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Extending tamoxifen use improves breast cancer outcomes
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Overall mortality rate was also reduced in the tamoxifen continuation arm (639 vs 722 deaths.3 Jan-Feb 2013 Extending tamoxifen use improves breast cancer outcomes Naomi Rodrig T reating women with estrogen receptor (ER)-positive breast cancer with tamoxifen for 10 years reduced the rates of late recurrence and breast cancer mortality compared with the current standard of 5 years.Longer Against Shorter) study. [doi:10. the women who continued tamoxifen had a significantly lower recurrence rate (617 recurrences in 3. The greatest benefit was observed during 10 to 14 years after diagnosis. Risk of death from breast cancer 5 to 14 years after diagnosis was 12. p=0.846 women with ER-positive breast cancer between 1996 and 2005.328 breast cancer recurrences and 728 deaths after recurrence. All the women had been using tamoxifen for 5 years. and were then randomly assigned to continue treatment for another 5 years or stop. who presented the results at the 2012 CTRC-AACR* San Antonio Breast Cancer Symposium last month. Treatment allocation had little effect on either recurrence or death rates during the period of 5 to 9 years after diagnosis. p=0. [Lancet 2011.2 percent among those who continued use vs 15 percent among those who stopped.418 controls. Oxford University. “Five years of adjuvant tamoxifen is already an excellent treatment that substantially reduces the 15-year risk for recurrence and death from ER-positive breast cancer. p=0. according to the international ATLAS (Adjuvant Tamoxifen .428 women allocated to continue vs 711 in 3. After about 8 years of follow-up. Half had node-positive disease. there were 1. The study was simultaneously published in The Lancet.1016/S0140-6736(12)61963-1] The investigators enrolled 6.378:771-784] ATLAS now shows that 10 years of tamoxifen is even more effective. UK.01) than those who stopped after 5 years.01). However. “The main additional benefit from continuing tamoxifen treatment is to reduce breast cancer mortality during the second decade after .” said Dr. during the second decade following diagnosis.002) and a 29 percent lower breast cancer mortality rate (331 vs 397 deaths. Christina Davies.
which led to its accelerated approval by the US FDA recently. there was no apparent excess of endometrial cancer.” said Davies. Women and their doctors should be aware of this evidence when deciding how long to continue tamoxifen. “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. offering potential benefits with extended use of tamoxifen.2 percent) for controls. Happy New Year! The Editor . with endometrial cancer being the most life-threatening. Also reported in this issue are the 19th Hong Kong International Cancer Congress. overall mortality was significantly reduced by longer treatment. The study data may be practice changing.” She noted that continuing tamoxifen use can increase side effects.4 Jan-Feb 2013 premenopausal women. AACR: American Association for Cancer Research diagnosis. Because this risk is heavily outweighed by the reduction in breast cancer deaths.” Davies said.4 percent) for women randomized to continue vs 1.6 percent (mortality 0. The latest results suggest that 10 years of tamoxifen treatment can approximately halve breast cancer mortality during the second decade after diagnosis. As reported in this issue. “ATLAS showed that protection against breast cancer recurrence and death is greater with 10 years than with 5 years of tamoxifen use. In Progress in 2012 and beyond T he year 2012 concluded with two important conferences – the 35th Annual San Antonio Breast Cancer Symposium and the 54th American Society of Hematology Annual Meeting and Exposition. “The current recommendation is to stop tamoxifen or any other endocrine treatment after 5 years. The cumulative risk of endometrial cancer during years 5 to 14 was 3. and highlights from the American Society of Clinical Oncology’s 2012 annual report that summarizes major achievements in the field of cancer management. for whom tamoxifen is often the endocrine treatment of choice.” * CTRC: Cancer Therapy and Research Center. or any other endocrine treatment. key findings include the benefit of extending tamoxifen use to 10 years in patients with estrogen receptorpositive breast cancer and the efficacy of ponatinib in certain forms of drug-resistant leukemia.1 percent (mortality 0. We look forward to more exciting developments in 2013.
056).5 months for capecitabine (p=0.1 vs 4.2 months (p=0. 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. [DOI: 10.1200/JCO. Those in the intervention group also reported more knowledge about CPR after watching the video.9 vs 13.9570] The investigators randomized 150 patients with advanced cancer to listen to a verbal narrative describing CPR and the likelihood of successful resuscitation (control group. and those with triple-negative disease (14.2012. 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=1.4 vs 9.5 months).102). while median progression-free survival (PFS) was 4. [Abstract S6-6] Median OS was 15.4 months). n=80) or listen to an identical narrative and view a 3-minute video of a patient on ventilator and CPR being performed on a simulated patient (intervention arm. compared with 51 percent in the control group. Following the presentations. 79 percent of patients in the intervention group said they wanted no CPR. n=70). . suggesting that particular patient subgroups may benefit from eribulin therapy.5 months). However. No OS advantage for eribulin A phase III.5 Jan-Feb 2013 Briefs 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. 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.4 vs 10.3050). those with estrogen receptor (ER)-negative disease (14.43.9 months for eribulin vs 14. there was a trend towards longer OS with eribulin among patients with HER2negative breast cancer (15.
2 vs 85.. according to a study by the Australasian Laparoscopic Colon Cancer Study Group. Primary endpoints were 5-year overall survival.2 percent. The bimonthly journal is proud to announce its CME-accreditation in the following Asian countries: HONG KONG. peer-reviewed journal of paediatrics. . or freedom from recurrence (86. INDONESIA. p=0. From the research bench to your patient’s bedside – JPOG raises the quality of life of women and children in Asia.jpog.256:915-919] The trial investigated whether the short-term benefits associated with LCR [shorter hospitalization. and freedom from recurrence. Pick up a copy today and start earning CME points. less scarring. etc] could be achieved safely. For further details.com today. [Ann Surgery 2012. in Hong Kong. obstetrics and gynaecology in Asia. recurrence-free survival. MALAYSIA and SINGAPORE. At 5-year follow-up. A total of 601 patients with potentially curable colon cancer were randomized to receive LCR or OCR.0 percent.6 Jan-Feb 2013 Briefs Laparoscopic resection for colon cancer as good as open surgery L ong-term outcomes of laparoscopic-assisted colon resection (LCR) for colon cancer are comparable with those of open colon resection (OCR).64).6 percent. visit www. Malaysia and Singapore For over 35 years..85).70). without survival disadvantages.7 vs 76. JPOG has been the only regional. recurrence-free survival (72.7 vs 71. there were no significant differences between the LCR and OCR groups in overall survival (77. p=0. JPOG is NOW CME-Accredited. p=0. Indonesia.
has developed a cytolytic virus activation (CLVA) therapy for NPC. 8-9 November 2012 – Christina Lau reports Studies investigate EBV-targeted therapies for NPC R ecent understanding of the role of Epstein-Barr virus (EBV) infection in cancer pathogenesis has led researchers to develop EBV-targeted therapies for nasopharyngeal carcinoma (NPC). occasionally leading to the development of malignancies in the epithelium. EBV may remain latent.” Young noted.3 percent are EBV-associated lymphomas and carcinomas. J Immunother 2010. increasing the chances of developing EBV-associated malignancies. The development of EBV-associated cancer is an accident. EBV infects more than 90 percent of human population. CLVA therapy led to disease stabilization and was well tolerated. If epithelial cells are unable to differentiate. UK. around 2 million cancer cases per year are attributable to infections. for example. 10.” A Dutch team. “Globally.” he continued.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. University of Hong Kong. “In normal differentiating epithelial cells.” said Young.105:1898-1904.” said Professor Lawrence Young of the University of Birmingham. Of these cases.33:983-990] “Therapeutic vaccination represents a very exciting approach in NPC.” he said. These include EBV nuclear antigens [EBNAs] and latent membrane proteins [LMPs]. [Blood 2005. According to Young. researchers have started to develop EBV-targeted therapies that aim to activate the latent virus and then kill it when it replicates. “What EBV wants to do is to persist in a normal host and replicate. In three patients with refractory NPC. Success has been shown in patients with relapsed or refractory NPC.” As the EBV replication cycle is controlled by T cells. [Clin Cancer Res 2012. “Based on understanding of the impact of EBV latent gene expression on the oncogenic process. followed by the antiviral drug ganciclovir to block EBV replication and kill proliferating EBV-infected cells. “Researchers have produced a therapeutic vaccine by inserting inactive EBV EBNA1 and LMP2 genes into a safe virus vector . “Studies have shown that EBV adopts different forms of latent gene expression in different malignancies. The therapy involves the use of gemcitabine and valproic acid to induce EBV lytic cycle. Young suggested that anything affecting T cell immune response could allow EBV to replicate more and infect more cells.7 Jan-Feb 2013 Conference Covera ge 19th Hong Kong International Cancer Congress. however. The infection is predominantly asymptomatic with the virus establishing a lifelong persistent infection in the memory B cell compartment. the virus is able to replicate after epithelial infection.
Waddell TS et al. [J Clin Oncol 2011. this complex heterogeneity may explain the negative results of targeted therapies in the AVAGAST (Avastin in Gastric Cancer). According to Wong. In contrast. mTOR-. negative results of other targeted therapies can be explained by the highly heterogeneous nature of gastric cancer.30(suppl 4): abstract 5.” she said. Intratumoral heterogeneity adds another level of complexity. J Clin Oncol 2012. ESMO 2012. REAL-3 (Randomized Trial of EOC ± Panitumumab for Advanced and Locally Advanced Esophagogastric Cancer) and GRANITE-1 (Gastric Antitumor Trial with Everolimus) trials. ESMO 2012] There is currently little evidence on the predominant molecular aberrations in each histological. A Gastric cancer heterogeneity: Difficulty or opportunity? B reakthroughs in targeted therapy for advanced gastric cancer have come to a near standstill after the approval of trastuzumab for HER2-positive disease. EGFR and MET pathways are predominantly implicated in proximal non-diffuse tumors. This vaccine was shown to significantly boost T cell response in 15 of 18 NPC patients. while VEGF-related signaling is more common in the distal non-diffuse subtype. recurrent or metastatic EBV-positive NPC. EXPAND (Xeloda and Cisplatin in Advanced Esophagogastric Cancer). anatomical. According to a Hong Kong expert. In a review of the literature.29:3968-3976.8 Jan-Feb 2013 Conference Covera ge single-arm phase II clinical trial is ongoing in Hong Kong in patients with persistent. which can be used to refine patient selection for potential benefit.and MMP-related .30(suppl 15): abstract LBA4000. [J Clin Oncol 2012. which were conducted in unselected patient populations.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.” [modified vaccinia Ankara. “There are multiple subtypes of gastric cancer based on histological. HER3. anatomical or epidemiological subtype of gastric cancer. MVA]. J Clin Oncol 2012. epidemiological and molecular classifications. Lordick F et al. Hilda Wong of the Queen Mary Hospital. loss of E-cadherin and FGFR2-.” said Dr. Wong and colleagues found that HER2.
4 months.” she said. the majority of patients (93. BCLC B. 10 months). 16. In that trial. “In addition.3 percent) had . while discordance between metastasis and primary tumor and between immunohistochemistry and FISH assays is also common. including HCC with portal vein involvement. The efficacy and safety of SIRT with yttrium-90 was demonstrated in several trials. especially since we have no validated. as well as refractory colorectal cancer liver metastases and neuroendocrine tumor metastases. “SIRT with yttrium-90 is indicated for inoperable larger or multifocal HCC. [Therap Adv Gastroenterol 2012.” SIRT and TomoTherapy for HCC: Asian perspective S elective internal radiaton therapy (SIRT) in combination with sorafenib has demonstrated encouraging results in a recent study of Asian patients with non-resectable hepatocellular carcinoma (HCC).9 months. median survival was 12.pathways is more frequently involved in diffuse tumors. intratumoral heterogeneity and clinicopathological characteristics will provide insights into tumor biology and facilitate clinical selection of patients for targeted therapy. The disease control rate is approximately 80 percent. while data from Korea suggest that TomoTherapy is more effective than 3D conformal RT in locally advanced HCC. “Clarification of the correlation between molecular profile. e-pub 9 July] “These clinical classifications may contribute to the prospective selection of patients for targeted therapy. Studies have shown discordance within or between sections of the primary tumor in up to 79 percent of HER2-positive cases. BCLC C. compared with 40 percent with transarterial chemoembolization [TACE]. accessible and predictive biomarker for direct patient selection to date except HER2.8 months (BCLC A. 24. intratumoral heterogeneity of HER2 overexpression/amplification is of particular therapeutic relevance.” said Professor Pierce Chow of the National University of Singapore and Singapore General Hospital. including a multicenter European trial on HCC across all Barcelona Clinic Liver Cancer (BCLC) stages.” she continued.
Tumor response rate was 33.9 Jan-Feb 2013 Conference Covera ge line therapy for inoperable HCC without metastasis.5 percent. The phase I/II trial.” only one SIRT session. significant benefits in PFS and OS were seen in tumors larger than 5 cm. 23. 31.” said Chow.5 percent achieving partial regression. Median survival was 20.8 percent. and 44 percent achieving stable disease. 42.6 vs 25. “While the two modalities showed similar progression-free survival [PFS] and OS in tumors ≤5 cm.” reported Chow. with 12 percent of patients achieving complete regression.” In another study (n=106).2 months for those with BCLC C disease. “The median time to progression was 39 weeks.” said investigator Professor Jinsil Seong. and 8.” “As there is currently no established first- . “Tumor response was encouraging. 2-year. new lesions can arise from the liver or from metastasis. 81. known as AHCC005. while disease control rate was 79. The Asia-Pacific HCC Trials Group tested yittrium-90 followed by sorafenib. “We therefore strongly suggest TomoTherapy for locally advanced HCC patients with tumors larger than 5 cm.5 percent.54: 868-878] “While yttrium-90 is efficacious in causing complete or partial destruction of the tumor.9 percent) with TomoTherapy vs 3D conformal RT in patients with locally advanced HCC.” he continued.2 vs 30. included 34 patients with BCLC B or C HCC. researchers from the Yonsei University.2 percent.1 vs 52. TACE or radiofrequency ablation are eligible.6 months for patients with BCLC B disease. to see if this can prevent or delay the development of new lesions and improve outcomes in advanced HCC. [Hepatology 2011. and patients previously treated with surgery. Korea have shown significantly longer overall survival (OS) (1-year. 3-year. the HCC Trials Group has started a phase III randomized controlled trial to compare SIRT with sorafenib in patients with locally advanced HCC. “Recruitment is ongoing.
USA. “At 1 year. In the PACE (Ponatinib Ph+ ALL and CML Evaluation) trial. has demonstrated activity in drug-resistant chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphocytic leukemia (Ph+ ALL) in adults in a pivotal phase II trial. 91 percent of these patients remained in MCyR. dasatinib. Atlanta. 8-11 December 2012. and/or nilotinib). which confers resistance to currently approved TKIs for CML and Ph+ ALL and is found in 5-20 percent of patients. Ponatinib is a pan-BCR ABL TKI with potent activity against native and mutant forms of the BCR-ABL protein and other kinases. The primary endpoint was major cytogenetic response (MCyR) within 12 months of treatment for those with chronicphase CML. gets FDA nod Christina Lau P onatinib. Nearly all patients were previously treated with ≥2 available TKIs (imatinib. and major hematologic response within 6 months after treatment for those with advanced-phase CML or Ph+ ALL.” reported lead investigator Professor Jorge E Cortes of the University of Texas MD Anderson Cancer Center in Houston.10 Jan-Feb 2013 Conference Covera ge 54th American Society of Hematology (ASH) Annual Meeting and Exposition. [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. a new oral tyrosine-kinase inhibitor (TKI). It targets cells with the “gatekeeper” T315I mutation. 55 percent achieved MCyR.” Major hematologic response was achieved in 58 percent of patients with accelerated-phase CML (57 percent of R/I patients and 50 percent . researchers assessed ponatinib in 499 patients with CML and Ph+ ALL who were either resistant to or intolerant of dasatinib or nilotinib (R/I patients) or had the T3151 mutation. “In chronic-phase CML patients. USA Ponatinib active in drug-resistant CML and ALL. including 50 percent of R/I patients and 70 percent of those with T3151 mutation.
Pomalidomide is a novel drug with immunomodulatory and anti-angiogenic properties. which has shown activity in relapsed and refractory MM. The primary endpoint was PFS.53.7 vs 8. 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).0 weeks.11 Jan-Feb 2013 Conference Covera ge mutations are not detected. elevation of pancreatic enzymes and/or pancreatitis. [Abstract LBA 6] Current MM treatments include combinations of steroids like DEX with targeted therapies such as bortezomib and lenalidomide. 15. “Ponatinib may be able to transform highly fatal forms of leukemia into a curable disease.” he suggested. “Complete cytogenetic response was achieved in 46 percent of patients with chronicphase CML. p<0. and quality of life. p<0. the most common adverse events were skin toxicity. Greece. According to Cortes. not reached vs 34 weeks. 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 Pomalidomide/dexamethasone combo improves MM outcomes Naomi Rodrig A phase III. PFS was significantly longer with POM + LoDEX vs HiDEX [median. crossing the prespecified superiority boundary. with higher response rates in patients who were exposed to fewer prior TKIs and those with shorter disease duration.001). We have simply never had any treatment produce such high rates of durable response in such a heavily treated group of patients.45. OS. However.001]. secondary endpoints included safety. 0. “Our next step is to test ponatinib’s potential as an initial therapy to prevent relapse. hazard ratio (HR). 0. HR.” Ponatinib was well tolerated with minimal toxicities. In the trial.” reported lead author Professor Meletios Dimopoulos of the Alexandra Hospital in Athens. An interim analysis showed that OS was also significantly longer with POM + LoDEX vs HiDEX alone (median. In the trial. “After a median follow-up of 18 weeks. 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). 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. This . many patients eventually become resistant to these therapies and have a poor prognosis.” he pointed out. and myelosuppression.
and febrile neutropenia (7 vs 0 percent). researchers evaluated 1.” he said. and glucose intolerance. included 45 patients who received POM after progressing on HiDEX. [Abstract 135] Patients with standard-risk ALL are commonly treated with regimens that include initial infusions of daunorubicin. hemorrhage (3 vs 5 percent). 25 percent of patients in the combination arm and 38 percent on HiDEX monotherapy died.4 weeks in the combination arm and 8 weeks in the HiDEX arm.128 children (age 1-9 years) with ALL admitted . mostly due to progressive disease and infections.” Overall. To determine whether daunorubicin can be safely left out of an initial 1-month induction regimen. prolonged use is associated with cardiomyopathy and heart failure. “Once the OS advantage of the combination regimen was confirmed. results of a randomized controlled phase III trial suggest. the DSMB [Data and Safety Monitoring Board] recommended an immediate crossover from HiDEX to POM + LoDEX. The primary reason Anthracycline can be safely omitted from B-cell ALL induction therapy Elvira Manzano T he anthracycline daunorubicin can be safely omitted during induction therapy for patients with standard-risk B-cell acute lymphoblastic leukemia (ALL). “We are excited about these results. Median duration of treatment was 12. thrombocytopenia (21 vs 24 percent). Other grade 3/4 toxicities were predominantly infections (24 vs 23 percent). Frequent grade 3/4 hematologic toxicities included neutropenia (42 percent on POM + LoDEX vs 15 percent on HiDEX). and may even offer greater benefit among less heavily treated patients as a first-line therapy.” suggested Dimopoulos. as they show that a combination approach with POM + LoDEX is superior to current treatment options for hard-to-treat myeloma patients.12 Jan-Feb 2013 Conference Covera ge for discontinuation was progressive disease. “We believe that this study provides the basis to consider the POM + LoDEX combination as a new standard of care for patients who have exhausted most standard treatments for refractory disease. While the therapy is effective.
Armaud Keating of the University of Toronto. said the study is important as the complication can be devastating in some patients.85]. dexamethasone. we now know that eliminating harmful chemotherapy from their treatment can help minimize their risk of heart damage later in life. All were initially treated with prednisone prephase plus methotrexate. who constitute the majority of ALL patients. EFS.2 percent [p=0.2 vs 98. “Some eventually succumb to heart failure and may even become candidates for a heart transplant.” Commenting on the study.” at 21 centers in France and Belgium. After randomization.” “There is no difference in complete remission rate.000 IU/m2 for nine infusions and had a good response. In the study. Canada. cumulative incidence of relapse [or] secondary malignancy in the randomized population. followed by 24 months of maintenance therapy. “We now have strong evidence that reducing the amount of chemotherapy initially . does not negatively affect their immediate outcome. MRD levels. while overall survival (OS) rate was 97.7 percent complete response rate.3 percent without daunorubicin (p=0.9 percent with daunorubicin vs 93. or no daunorubicin.” said study author Dr. France. “We conclude that daunorubicin is dispensable during induction therapy in children with standard-risk B-cell ALL with good early response to vincristine. resulting in a 99.89). No leukemic induction failure was observed. Andre Baruchel of the Robert Debré University Hospital in Paris. outcomes were similar whether or not patients received daunorubicin. ASH President Dr. “Perhaps more importantly. vincristine and L-asparaginase 6. dexamethasone and asparaginase. There was also no difference in complete remission rates or minimal residual disease (MRD) between groups. the event-free survival (EFS) rate was 92.” Baruchel said. OS.13 Jan-Feb 2013 Conference Covera ge administered to these children. Over a 5-year period. They were then randomized to receive a standard dose of daunorubicin (40 mg/m2 on days 22 and 29). all patients received doxorubicin-based delayed intensification therapy.
However. MRI of the spine showed bone metastases with a T10 compression fracture. and received postoperative radiotherapy to T6–L1. T1cN1aM0. before capecitabine treatment. for which she underwent a modified radical mastectomy in December 2004. after four cycles of capecitabine. Exemestane and zoledronic acid were discontin- Figure 1. CT scans in March and June 2009 showed enlargement of a previously noted right superior mediastinal lymph node. Surgical margins were close. She also underwent ovarian ablation by radiation therapy. as well as development of a new right cervical node and multiple liver metastases. postoperative staging was IIa. with progression of bone metastases on follow-up CT. which showed metastases to multiple bones and to locoregional. showing multiple liver metastases Figure 2. The patient received adjuvant chemotherapy with four cycles of doxorubicin and cyclophosphamide.14 Jan-Feb 2013 Case Stud y Capecitabine treatment in metastatic breast cancer Dr. February 2010. hormonal therapy was changed to exemestane in February 2008. followed by radiotherapy to the chest wall and hormonal therapy with tamoxifen. Ting-Ying Ng Associate Consultant Department of Clinical Oncology Tuen Mun Hospital Hong Kong Presentation and management A 44-year-old Chinese woman presented in 2004 with a mass in her right breast. Pathology revealed a grade 2 invasive ductal carcinoma. The patient underwent a T10 laminectomy and T7–T12 internal fixation. this was confirmed by a subsequent PET-CT scan in August 2007. showing reduction in size of metastases . November 2009. mediastinal and neck nodes. In 2007. Estrogen receptor (ER) was positive. and was commenced on zoledronic acid in September 2007 and letrozole in November 2007.
if possible. revealed a good partial response: there was a marked decrease in size of some of the liver metastases. transient thrombocytopenia) necessitated short treatment delays. rapidly progressive visceral disease. Re-assessment in February 2010.7 months.500 mg/m2 daily for 2 weeks in each 3-weekly cycle). Discussion Breast cancer is the most common malignancy in women and the fifth most common cause of cancer mortality in Hong Kong. receiving 34 cycles of chemotherapy before documentation of progressive disease.2 Cytotoxic chemotherapy is appropriate for those with hormone refracto- . as yet. the median overall response rate was 28 percent. diarrhea (48 percent) and nausea (42 percent). Pooled data from 875 patients with metastatic breast cancer treated with capecitabine showed that the most frequently reported side effects were hand-foot syndrome (52 percent). the patient received chemotherapy with paclitaxel and carboplatin for six cycles. thereafter. or as monotherapy after anthracycline or taxane failure? The published literature does not. The regimen was generally well tolerated.4 Adverse events were typically mild to moderate in intensity and could be controlled with treatment interruption and dose adjustment. Anthracyclines and taxanes are the most preferred treatment options in this setting. and the median overall survival was 11.15 Jan-Feb 2013 Case Stud y ry-disease.2 Given the wide range of available chemotherapeutic agents. it is important to individualize therapy as much as possible. the median time to progression was 4. (Figure 2) Follow-up CT scan in September 2010 showed a further interval decrease in size and number of liver metastases. For example. follow-up CT scan revealed disease progression. (Figure 1) Subsequently. the patient was commenced on second-line chemotherapy with capecitabine (2. with note of new and enlarging liver and bone metastases.0 months. or early relapse after adjuvant therapy. Single-agent capecitabine has demonstrated good efficacy in these poor-prognosis patients: in studies of patients previously treated with an anthracycline and/or a taxane.1 In those with metastatic disease. The patient was maintained on single-agent capecitabine for more than 2 years. occasional side effects (grade 1/2 hand-foot syndrome. Should capecitabine be used in combination with taxane. provide a definitive answer to this question. the goals of therapy are to optimize quality of life and. with our patient notably having stable disease for more than 2 years while on capecitabine monotherapy. However. the combination of capecitabine and docetaxel resulted in significantly superior efficacy in time to disease progression (median. In November 2009. Our patient’s hand-foot syndrome subsided with temporary discontinuation of capecitabine treatment.3 Our experience corroborates this data. prolong time to disease progression and death. though the number of liver metastases remained static. increasing early use of anthracyclines and taxanes has increased the likelihood of recurrent metastatic disease that is resistant to these agents.1 vs ued. after four cycles of chemotherapy.2 Initial palliation with endocrine therapy should be the primary consideration for patients with metastatic. hormone receptorpositive tumors. 6.
22:614-623.40:536-542. 4.5 months).006) compared with docetaxel alone.hk/cancereg/statistics. 7. six of the 12 patients treated with a standard oral capecitabine regimen had improved QoL References: 1. 4. significant improvements in mean Global Health Status from baseline were recorded after six and 12 treatment cycles with single-agent capecitabine. Oncology (Williston Park) 2008.html. 5. Anticancer Drugs 2002.13:405-410. Eur J Cancer 2004. p=0. . http://www3. 14.7 In summary.2 months). 2. and objective tumor response rate (42 vs 30 percent. overall survival (median.ha. the treatment resulted in a fairly long duration of disease control and was well tolerated. J Clin Oncol 2002. given that it is an oral therapy that can be taken at home. but was associated with more gastrointestinal side effects and handfoot syndrome.org. 3.20:2812-2823.6 and in another.6:56-64. Treatment with capecitabine is associated with a substantial positive impact on quality of life (QoL): in one study. The Oncologist 2006. In our patient. 6.11:325-335. convenient treatment option for cancer patients. Top 10 Cancers in 2010. The Oncologist 2001.5 vs 11.16 Jan-Feb 2013 Case Stud y scores. this case illustrates the successful use of single-agent capecitabine in the management of advanced metastatic breast cancer.5 Single-agent capecitabine is an attractive.
screening. 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). and/or reports on treatments that received US FDA approval in the past year. even in malignancies that have previously had few treatment options. was developed under the guidance of a 21-person editorial board of renowned experts in specific fields of cancer research. now in its th 8 year. patient care. Co-Executive Editor of the report. • A new targeted treatment extends survival for patients with advanced prostate cancer. • Preoperative chemotherapy and radiation improves survival for patients with esophageal cancer. to selectively deliver medicine to HER2-positive breast cancer cells without affecting normal cells.17 Jan-Feb 2013 News 2012 in retrospective: Report highlights advances in oncology Naomi Rodrig L ast month. biomarkers. Clinical Cancer Advances (CCA). This research has led to new FDA approvals for anticancer agents in 2012.Adding targeted therapy to hormonal therapy delays disease progression in postmenopausal women with advanced hormone receptor-positive breast cancer. as well as defining factors that will predict for response to treatment. treatment. trastuzumab emtansine (TDM-1). The 2012 CCA features a total of 87 studies. significant achievements are being made in oncology care with novel therapeutics.Use of an ‘armed’ antibody. the American Society of Clinical Oncology (ASCO) released its annual report on the top cancer advances of 2012.” said Dr. -. some of which are . tumor biology. MD. • Two new therapies which delay progression of advanced breast cancer: -. cancer screening and overcoming treatment resistance. which enables development of targeted drugs and treatments tailored to molecular characteristics of individual patients and their tumors. Many of the top clinical research advances of 2012 involve therapeutic approaches that stem from a growing understanding of the complex biology of cancer. early detection. Reviewed research covers the full range of clinical research disciplines: epidemiology. • Screening with flexible sigmoidoscopy reduces colorectal cancer incidence and mortality. Bruce Roth. “Consistent. 17 of which are considered major. ASCO’s report distills the most significant of these advances that are impacting the lives of cancer patients today. prevention. highlighting major achievements in precision medicine. and cancer disparities. meaning they represent practice-changing results published in a peer-reviewed journal.
” she added. leukemia (liposomal vincristine). and pancreatic cancers. “We offer. Almost all of the newly approved drugs are targeted agents.18 Jan-Feb 2013 News survival. breast cancer (pertuzumab and everolimus). Referring to the impending spending cuts for cancer research. so they can be directed to alternative. ASCO President Dr. and soft tissue sarcoma (pazopanib). Sandra Swain remarked. future progress in cancer research will be seriously undermined. It is now being evaluated in clinical trials for colorectal. around the world. prostate cancer (enzalutamide). Vismodegib marks the first FDA approval of a drug targeting the hedgehog signaling pathway. potentially effective treatments while being spared the adverse effects of regimens that are not likely to benefit them. bridges that will improve care for all patients. gastrointestinal stromal tumors (imatinib mesylate). kidney cancer (axitinib). for treatment-resistant tumor types. reveal that epigenetic regulation is critical for cancer cell . and regorafenib). Several other studies featured in the report address the need to identify treatment-resistant patients early. In addition. stomach. bridges that will enable us to share information and learn what works in real time. we need to build bridges to the future: Bridges that will get scientific advances to the patient’s bedside quicker. but with a cautionary note: If current threats to federal funding materialize. skin cancer (vismodegib). ziv-aflibercept. the regulatory agency approved seven new anticancer drugs and expanded indications for five existing agents to provide new treatment options for patients with certain forms of myeloma (carfilzomib). Between October 2011 and October 2012. colorectal cancer (cetuximab. again. which plays an important role in tissue growth and repair. an inspiring perspective on clinical cancer advances over the past year. new data from The Cancer Genome Atlas Project identify potential new drug targets in colorectal cancer.” “To conquer cancer. and propose innovative technologies for predicting chemotherapy response in patients with ovarian cancer.
the authors noted. 0. plus best supportive care in both groups. Regorafenib – an oral multi-kinase inhibitor that targets angiogenic. placebo patients who progressed could crossover to open-label regorafenib. resulting in fatal disease progression.0001).9 months for placebo (hazard ratio [HR]. Median PFS by independent review was 4. and diarrhea (5 percent). a recent study has shown. only imatinib and sunitinib have proven clinical benefits in advanced GIST. The primary endpoint was PFS. 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. The latest phase III trial enrolled 199 patients with advanced GIST from 17 countries.2. [Lancet. stromal and oncogenic receptor tyrosine kinases – has been approved last year by the US FDA for previously treated metastatic colorectal cancer (mCRC). . e-pub ahead of print. Drug-related adverse events were reported in 98 percent of patients assigned regorafenib and 68 percent of those on placebo.1016/S0140-6736(12)61857-1] Until now. DOI: 10.19 Jan-Feb 2013 News Regorafenib effective in GIST after standard treatment failure Rajesh Kumar R egorafenib prolongs progression-free survival (PFS) in patients with gastrointestinal stromal tumors (GIST) who had failed prior treatment with imatinib and/or sunitinib. but almost all patients eventually develop resistance to these agents. The most common regorafenib-related adverse events of grade >3 were hypertension (23 percent). p<0. After progression. 56 placebo patients (85 percent) crossed over to regorafenib.8 months for regorafenib and 0. handfoot skin reaction (20 percent).
According to the authors. according to a study published recently in the Hong Kong Medical Journal. Eur Urol 2008. 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 commercial test from Gen-Probe was still unavailable in our region. In the second part of the study. its positive predictive value is low. Urine levels of PCA3 and PSA mRNA were measured. evidence supporting the beneficial role of PCA3 in diagnosing prostate cancer comes mainly from Western populations. “Information regarding its utility in the Chinese is scanty.20 Jan-Feb 2013 News PCA3 helps diagnose prostate cancer.59:5975-5979. the combination of serum PSA and PCA3 may help improve the diagnostic yield in patients with elevated serum . The study included a total of 149 patients and was carried out in two parts. “There is therefore a need to develop more specific prostate cancer markers to improve the diagnostic yield.127. which is shown to be more sensitive and specific than serum PSA alone. Clin Cancer Res 2007.13:939-943.127. This cut-off value offered a high sensitivity of 71 percent and high specificity of 92 percent in diagnosing prostate cancer.54:1081-1088] However. [Cancer Res 1999.” the authors noted. who conducted the study. measurement of PCA3 in post-prostatic massage urine has become a new screening test for the malignancy. The best cut-off for the PCA3 ratio (ratio of the Ct value of PCA3/PSA mRNA) in differentiating prostate cancer was 1. 102 post-prostatic massage urine samples were collected from patients with known prostate cancer (n=38) and controls with normal digital rectal examination and serum PSA <4 ng/mL (n=64). In the first part. avoid unnecessary biopsies Christina Lau P rostate cancer antigen 3 (PCA3) can aid the diag-nosis of prostate cancer in Chinese patients with elevated prostate-specific antigen (PSA) levels and help avoid unnecessary biopsies. many patients are subjected to transrectal ultrasound-guided prostate biopsy (TRUSPB) with negative results. post-prostatic massage urine samples from 47 patients with clinically suspected prostate cancer were collected before prostate biopsy. The performance of PCA3 as a diagnostic aid for prostate cancer was then assessed using the cut-off of 1. During the design of this study.” [Hong Kong Med J 2012.18:459-465] As PCA3 is over-expressed in prostate cancer. CF Ng and colleagues from the Division of Urology. As a result.” wrote Dr. “Although PSA level remains the most often used marker for screening of the disease [prostate cancer]. Chinese University of Hong Kong and Diagcor Bioscience Incorporation Limited.
PSA who were planned for TRUSPB (positive predictive value. the American College of Radiology (ACR) disputes the findings. and post-prostatic massage urine PCA3 levels could help in the counselling of patients with suspected prostate cancer. [N Engl J Med 2012:367:1998-2005] The findings provoked a strong public reaction. Epidemiology and End Results (SEER) database. when in fact they only had early-stage tumors which would not progress to advanced disease. “In future. the study investigators 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. it seems the question will remain open for some time. Download the digital edition today at www. according to the ACR. Conversely.com . accounting for about one third of all diagnosed cases.000 women. arguing the article was “deeply flawed and misleading” and based on false assumptions. a recent study found.21 Jan-Feb 2013 News tion.C a n c e r . which warned. the cost may be lost lives.” However. only a small effect on the rate of death from breast cancer. “If such misinformation is used to determine screening guidelines and recommendations.S c r e e n i n g . They estimated that 1.org/NewsPublications/News/News-Articles/2012/ Quality-Care/20121112-ACRSBI-Bleyera n d -We l c h .” [http://www. In 2008 alone. READ JPOG ANYTIME. ANYWHERE. combining clinical informa- Mammography screening: Debate ongoing Naomi Rodrig R outine mammography screening has led to substantial overdiagnosis of breast cancer in the USA while having only a small effect on mortality from the disease.3 million women were mistakenly diagnosed with breast cancer.B r e a s t . the baseline incidence of breast cancer was incorrectly determined.” they concluded. at best.jpog. The authors concluded that “screening is having. 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. and did not require treatment. with some patient groups blaming the oncology community for unnecessary testing and treatment. Specifically. 47 percent with elevated serum PSA alone vs 92 percent with elevated serum PSA plus positive PCA3 result). Using the Surveillance. accessed 19 December 2012] With such strong opinions for and against mass screening.acr. serum PSA. breast cancer was ‘over-diagnosed’ in >70. whenever the possibility of TRUSPB is under consideration.
1182/blood-2011-03-340166. 8.fda. http://www.363:1889-1899. 6. 3. 2.15:956-976. 9. Am J Haematol 2012.gov/NewsEvents/ Newsroom/PressAnnouncements/2008/ucm116938.news-medical. Packing insert of Nplate.87:558-561.3 • Safe and effective for long-term treatment of chronic ITP4-6 • Without Black Box Warning for the risk of hepatotoxicity1 • Improving patients’ health-related quality of life7-10 References: 1.144:409-415. 10.22 Jan-Feb 2013 News MARKET WATCH NPLATE®– Romiplostim Powder for Solution for Injection (Vial) – Kyowa Hakko Kirin Boosting platelet production with onceweekly romiplostim • Single-use 250 µg/vial1 • First TPO-receptor agonist approved by FDA2. Blood doi:10. J Med Econ 2012. Blood doi:10. Int J Hematol doi: 10.1007/s12185. 4. N Engl J Med 2010.1182/ blood-2008-04-150078. Br J Haematol 2008.aspx. http://www.net/news/2008/08/24/40859.htm. 5. .012-1065-2 7.
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