer

Dr. Ting-Ying NgAssociate ConsultantDepartment of Clinical OncologyTuen Mun HospitalHong Kong

Presentation and managementA 44-year-old Chinese woman presented

in 2004 with a mass in her right breast, for which she underwent a modified radical mastectomy in December 2004. Pathology re-vealed a grade 2 invasive ductal carcinoma; postoperative staging was IIa, T1cN1aM0. Surgical margins were close. Estrogen recep-tor (ER) was positive. The patient received adjuvant chemotherapy with four cycles of doxorubicin and cyclophosphamide, fol-lowed by radiotherapy to the chest wall and hormonal therapy with tamoxifen.

In 2007, MRI of the spine showed bone

metastases with a T10 compression fracture; this was confirmed by a subsequent PET-CT scan in August 2007, which showed metas-tases to multiple bones and to locoregional, mediastinal and neck nodes. The patient underwent a T10 laminectomy and T7–T12 internal fixation, and received postoperative radiotherapy to T6–L1. She also underwent ovarian ablation by radiation therapy, and was commenced on zoledronic acid in Sep-tember 2007 and letrozole in November 2007. However, with progression of bone metasta-ses on follow-up CT, hormonal therapy was changed to exemestane in February 2008.

CT scans in March and June 2009 showed enlargement of a previously noted right su-perior mediastinal lymph node, as well as development of a new right cervical node and multiple liver metastases. Exemes-tane and zoledronic acid were discontin-

Figure 1. November 2009, before capecitabine treatment, showing multiple liver metastases

Figure 2. February 2010, after four cycles of capecitabine, showing reduction in size of metastases

Case StudyJan-Feb 201315ued; thereafter, the patient received chemo-therapy with paclitaxel and carboplatin for six cycles.

In November 2009, follow-up CT scan revealed disease progression, with note of new and enlarging liver and bone metasta-ses. (Figure 1) Subsequently, the patient was commenced on second-line chemotherapy with capecitabine (2,500 mg/m2 daily for 2 weeks in each 3-weekly cycle). Re-assess-ment in February 2010, after four cycles of chemotherapy, revealed a good partial re-sponse: there was a marked decrease in size of some of the liver metastases, though the number of liver metastases remained static. (Figure 2)

Follow-up CT scan in September 2010 showed a further interval decrease in size and number of liver metastases. The patient was maintained on single-agent capecitabine for more than 2 years, receiving 34 cycles of chemotherapy before documentation of pro-gressive disease. The regimen was generally well tolerated; occasional side effects (grade 1/2 hand-foot syndrome, transient thrombo-cytopenia) necessitated short treatment de-lays.

DiscussionBreast cancer is the most common malig-

nancy in women and the fifth most common cause of cancer mortality in Hong Kong.1 In those with metastatic disease, the goals of therapy are to optimize quality of life and, if possible, prolong time to disease progres-sion and death.2

Initial palliation with endocrine therapy should be the primary consideration for pa-tients with metastatic, hormone receptor-positive tumors.2 Cytotoxic chemotherapy is appropriate for those with hormone refracto-

ry-disease, rapidly progressive visceral dis-ease, or early relapse after adjuvant therapy.2 Given the wide range of available chemo-therapeutic agents, it is important to individ-ualize therapy as much as possible. Anthra-cyclines and taxanes are the most preferred treatment options in this setting.

However, increasing early use of anthra-cyclines and taxanes has increased the like-lihood of recurrent metastatic disease that is resistant to these agents. Single-agent capecitabine has demonstrated good efficacy in these poor-prognosis patients: in studies of patients previously treated with an an-thracycline and/or a taxane, the median over-all response rate was 28 percent, the median time to progression was 4.7 months, and the median overall survival was 11.0 months.3 Our experience corroborates this data, with our patient notably having stable disease for more than 2 years while on capecitabine monotherapy.

Pooled data from 875 patients with meta-static breast cancer treated with capecitabine showed that the most frequently reported side effects were hand-foot syndrome (52 percent), diarrhea (48 percent) and nausea (42 percent).4 Adverse events were typically mild to moderate in intensity and could be controlled with treatment interruption and dose adjustment. Our patient’s hand-foot syndrome subsided with temporary discon-tinuation of capecitabine treatment.

Should capecitabine be used in combina-tion with taxane, or as monotherapy after an-thracycline or taxane failure? The published literature does not, as yet, provide a defini-tive answer to this question. For example, the combination of capecitabine and docetaxel resulted in significantly superior efficacy in time to disease progression (median, 6.1 vs

Case StudyJan-Feb 2013164.2 months), overall survival (median, 14.5 vs 11.5 months), and objective tumor response rate (42 vs 30 percent; p=0.006) compared with docetaxel alone, but was associated with more gastrointestinal side effects and hand-foot syndrome.5

Single-agent capecitabine is an attractive, convenient treatment option for cancer pa-tients, given that it is an oral therapy that can be taken at home. Treatment with capecitabine is associated with a substantial positive im-pact on quality of life (QoL): in one study, six of the 12 patients treated with a standard oral capecitabine regimen had improved QoL

scores,6 and in another, significant improve-ments in mean Global Health Status from baseline were recorded after six and 12 treat-ment cycles with single-agent capecitabine.7

In summary, this case illustrates the success-ful use of single-agent capecitabine in the man-agement of advanced metastatic breast cancer. In our patient, the treatment resulted in a fair-ly long duration of disease control and was well tolerated.

References:1. Top 10 Cancers in 2010. http://www3.ha.org.hk/cancereg/statistics.html.  2. Oncology (Williston Park) 2008;22:614-623. 3. The Oncologist 2006;11:325-335. 4. The Oncologist 2001;6:56-64. 5. J Clin Oncol 2002;20:2812-2823. 6. Anticancer Drugs 2002;13:405-410. 7. Eur J Cancer 2004;40:536-542.

NewsJan-Feb 201317

2012 in retrospective: Report highlights advances in oncology

Naomi Rodrig

Last month, the American Society of Clinical Oncology (ASCO) released its annual report on the top cancer advanc-

es of 2012, highlighting major achievements in precision medicine, cancer screening and over-coming treatment resistance.

Clinical Cancer Advances (CCA), now in its 8th year, was developed under the guidance of a 21-person editorial board of renowned experts in specific fields of cancer research. The editors reviewed studies published in peer-reviewed scientific or medical journals and presented at major scientific meetings over a 1-year period (October 2011-September 2012). Reviewed research covers the full range of clinical research disciplines: epidemiology, prevention, screening, early detection, treat-ment, patient care, biomarkers, tumor biology, and cancer disparities.

The 2012 CCA features a total of 87 studies, 17 of which are considered major, meaning they represent practice-changing results published in a peer-reviewed journal, and/or reports on treatments that received US FDA approval in the past year.

“Consistent, significant achievements are being made in oncology care with novel therapeutics, even in malignancies that have previously had few treatment options, as well as defining factors that will predict for response to treatment. ASCO’s report distills the most significant of these advances that are impacting the lives of cancer patients today,” said Dr. Bruce Roth, MD, Co-Executive Editor

of the report.• Two new therapies which delay progres-

sion of advanced breast cancer: - Adding targeted therapy to hormonal

therapy delays disease progression in postmenopausal women with advanced hormone receptor-positive breast cancer;

- Use of an ‘armed’ antibody, trastuzumab emtansine (TDM-1), to selectively deliver medicine to HER2-positive breast cancer cells without affecting normal cells.

• Preoperative chemotherapy and radiation improves survival for patients with esoph-ageal cancer.

• Screening with flexible sigmoidoscopy reduces colorectal cancer incidence and mortality.

• A new targeted treatment extends survival for patients with advanced prostate cancer.Many of the top clinical research advances

of 2012 involve therapeutic approaches that stem from a growing understanding of the complex biology of cancer, which enables development of targeted drugs and treat-ments tailored to molecular characteristics of individual patients and their tumors. This research has led to new FDA approvals for anticancer agents in 2012, some of which are

NewsJan-Feb 201318for treatment-resistant tumor types.

Between October 2011 and October 2012, the regulatory agency approved seven new anticancer drugs and expanded indications for five existing agents to provide new treat-ment options for patients with certain forms of myeloma (carfilzomib), leukemia (liposomal vincristine), breast cancer (pertuzumab and everolimus), skin cancer (vismodegib), prostate cancer (enzalutamide), gastroin-testinal stromal tumors (imatinib mesylate), colorectal cancer (cetuximab, ziv-aflibercept, and regorafenib), kidney cancer (axitinib), and soft tissue sarcoma (pazopanib).

Almost all of the newly approved drugs are targeted agents. Vismodegib marks the first FDA approval of a drug targeting the hedgehog signaling pathway, which plays an important role in tissue growth and repair. It is now being evaluated in clinical trials for colorectal, stomach, and pancreatic cancers.

In addition, new data from The Cancer Genome Atlas Project identify potential new drug targets in colorectal cancer, reveal that epigenetic regulation is critical for cancer cell

survival, and propose innovative technolo-gies for predicting chemotherapy response in patients with ovarian cancer.

Several other studies featured in the report address the need to identify treatment-resistant patients early, so they can be directed to alter-native, potentially effective treatments while being spared the adverse effects of regimens that are not likely to benefit them.

Referring to the impending spending cuts for cancer research, ASCO President Dr. Sandra Swain remarked, “We offer, again, an inspiring perspective on clinical cancer advances over the past year, but with a cautionary note: If current threats to federal funding materialize, future progress in cancer research will be seriously undermined.”

“To conquer cancer, we need to build bridges to the future: Bridges that will get scientific advances to the patient’s bedside quicker; bridges that will enable us to share information and learn what works in real time; bridges that will improve care for all patients, around the world,” she added.

NewsJan-Feb 201319

Regorafenib effective in GIST after standard treatment failure

Rajesh Kumar

Regorafenib prolongs progression-free survival (PFS) in patients with gastroin-

testinal stromal tumors (GIST) who had failed prior treatment with imatinib and/or sunitinib, a recent study has shown. [Lancet, e-pub ahead of print, DOI: 10.1016/S0140-6736(12)61857-1]

Until now, only imatinib and sunitinib have proven clinical benefits in advanced GIST, but almost all patients eventu-ally develop resistance to these agents, resulting in fatal disease progression, the authors noted.

Regorafenib – an oral multi-kinase inhib-itor that targets angiogenic, stromal and oncogenic receptor tyrosine kinases – has been approved last year by the US FDA for previously treated metastatic colorectal cancer (mCRC).

The latest phase III trial enrolled 199

patients with advanced GIST from 17 countries. Patients had failed at least previous imatinib or sunitinib and were randomized in a 2:1 ratio to receive either regorafenib 160 mg daily or placebo for the first 3 weeks of each 4-week cycle, plus best supportive care in both groups. The primary endpoint was PFS; placebo patients who progressed could cross-over to open-label regorafenib.

Median PFS by independent review was 4.8 months for regorafenib and 0.9 months for placebo (hazard ratio [HR], 0.2; p<0.0001). After progression, 56 placebo patients (85 percent) crossed over to regorafenib.

Drug-related adverse events were reported in 98 percent of patients assigned regorafenib and 68 percent of those on placebo. The most common regorafenib-related adverse events of grade >3 were hypertension (23 percent), hand-foot skin reaction (20 percent), and diarrhea (5 percent).

NewsJan-Feb 201320

PCA3 helps diagnose prostate cancer, avoid unnecessary biopsies

Christina Lau

Prostate cancer antigen 3 (PCA3) can aid the diag-nosis of pros-tate cancer in Chinese patients with

elevated prostate-specific antigen (PSA) lev-els and help avoid unnecessary biopsies, ac-cording to a study published recently in the Hong Kong Medical Journal.

“Although PSA level remains the most of-ten used marker for screening of the disease [prostate cancer], its positive predictive value is low. As a result, many patients are subjected to transrectal ultrasound-guided prostate bi-opsy (TRUSPB) with negative results,” wrote Dr. CF Ng and colleagues from the Division of Urology, Chinese University of Hong Kong and Diagcor Bioscience Incorporation Limited, who conducted the study. “There is therefore a need to develop more specific prostate can-cer markers to improve the diagnostic yield.” [Hong Kong Med J 2012;18:459-465]

As PCA3 is over-expressed in prostate can-cer, measurement of PCA3 in post-prostatic massage urine has become a new screening test for the malignancy, which is shown to be more sensitive and specific than serum PSA alone. [Cancer Res 1999;59:5975-5979; Clin Cancer Res 2007;13:939-943; Eur Urol 2008;54:1081-1088]

However, evidence supporting the benefi-cial role of PCA3 in diagnosing prostate cancer comes mainly from Western populations. “In-formation regarding its utility in the Chinese is scanty. During the design of this study, the commercial test from Gen-Probe was still un-available in our region,” the authors noted.

The team conducted a cross-sectional study to establish and verify the utility of measuring urine PCA3 mRNA levels in the diagnosis of prostate cancer among Hong Kong Chinese patients.

The study included a total of 149 patients and was carried out in two parts. In the first part, 102 post-prostatic massage urine samples were collected from patients with known pros-tate cancer (n=38) and controls with normal digital rectal examination and serum PSA <4 ng/mL (n=64). Urine levels of PCA3 and PSA mRNA were measured. The best cut-off for the PCA3 ratio (ratio of the Ct value of PCA3/PSA mRNA) in differentiating prostate cancer was 1.127.

In the second part of the study, post-pros-tatic massage urine samples from 47 patients with clinically suspected prostate cancer were collected before prostate biopsy. The perfor-mance of PCA3 as a diagnostic aid for prostate cancer was then assessed using the cut-off of 1.127. This cut-off value offered a high sensi-tivity of 71 percent and high specificity of 92 percent in diagnosing prostate cancer.

According to the authors, the combination of serum PSA and PCA3 may help improve the diagnostic yield in patients with elevated serum

NewsJan-Feb 201321PSA who were planned for TRUSPB (positive predictive value, 47 percent with elevated se-rum PSA alone vs 92 percent with elevated se-rum PSA plus positive PCA3 result).

“In future, combining clinical informa-

tion, serum PSA, and post-prostatic massage urine PCA3 levels could help in the counsel-ling of patients with suspected prostate cancer, whenever the possibility of TRUSPB is under consideration,” they concluded.

Mammography screening: Debate ongoing

Naomi Rodrig

Routine mammography screening has led to substantial overdiagnosis of breast cancer in the USA while hav-

ing only a small effect on mortality from the disease, a recent study found. [N Engl J Med 2012:367:1998-2005]

The findings provoked a strong public reaction, with some patient groups blaming the oncology community for unnecessary testing and treatment.

Using the Surveillance, Epidemiology and End Results (SEER) database, the study inves-tigators examined trends from 1976 through 2008 in the incidence of ductal carcinoma in situ and late-stage breast cancer among women >40 years of age.

They estimated that 1.3 million women were mistakenly diagnosed with breast cancer, when in fact they only had early-stage tumors which would not progress to advanced disease, and did not require treatment. In 2008 alone, breast cancer was ‘over-diagnosed’ in >70,000 women, accounting for about one third of all diagnosed cases.

Conversely, mammography screening has only marginally reduced the rate of advanced cancer presentation (by 8 percent) during the 3 decades despite substantial increases in the detection of early-stage cases. The authors concluded that “screening is having, at best, only a small effect on the rate of death from breast cancer.”

However, the American College of Radiology (ACR) disputes the findings, arguing the article was “deeply flawed and misleading” and based on false assumptions. Specifically, the baseline incidence of breast cancer was incor-rectly determined, according to the ACR, which warned, “If such misinformation is used to determine screening guidelines and recommendations, the cost may be lost lives.” [http://www.acr.org/News-Publications/News/News-Articles/2012/Quality-Care/20121112-ACRSBI-Bleyer-and-Welch-Breas t -Cancer-Screening , accessed 19 December 2012]

With such strong opinions for and against mass screening, it seems the question will remain open for some time.

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NewsJan-Feb 201322

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References:1.Packing insertofNplate. 2.http://www.news-medical.net/news/2008/08/24/40859.aspx. 3.http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2008/ucm116938.htm. 4. Blood doi:10.1182/blood-2011-03-340166. 5. Blood doi:10.1182/blood-2008-04-150078. 6. Int J Hematol doi: 10.1007/s12185.012-1065-2 7. Br J Haematol 2008;144:409-415. 8. J Med Econ2012;15:956-976.9.AmJHaematol2012;87:558-561.10.NEnglJMed2010;363:1889-1899.

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CalendarJan-Feb 201324Tumor Invasion and Metastasis20/1/2013 to 23/1/2013San Diego, USATel: +001 215 440 9300 / 866 423 3965Fax: +001 215 9313E-mail: aacr@aacr.orghttp://www.aacr.org/home/scientists/meetings--workshops/special-conferences/tumor-invasion-and-metastasis.aspx

2013 Gastrointestinal Cancers Symposium – Science and Multidisciplinary Management of GI Malignancies24/1/2013 to 26/1/2013San Francisco, USATel: +001 888 788 1522 / 703 449 6418Fax: +001 703 563 2715 E-mail: giregistration@jspargo.com http://www.gicasym.org/

2013 Genitourinary Cancers Symposium14/2/2012 to 16/2/2012Orlando, USATel: +001 888 788 1522 / 703 449 6418Fax: +001 703 563 2715E-mail: guregistration@jspargo.comhttp://gucasym.org

AACR/JCA Joint Conference: Breakthroughs in Basic and Translational Cancer Research21/2/2013 to 25/2/2013Maui, USATel: +001 215 440 9300Fax: +001 215 351 9165E-mail:myaacr@aacr.orghttp://www.aacr.org

European Society of Breast Imaging (EUSOBI) Breast MRI Training Course 20135/3/2013 to 6/3/2013Vienna, AustriaTel: +43 1 535 89 25E-mail: office@eusobi.orghttp://www.eusobi.org/cms/website.php?id=/en/index/eu-sobi_ws_03.htm

American Society of Preventive Oncology 37th Annual Meeting9/3/2013 to 12/3/2013Memphis, USAInfo: Heidi SahelTel: +608 263 9515Fax: +608 263 4497E-mail: hasahel@wisc.eduwww.aspo.org

13th St. Gallen International Breast CancerConference 201313/3/2013 to 16/3/2013St. Gallen, SwitzerlandInfo: Q Events AGTel: +041 71 228 58 08Fax: +041 71 228 58 09E-mail: bcc@qevent to s.bizhttp://www.oncoconferences.ch/dynasite.cfm?dsmid=111783

1st International Congress on Oncological Perspectives of Fertility Preservation: Gynecological & Breast Cancer21/3/2013 to 23/3/2013Berlin, GermanyTel: +972 3 5666166Fax: +972 3 5666177E-mail: info@comtecmed.comhttp://comtecmed.com/opfp/2013/Default.aspx

EORTC/EANO/ESMO 2013 – Trends in Central Nervous System Malignancies22/3/2013 to 23/3/2013Prague, Czech RepublicTel: +032 2 775 02 01Fax: +032 2 775 02 00E-mail: eortceanoesmo@ecco-org.euhttp://www.ecco-org.eu/Conferences/Conferences/EORTC_EANO_ESMO.aspx

8th International European Federation for ColoRectal (EFR) Cancer Congress4/4/2013 to 6/4/2013Vienna, AustriaTel: +001 319 76 90 Fax: +001 319 11 80E-mail: efr2013@at.kuoni.comhttp://www.efrcancer.org

CalendarJan-Feb 201325American Association for Cancer Research Annual Meeting 20136/4/2013 to 10/4/2013Washington DC, USA Tel: +001 708 486 0720E-mail: aacr@compusystems.comhttp://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2013.aspx

26th Annual Meeting of the American Society of Pediatric Hematology/Oncology24/4/2013 to 27/4/2013Miami, USATel: +001 847 375 4716Fax: +001 847 375 6483E-mail: info@aspho.orghttp://www.aspho.org/education/content/meeting.html

5th IMPAKT Breast Cancer Conference2/5/2013 to 4/5/2013 Brussels, BelgiumInfo: Nicole BulloTel: +041 91 973 19 39Fax: +041 91 973 19 18http://www.esmo.org/events/breast-2013-impakt.html

2013 ASCO Annual Meeting31/5/2013 to 4/6/2013Chicago, USATel: +001 703 449 6418Fax: +001 703 563 2715E-mail: ascoregistration@jspargo.comhttp://chicago2013.asco.org/

18th Congress of European Hematology Association (EHA)13/6/2013 to 16/6/2013Stockholm, SwedenTel: +031 20 679 3411E-mail: eha@mci.group.comhttp://ehaweb.org/congress-and-events/18th-congress/key-information/

Oncology Tribune is published 6 times a year by UBM Medica, a division of United Business Media. Oncology Tribune is a controlled circulation publication to medical practitioners in Asia. It is also available on subscription to members of allied professions. The price per annum is US$48 (surface mail) and US$60 (overseas airmail); back issues at US$5 per copy. Editorial matter published herein has been prepared by professional editorial staff. Views expressed are not necessarily those of UBM Medica. Although great effort has been made in compiling and checking the information given in this publication to ensure that it is accurate, the authors, the publisher and their servants or agents shall not be responsible or in any way liable for the continued currency of the information or for any errors, omissions or inaccuracies in this publication whether arising from negligence or otherwise howsoever, or for any consequences arising therefrom. The inclusion or exclusion of any product does not mean that the publisher advocates or rejects its use either generally or in any particular field or fields. The information contained within should not be relied upon solely for final treatment decisions.

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ISSN: 2078-2535

Dr. Michael Cheung Ming-Chee (Asia Cancer & Hematology Centre)

Dr. Daniel Chua Tsin-Tien (Hong Kong Sanatorium & Hospital)

Dr. William Foo (Hong Kong Baptist Hospital)

Dr. Carol Kwok (Princess Margaret Hospital)

Dr. Philip Kwok (Queen Elizabeth Hospital)

Dr. Ava Kwong (University of Hong Kong)

Editorial Advisory Board – Hong Kong

Oncology Tribune contains articles from Cancer Network, under license from UBM Medica LLC. Copyright © 2013 UBM Medica LLC.

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