Description

The next few decades will see dramatic changes within the field of oncology. Whilst the burden of disease is set to increase, the available armamentarium to the oncologist will be greater, more robust and offer the potential to focus on individual needs. Future Oncology (ISSN 1479-6694) provides a forum for a new era of cancer care. The journal focuses on the most important advances and highlights their relevance in the clinical setting. Furthermore, Future Oncology delivers essential information in concise, at-a-glance article formats - vital in delivering information to an increasingly time-constrained community. The journal takes a forward-looking stance toward the scientific and clinical issues, together with the economic and policy issues, that confront us in a new era of cancer care. The journal includes news and views, literature awareness regarding new biomarkers, concise commentary and analysis, reports from the conference circuit and full review articles. Topics addressed include: Biological processes involved in cancer and how new understanding will impact treatment; Clinical implications and applications for new biomarkers; Impact of molecular genetics on prevention, screening, diagnosis and treatment; Integration of diagnostic and therapeutic approaches; Profiles of new anticancer agents; Selective and 'personalized' approaches; Screening programs and methodology.

Publisher details

Future Medicine

Publications in this journal

• Rethinking the war on cancer: multidisciplinary collaborations between biologists and physical scientists.

  Authors: Devin T Rosenthal, Sofia D Merajver

  Future oncology (London, England). 8(4):339-41.

• Efficacy of tosedostat, a novel, oral agent for elderly patients with relapsed or refractory acute myeloid leukemia: a review of the Phase II OPAL trial.

  Authors: Michael S Mathisen, Farhad Ravandi

  Future oncology (London, England). 8(4):351-7.

  Acute myeloid leukemia is most often diagnosed in patients older than 60 years of age. Overall, these patients have a poor prognosis, partly because they are typically unable to tolerate intensiveAcute myeloid leukemia is most often diagnosed in patients older than 60 years of age. Overall, these patients have a poor prognosis, partly because they are typically unable to tolerate intensive chemotherapy regimens traditionally offered to younger individuals. Furthermore, responses attained in these older patients are not durable, with most experiencing relapse within 1-2 years. Therefore, new strategies are needed to improve the outcome of older patients with acute myeloid leukemia. Tosedostat is an orally available aminopeptidase inhibitor shown to have activity in leukemia. This commentary discusses the background and results of an ongoing Phase II evaluation of tosedostat in elderly patients with relapsed or refractory acute myeloid leukemia. The data available to date is analyzed and future perspectives regarding the development of this agent is discussed.

• Panitumumab: a summary of clinical development in colorectal cancer and future directions.

  Authors: Guillem Argiles, Rodrigo Dienstmann, Elena Elez, Josep Tabernero

  Future oncology (London, England). 8(4):373-89.

  Panitumumab is a fully human, monoclonal antibody targeting the EGF receptor with proven clinical activity in KRAS wild-type metastatic colorectal carcinoma. Treatment with panitumumab has been shownPanitumumab is a fully human, monoclonal antibody targeting the EGF receptor with proven clinical activity in KRAS wild-type metastatic colorectal carcinoma. Treatment with panitumumab has been shown to significantly improve response rate and progression-free survival in this subgroup of patients, with a manageable toxicity profile. Panitumumab's first worldwide indication was as a single agent in chemorefractory patients. Recently, the EMA approved its use as part of a chemotherapy regimen in first- and second-line settings, following the encouraging results of large randomized Phase III trials. In order to identify patients with higher chances of benefiting from the treatment, additional molecular aberrations in the EGF receptor signaling pathway are being investigated as predictive biomarkers. In this article we review 10 years of drug development, focusing on the clinical evidence for panitumumab's indication in metastatic colorectal cancer and future strategies of investigation.

• PKM2: a new player in the β-catenin game.

  Authors: Frédéric Canal, Christine Perret

  Future oncology (London, England). 8(4):395-8.

  Evaluation of: Yang W, Xia Y, Ji H et al. Nuclear PKM2 regulates β-catenin transactivation upon EGFR activation. Nature 480(7375), 118-122 (2011). β-catenin is a key player in the regulation of geneEvaluation of: Yang W, Xia Y, Ji H et al. Nuclear PKM2 regulates β-catenin transactivation upon EGFR activation. Nature 480(7375), 118-122 (2011). β-catenin is a key player in the regulation of gene expression during morphogenesis and tumorigenesis. Although its transactivation often results from stimulation of the Wnt signaling pathway, Wnt-independent regulation of β-catenin has also been observed in cancer cells. This study discloses a new mechanism for the transactivation of β-catenin upon EGF receptor activation that relies on the binding of β-catenin to the PKM2 isoform in the nucleus. This interaction requires phosphorylation of β-catenin on the Y333 residue by c-Src and the PKM2 domain that binds phosphotyrosine. Importantly, the authors demonstrated that EGF-induced transactivation of β-catenin is necessary for brain tumor growth and that high levels of c-Src activity, Y333 β-catenin phosphorylation and nuclear localization of PKM2 altogether correlate with high aggressiveness of tumors in glioblastoma multiforme. Remarkably, this study reveals a novel role for PKM2 in cancer cells where PKM2 appears to be, in addition to its established role in aerobic glycolysis, a major coactivator of β-catenin transactivation. This nuclear function of PKM2 is shared with other transcription factors such as HIF-1α and OCT4, and highlights the nonmetabolic role of PKM2 during tumorigenesis.

• Bevacizumab and breast cancer: what does the future hold?

  Authors: Christina E Stevenson, Masayuki Nagahashi, Subramaniam Ramachandran, Akimitsu Yamada, Harry D Bear, Kazuaki Takabe

  Future oncology (London, England). 8(4):403-14.

  Breast cancer is a major health concern for many women, but despite the current standard therapies, many women still die of metastatic disease. Angiogenesis has been evaluated as a possible targetBreast cancer is a major health concern for many women, but despite the current standard therapies, many women still die of metastatic disease. Angiogenesis has been evaluated as a possible target for therapy and bevacizumab (Avastin(®), Genentech/Roche, CA, USA), a monoclonal antibody against VEGF-A, has been developed to target this. Current clinical trials utilizing bevacizumab have shown an increase in progression-free survival, but this has not translated to an increase in overall survival in breast cancer patients. In this article, we summarize the currently published trials utilizing bevacizumab in the treatment of breast cancer and describe various methods of measuring angiogenesis in vitro and in vivo. We also describe the related process of lymphangiogenesis, as this may contribute to the mechanism of cancer progression and may be a potential target for therapy in the future. Understanding these processes may help us develop new treatments for breast cancer.

• GPR56 in cancer progression: current status and future perspective.

  Authors: Liquan Yang, Lei Xu

  Future oncology (London, England). 8(4):431-40.

  Cell adhesion is a critical process during cancer progression and is mediated by transmembrane receptors. Recently, GPR56, a member of the adhesion family of G protein-coupled receptors, wasCell adhesion is a critical process during cancer progression and is mediated by transmembrane receptors. Recently, GPR56, a member of the adhesion family of G protein-coupled receptors, was established as a new type of adhesion receptor that binds to extracellular matrix proteins and shown to play inhibitory roles in melanoma progression. Further studies revealed that the extracellular portion and the seven transmembrane domains of GPR56 function antagonistically to regulate VEGF production and angiogenesis via a signaling pathway mediated by PKCα. Tissue transglutaminase was identified as the first extracellular matrix protein that binds to GPR56. It is a crosslinking enzyme in the extracellular matrix but is also expressed in the cytosol. Tissue transglutaminase plays pleiotropic roles in cancer progression. Whether and how it might mediate GPR56-regulated cancer progression awaits further investigation.

• Differences in outcome and toxicity between Asian and caucasian patients with lung cancer treated with systemic therapy.

  Authors: Ross A Soo, Tomoya Kawaguchi, Marie Loh, Sai-Hong I Ou, Marie P Shieh, Byoung-Chul Cho, Tony S Mok, Richie Soong

  Future oncology (London, England). 8(4):451-62.

  It is increasingly recognized that differences in overall survival and toxicity exist between Asian and caucasian patients with small-cell and non-small-cell lung cancer, with a longer survival,It is increasingly recognized that differences in overall survival and toxicity exist between Asian and caucasian patients with small-cell and non-small-cell lung cancer, with a longer survival, higher response rates and greater toxicity to chemotherapy and targeted therapy reported in Asian patients. Two global studies are used to illustrate how the proportions of Asian patients can influence survival outcome. Ethnicity is an important and complex characteristic that should considered in the design and conduct of a global clinical study, as the safety, tolerability and response may vary between Asian and caucasian patients. Whether ethnic differences in lung cancer survival are attributed to genetic differences among races or are simply a surrogate marker of differences in access to healthcare because of socioeconomic differences is unclear. Carefully designed prospective studies investigating ethnic-specific determinants of sensitivity and toxicity to systemic therapy are warranted.

• Complete response to exemestane in a patient with a desmoid tumor.

  Authors: Marc Debled, François Le Loarer, Françoise Callonnec, Isabelle Soubeyran, Chantal Cambon-Michot, Franck Dujardin, Antoine Italiano

  Future oncology (London, England). 8(4):483-6.

  Desmoid tumors are rare mesenchymal neoplasms without metastatic potential. Despite the benign nature of this condition, some patients develop disease progression despite all locoregional options forDesmoid tumors are rare mesenchymal neoplasms without metastatic potential. Despite the benign nature of this condition, some patients develop disease progression despite all locoregional options for care. Aggressive forms of desmoid tumors may induce morbidity that can lead to physical impairment and mortality that is occasionally observed as a result of local infiltrative growth and tissue invasion, in particular with abdominal disease. Few therapeutic options are available for patients with recurrent/unresectable desmoid tumors. Several studies have suggested the potential benefit of antiestrogens such as tamoxifen in this setting. Here we report the first description of the efficacy of an aromatase inhibitor in a patient with a desmoid tumor.

• Future approaches for the therapy of malignant glioma: targeting genes mediating invasion.

  Authors: Luni Emdad, Paul Dent, Devanand Sarkar, Paul B Fisher

  Future oncology (London, England). 8(4):343-6.

• Bortezomib: a proteasome inhibitor with an evolving role in select subtypes of B-cell non-Hodgkin's lymphoma.

  Authors: Jamie L Koprivnikar, Bruce D Cheson

  Future oncology (London, England). 8(4):359-71.

  Bortezomib is a novel proteasome inhibitor initially approved for use in multiple myeloma and currently under continued investigation as a treatment for numerous subtypes of non-Hodgkin's lymphoma.Bortezomib is a novel proteasome inhibitor initially approved for use in multiple myeloma and currently under continued investigation as a treatment for numerous subtypes of non-Hodgkin's lymphoma. One postulated mechanism of action in non-Hodgkin's lymphoma is the ability of bortezomib to ameliorate molecular dysregulation in NF-κB activation and regain cell cycle control. Results of clinical trials have varied widely based on lymphoma subtype. While response to bortezomib has been dismal in chronic lymphocytic leukemia and small lymphocytic lymphoma, reasonable responses have been attained in mantle cell lymphoma leading to its US FDA approval as a second-line agent for the treatment of mantle cell lymphoma in 2006. Bortezomib in combination with R-CHOP has also been suggested to improve response in certain molecular subgroups of diffuse large B-cell lymphoma. The role of bortezomib in follicular and marginal zone lymphomas remains less clear.

• New developments in the treatment of hepatic tumors.

  Authors: Isidoro Di Carlo, Adriana Toro

  Future oncology (London, England). 8(4):391-4.

  The International Association of Surgeons, Gastroenterologists and Oncologists (IASGO) hosted their annual world congress under the auspices of president Masatoshi Makuuchi from Japan and the generalThe International Association of Surgeons, Gastroenterologists and Oncologists (IASGO) hosted their annual world congress under the auspices of president Masatoshi Makuuchi from Japan and the general secretary Nicolas J Lygidakis. This year the congress was held in Tokyo, and the president was Wataru Kimura of Yamagata University. It is common knowledge that a major triple disaster struck Japan in March 2011. It was thought, for a time, that the congress would not take place, but the great courage and determination of the hosts allowed the conference to continue as scheduled. This congress was one of the most interesting hosted by the IASGO, evidenced by the presence of 909 participants from 59 countries, including invited speakers from Europe, America, Africa and Asia. The congress provided an opportunity to exchange knowledge of new techniques, methods of diagnosis and therapy. The program included symposiums, video presentations, free papers and poster presentations. This manuscript highlights presentations of the newest and most original material concerning the treatment of liver tumors, especially hepatocellular carcinoma.

• Elevated levels of HSF1 indicate a poor prognosis in breast cancer.

  Authors: Stuart K Calderwood

  Future oncology (London, England). 8(4):399-401.

  Evaluation of: Santagata S, Hu R, Lin NU et al. High levels of nuclear heat shock factor 1 (HSF1) are associated with poor prognosis in breast cancer. Proc. Natl Acad. Sci. USA 108, 18378-18383Evaluation of: Santagata S, Hu R, Lin NU et al. High levels of nuclear heat shock factor 1 (HSF1) are associated with poor prognosis in breast cancer. Proc. Natl Acad. Sci. USA 108, 18378-18383 (2011). HSF1 is the transcriptional activator of heat shock protein genes in both cell stress and cancer. The studies of Santagata et al. clearly establish that HSF1 levels are increased in the nuclei of mammary cancer cells, both at the in situ and invasive stages, and that these levels are closely correlated with increased mortality. HSF1 levels were elevated in estrogen receptor-positive cells, as well as HER2-expressing and triple-negative breast cancer cells, and higher levels of nuclear HSF1 were associated with a poor prognosis. These studies establish a clear role for HSF1 in human mammary carcinoma and suggest the potential for targeting HSF1 in breast cancer treatment.

• Preclinical imaging of the cellular and molecular events in the multistep process of bone metastasis.

  Authors: Geertje van der Horst, Gabri van der Pluijm

  Future oncology (London, England). 8(4):415-30.

  Bone metastasis is a complex process that ultimately leads to devastating metastatic bone disease. It is therefore of key interest to unravel the mechanisms underlying the multistep process ofBone metastasis is a complex process that ultimately leads to devastating metastatic bone disease. It is therefore of key interest to unravel the mechanisms underlying the multistep process of skeletal metastasis and cancer-induced bone disease, and to develop better treatment and management of patients with this devastating disease. Fortunately, novel technologies are rapidly emerging that allow real-time imaging of molecules, pathogenic processes, drug delivery and drug response in preclinical in vivo models. The outcome of these experimental studies will facilitate clinical cancer research by improving the detection of cancer cell invasion, metastasis and therapy response.

• Germline copy number variations and cancer predisposition.

  Authors: Ana Cristina Victorino Krepischi, Peter Lees Pearson, Carla Rosenberg

  Future oncology (London, England). 8(4):441-50.

  We present an overview of the role of germline copy number variations (CNVs) in cancer predisposition. CNVs represent a significant source of genetic diversity, although the mechanisms by which theyWe present an overview of the role of germline copy number variations (CNVs) in cancer predisposition. CNVs represent a significant source of genetic diversity, although the mechanisms by which they influence cancer susceptibility still remain largely unknown. Approximately 100 highly penetrant germline mutant genes are now known to cause cancer predisposition inherited in a Mendelian fashion; in this review, we show that nearly half of these genes have also been observed as rare CNVs associated with cancer. However, these highly penetrant alleles seem to account for less than 5% of all familial cancers. We surmise that most of the genetic risk of cancer in the general population must largely involve genes of low or moderate penetrance. In the last 5 years, studies have demonstrated that although common low penetrant CNVs are modest contributors to cancer individually, their combined impact on cancer predisposition must be taken into account in estimating cancer risk.

• Inactivation of X-linked tumor suppressor genes in human cancer.

  Authors: Runhua Liu, Mandy Kain, Lizhong Wang

  Future oncology (London, England). 8(4):463-81.

  Cancer cells silence autosomal tumor suppressor genes by Knudson's two-hit mechanism in which loss-of-function mutations and then loss of heterozygosity occur at the tumor suppressor gene loci.Cancer cells silence autosomal tumor suppressor genes by Knudson's two-hit mechanism in which loss-of-function mutations and then loss of heterozygosity occur at the tumor suppressor gene loci. However, the identification of X-linked tumor suppressor genes has challenged the traditional theory of 'two-hit inactivation' in tumor suppressor genes, introducing the novel concept that a single genetic hit can cause loss of tumor suppressor function. The mechanism through which these genes are silenced in human cancer is unclear, but elucidating the details will greatly enhance our understanding of the pathogenesis of human cancer. Here, we review the identification of X-linked tumor suppressor genes and discuss the potential mechanisms of their inactivation. In addition, we also discuss how the identification of X-linked tumor suppressor genes can potentially lead to new approaches in cancer therapy.

• Use of biosimilar epoetin to increase hemoglobin levels in patients with chemotherapy-induced anemia: real-life clinical experience.

  Authors: Leon Kerkhofs, Gilles Boschetti, Antonio Lugini, Dana-Lucia Stanculeanu, Andrés Garcia Palomo

  Future oncology (London, England).

  Aim: To evaluate the effectiveness of a biosimilar erythropoiesis-stimulating agent (Binocrit(®)) for the treatment of patients with cancer and chemotherapy-induced anemia in real-life clinicalAim: To evaluate the effectiveness of a biosimilar erythropoiesis-stimulating agent (Binocrit(®)) for the treatment of patients with cancer and chemotherapy-induced anemia in real-life clinical practice. Materials & methods: Data were collected retrospectively from patients at five European centers (in France, Italy, The Netherlands, Romania and Spain) who received treatment with Binocrit. Hemoglobin (Hb) levels were recorded at regular intervals during Binocrit therapy for up to 26 weeks. Hb response (an increase of ≥1 g/dl in 4 weeks or a Hb level in the range 10-12 g/dl during the study) was assessed in patients with a Hb level ≥8.5 g/dl at the start of therapy who received treatment for at least 6 weeks. Hb response rates in patients who did and did not receive intravenous (iv.) iron were also assessed, and data on any serious unexpected adverse events were collected. Results: Among evaluable patients (n = 113), 79% achieved a Hb response. Response rates were similar among evaluable patients who received an initial Binocrit dose of 30,000 or 40,000 IU/week (81 vs 78%; p = not significant). The Hb response rate was significantly greater in patients who received iv. iron than in patients who did not receive iv. iron (93 vs 77%; p < 0.05). No serious unexpected adverse events were reported. Conclusion: Use of the biosimilar erythropoiesis-stimulating agent Binocrit is effective and safe for the treatment of patients with cancer and chemotherapy-induced anemia. Supplementation with iv. iron increases the response rate compared with oral or no iron supplementation.

• Biosimilar medicines in oncology: single-center experience with biosimilar G-CSF.

  Authors: Nello Salesi, Barbara Di Cocco, Maria Colonna, Enzo Veltri

  Future oncology (London, England).

  Aims: A biosimilar medicine is one with proven similarity to a reference biological product for which the patent has expired and whose active ingredient is produced or derived from a living organism.Aims: A biosimilar medicine is one with proven similarity to a reference biological product for which the patent has expired and whose active ingredient is produced or derived from a living organism. Recombinant granulocyte colony-stimulating growth factors (G-CSF) are used for the prophylaxis of febrile neutropenia. Materials & methods: In this observational, single-center study, a total of 48 patients with solid tumors were treated with a new biosimilar G-CSF (Zarzio(®)) for 4-14 days from the day following the end of chemotherapy. Results: Between October 2010 and July 2011, biosimilar G-CSF was administered as primary prophylaxis in 37 patients and as secondary prophylaxis in 11 patients in our clinic. The median length of G-CSF administration was 7 days (range: 1-12 days). Three cases of febrile neutropenia were reported: two in patients with prostate adenocarcinoma and one in a patient with pulmonary squamous cell carcinoma and multiple secondary skeletal lesions. These patients were treated with antibiotics and improved within 24 h without the need for hospitalization. Nonfebrile grade 4 neutropenia was observed in a further six patients. Conclusion: Our experience indicates that the use of biosimilar G-CSF is safe and effective at reducing neutropenic complications in patients with solid tumors and may be associated with cost savings.

• Fighting fire with fire: rewiring tumor cells for oncolytic virotherapy.

  Authors: Douglas J Mahoney, David F Stojdl

  Future oncology (London, England). 8(3):219-21.

• Evaluation of MVA-5T4 as a novel immunotherapeutic vaccine in colorectal, renal and prostate cancer.

  Authors: Robert J Amato, Mika Stepankiw

  Future oncology (London, England). 8(3):231-7.

  This paper reviews the development of the combination of modified vaccinia Ankara (MVA) to deliver the tumor-associated antigen 5T4 as a novel immunotherapeutic vaccine. The oncofetal antigen 5T4 isThis paper reviews the development of the combination of modified vaccinia Ankara (MVA) to deliver the tumor-associated antigen 5T4 as a novel immunotherapeutic vaccine. The oncofetal antigen 5T4 is highly expressed in 80% of breast, kidney, colorectal, prostate and ovarian carcinomas, making it an ideal antigen for vaccine therapy. To date, more than 3000 doses of MVA-5T4 have been administered to colorectal, renal and prostate cancer patients, with rare occurrences of grade 3 or 4 vaccination-related adverse events being observed. Studies have demonstrated that MVA-5T4 is safe and highly immunogenic, both as monotherapy and in combination with other standard of care therapies. Although an immune response has been observed, antitumor activity has been modest or absent in clinical trials. A Phase III trial resulted in the development of an immune response surrogate that is to be applied to all future MVA-5T4 clinical trials. With minimal side effects and the ability to produce a strong immunogenic response, MVA-5T4 is a viable addition to the cancer therapy arsenal.

• Cortical dysplasia: a possible substrate for brain tumors.

  Authors: Shiyong Liu, Chunqing Zhang, Haifeng Shu, Didier Wion, Hui Yang

  Future oncology (London, England). 8(3):251-8.

  The similarities between brain tumor stem cells and neural stem cells suggest a possible stem cell origin of tumorigenesis. Recently, cells with features of stem cells have been observed in lesionsThe similarities between brain tumor stem cells and neural stem cells suggest a possible stem cell origin of tumorigenesis. Recently, cells with features of stem cells have been observed in lesions of adult and pediatric cortical dysplasia (CD). Given the evidence for a close relationship between CD and certain brain tumors, together with the finding that CD neural stem cells/progenitors are abnormally developed, we propose that CD is a possible substrate for brain tumors. The neural stem cells/progenitors in CD have accumulating abnormalities, and these abnormal stem/progenitor cells may be the initiating, transformed cells of brain tumors, when subsequently exposed to a carcinogen.

• Endocrine resistance in breast cancer: molecular pathways and rational development of targeted therapies.

  Authors: Ryan P Roop, Cynthia X Ma

  Future oncology (London, England). 8(3):273-92.

  Endocrine resistance presents a major challenge in the management of estrogen receptor (ER)-positive breast cancer and is an area under intense investigation. Although the underlying mechanism isEndocrine resistance presents a major challenge in the management of estrogen receptor (ER)-positive breast cancer and is an area under intense investigation. Although the underlying mechanism is still poorly understood, many studies point towards the 'cross-talk' between ER and growth factor receptor signaling pathways as the key in the development of estrogen-independent growth in breast cancer. This review aims to provide the reader our current understanding of various molecular pathways that mediate endocrine resistance and that are being evaluated as therapeutic targets for ER-positive breast cancer. While most of the agents that target these pathways have only been tested in Phase I or small Phase II trials, some have shown encouraging results. A critical issue that remains is the development of research strategies and clinical trials that take into account the molecular heterogeneity of ER-positive breast cancer.

• Optical spectroscopy: current advances and future applications in cancer diagnostics and therapy.

  Authors: Dj Evers, Bhw Hendriks, Gw Lucassen, Tjm Ruers

  Future oncology (London, England). 8(3):307-20.

  Optical spectroscopy (OS) is a tissue-sensing technique that could enhance cancer diagnosis and treatment in the near future. With OS, tissue is illuminated with a selected light spectrum. DifferentOptical spectroscopy (OS) is a tissue-sensing technique that could enhance cancer diagnosis and treatment in the near future. With OS, tissue is illuminated with a selected light spectrum. Different tissue types can be distinguished from each other based on specific changes in the reflected light spectrum that are a result of differences on a molecular level between compared tissues. Therefore, OS has the potential to become an important optical tool for cancer diagnosis and treatment monitoring. In recent years, significant progress has been made in the discriminating abilities of OS techniques between normal and cancer tissues of multiple human tissue types. This article provides an overview of the advances made with diffuse reflectance, fluorescence and Raman spectroscopy techniques in the field of clinical oncology, and focuses on the different clinical applications that OS could enhance.

• Anal metastasis from breast cancer: a case report and review of the literature.

  Authors: Annamaria Bochicchio, Alfredo Tartarone, Orazio Ignomirelli, Giuseppe Latorre, Rodolfo Cangiano, Giuseppina Gallucci, Mariarosa Coccaro, Elisa Feudale, Michele Aieta

  Future oncology (London, England). 8(3):333-6.

  Breast cancer usually metastasizes towards the lymph nodes, lung, bone, liver or brain; metastatic gastrointestinal involvement is rare and anal metastases are extremely rare. Necroscopic studiesBreast cancer usually metastasizes towards the lymph nodes, lung, bone, liver or brain; metastatic gastrointestinal involvement is rare and anal metastases are extremely rare. Necroscopic studies report a 6-18% incidence of extra-hepatic gastrointestinal metastases, and the most frequent sites of the GI tract involved are the stomach and the small intestine. We report a case with anal metastasis from breast cancer and a review of the associated literature.

• FoxM1: a potential drug target for glioma.

  Authors: Yu Li, Sicong Zhang, Suyun Huang

  Future oncology (London, England). 8(3):223-6.

• Surgical considerations in patients receiving neoadjuvant systemic therapy.

  Authors: Akhil Chawla, Kelly K Hunt, Elizabeth A Mittendorf

  Future oncology (London, England). 8(3):239-50.

  Neoadjuvant chemotherapy is being increasingly used in the treatment of patients presenting with early-stage, operable breast cancer. Neoadjuvant chemotherapy downsizes most tumors, allowingNeoadjuvant chemotherapy is being increasingly used in the treatment of patients presenting with early-stage, operable breast cancer. Neoadjuvant chemotherapy downsizes most tumors, allowing appropriately selected patients to undergo breast-conserving therapy. Management of the axilla in patients receiving neoadjuvant chemotherapy is dictated by whether patients present with clinically node-negative or node-positive disease. Patients with clinically node-negative disease can undergo sentinel lymph node dissection after neoadjuvant chemotherapy, with axillary lymph node dissection reserved for patients with a positive sentinel lymph node. For patients with clinically node-positive disease at presentation, the current standard of care is axillary lymph node dissection. An ongoing cooperative group trial is investigating the utility of sentinel lymph node surgery in the clinically node-positive population.

Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.