	Assistant Director of Cancer Health Equity

Non-small cell lung cancer (NSCLC) is no longer a single disease, but a constellation of cancer types pathologically classified by histology. Hence, a fundamental first step in diagnosis is the retrieval of adequate tissue for histological classification. Greater effort is required from pathologists to, whenever possible, avoid the diagnosis of carcinoma not otherwise specified (NOS).

With the majority of patients with NSCLC presenting with advanced disease, minimally invasive small volume biopsies are increasingly utilized for diagnosis. The fine-needle aspirate (FNA) is the most routinely utilized biopsy approach, and while sufficient for cancer diagnosis, the amount of cellular material from FNAs can be sparse. This is often cited as the limiting factor to the correct classification of NSCLC histology, a problem further compounded by the poor cellular differentiation characteristic of advanced-stage disease. Together, these limitations contribute to errors in NSCLC classification and interobserver disagreement among pathologists.

Despite the advancements in the identification of driver mutations and actionable targeted drugs like the ALK-inhibitor crizotinib and the EGFR-inhibitor erlotinib, chemotherapy remains standard care for the majority of patients with metastatic NSCLC. However, in recent years, NSCLC classification by histology has become essential for the optimal selection of treatment:

		There is confirmed differential efficacy of pemetrexed favoring overall survival in patients with advanced NSCLC with adenocarcinoma (AC) histology and less favorable therapeutic efficacy in tumors of squamous cell carcinoma (SCC) histology.

		The VEGF-inhibitor bevacizumab is approved for first-line treatment in patients with non- SCC histology. Bevacizumab has been shown to contribute to improved response rates when added to standard therapy, but has a significant increase in pulmonary hemorrhage in SCC histology, which may be fatal.

		Efficacy studies of frontline tyrosine kinase inhibitors have shown that AC—but not SCC&mdash;histology can predict response to treatment. Most recently, a randomized trial in advanced NSCLC using nab-paclitaxel suggests a differential response rate favoring the drug’s use in patients with SCC histology.

Thus, histological diagnosis in NSCLC has become a major determinant of drug efficacy and prevention of undue toxicity to patients.

Additional immunohistochemical (IHC) stains can aid in the classification of NSCLC. However, numerous tissue assays can significantly deplete the amount of tissue available for additional molecular testing. Testing for emerging predictive genomic biomarkers such as 

 testing, will only compound the issue of obtaining sufficient tissue from small volume biopsies.

Paramount to ensuring the retrieval of adequate tissue for comprehensive diagnosis of NSCLC is close collaboration and communication among all providers involved in the diagnosis, classification, and treatment of patients. At our institution, we have developed an algorithm that standardizes the retrieval of adequate tissue and the effective pathological processing of specimens for both histology and molecular characterization. Yet, there remain cases where the complete characterization of NSCLC is not possible due to the sparsity of viable tissue samples. This problem has been a central concern, motivating the development of diagnostic technologies that can accurately measure multiple biomarkers in minimal tissue specimens.

Several technologies are being developed to accurately differentiate between AC and SCC by analyzing protein, RNA, or DNA components of cancer tissues. By collaborating with RNA expression analysis experts, we have analyzed the gene expression profiles of hundreds of human lung tumors and identified a panel of eight genes that accurately discriminates NSCLC tumors by AC and SCC histology (

). We used a sensitive and reproducible gene expression profiling assay, Panomics QuantiGene Plex 2.0 expression analysis system (QGS). The QGS is a nucleic acid hybridization-based assay that allows direct quantification of mRNA transcripts from FFPE tissue sections. Our research team was able to validate the diagnostic accuracy of the eight-gene panel (termed the A/S signature) retrospectively by analyzing archival tissues derived from surgically resected NSCLC tumors.

This emerging technology may prove useful for discrimination of NSCLC tumor histologies that are otherwise difficult to define by conventional pathological means. There is clearly a need for a technology that can accomplish this goal, and many studies of alternative technologies are ongoing nationally.

		Figure. Confirmation of QuantiGene Performance

		Eight putative histotype-specific genes (on y axis) selected by microarray meta-analysis were profiled in 25 NSCLC tumors (FFPEs) using the QuantiGene RNA analysis system. By hierarchical cluster analysis, the gene expression patterns discern AC from SCC.

The pathologic analysis of lung cancer has become increasingly complex. The amount of tissue required for establishing not only a cancer diagnosis, but also a treatment plan, has also increased. While molecular genetic testing has increased in value, establishing the pathologic subtype continues to be of significant importance. This step is critical for selecting the most active chemotherapy agents and avoiding potentially fatal toxicities. Thus, we must continue to advance the emerging technologies under development for improving the accuracy of this assessment and reducing the amount of tissue required.

Articles

The pathologic analysis of lung cancer has become increasingly complex, calling for continued attention to improving the accuracy of the assessment and reducing the amount of tissue required.

Tissue Truly Is the Issue in Advanced Non-Small Cell Lung Cancer

	The FDA is currently reviewing New Drug Applications for idelalisib in chronic lymphocytic leukemia (CLL) and indolent non-Hodgkin lymphoma (iNHL). What has the data shown in support of the drug’s efficacy?

	Ibrutinib is now approved for mantle cell lymphoma and CLL. What are your thoughts on the potential for sequencing ibrutinib and idelalisib?

At the 18th Annual International Congress on Hematologic Malignancies, Anas Younes, MD, sat down with 

 to discuss trends in the management of hematologic malignances. Younes, who is chief of the Lymphoma Service at Memorial Sloan Kettering Cancer Center, discussed a wide range of topics, including novel targeted agents, chimeric antigen receptor (CAR)-modified T-cell therapy, and the appropriate role for oncologists on social media

The PI3K delta specific inhibitor idelalisib has demonstrated significant activity in both relapsed CLL and relapsed follicular lymphoma. The CLL results came from randomized trials, so it was easy to compare treatments and get the data. The relapsed follicular lymphoma data was in patients who were refractory to both alkylating agents and rituximab, which is an area of unmet medical need. About 57% of these patients responded to single-agent oral therapy, which is remarkable.

Right now, there is no guidance as to which one you should start with. It is going to be based on what is available, what sort of indication, what is the fine print on the indication, what are the future guidelines from the NCCN, and so forth. You will likely have a group of patients who could be eligible for both, and it is difficult to pick one over the other.

There are some groups, however, that have clear contraindications. For example, ibrutinib should not be given to patients on an anticoagulant, such as Coumadin. That set should receive idelalisib.

	Other agents being developed in this space include IPI-145 and ABT-199. What are your thoughts on these therapies?

This is not the first time where we have multiple options, and, in the end, the treating oncologist and the patient discuss the pros and cons of each one and decide to go with one over the other. It is good to have more than one option.

IPI-145 is a gamma and delta pathway kinase inhibitor, so it has a wider range of activity than idelalisib. It seems to have good activity across different lymphoma malignancies, including indolent lymphoma, MCL, CLL, and T-cell lymphoma. It will be interesting to see where this will go moving forward.

	What about the anti-CD20 agent obinutuzumab?

	Please discuss your research on brentuximab vedotin that was recently published in 

ABT-199 is a selective Bcl-2 inhibitor that induces cell death. In phase I trials the data were impressive in CLL and MCL, and there is even a good signal in there for it in larger lymphomas. Although it is too early to call, I think it is going to be an active agent that we should watch very closely.

Obinutuzumab was recently approved for the treatment of CLL, and it seems to be more effective than rituximab in some subsets of B-cell lymphomas. Now we have to go through multiple randomized trials to determine, in a more scientific way, whether substituting rituximab with obinutuzumab would be more beneficial in these diseases that have an indication for rituximab. There is a good chance to build up on the success in CLL and potentially change the treatment paradigm for other B-cell lymphomas by replacing rituximab with obinutuzumab.

The antibody-drug conjugate brentuximab vedotin targets CD-30. It is approved by the FDA for patients with relapsed classical Hodgkin lymphoma and anaplastic large cell lymphoma. In the relapse setting, single-agent activity for brentuximab vedotin exceeds 75% in Hodgkin lymphoma and 86% in anaplastic large cell lymphoma. This is remarkable single-agent activity, so it makes a lot of sense to take a highly effective agent in a relapse setting and move it upfront and combine it with effective regimens.

	At the ASH Annual Meeting in December, there was a lot of excitement surrounding CAR-modified T-cell therapy. Can you discuss this treatment strategy and potential implications for clinical practice?

And that is what we did in Hodgkin lymphoma. The most widely used regimen for a newly diagnosed patient with Hodgkin lymphoma is ABVD. We added brentuximab to ABVD in this setting to determine if outcomes could be improved. When we administered ABVD plus brentuximab, there was an unexpected pulmonary toxicity, so the bleomycin had to be dropped from the ABVD. So right now, the experimental arm is AVD plus brentuximab, which is being randomized against ABVD. If the AVD plus brentuximab is better than ABVD, hopefully the treatment paradigm for Hodgkin lymphoma will change.

CAR-modified T-cell therapy is a technology that allows you to target different antigens based on what you plan in advance. The one that is most widely used is the CAR CD-19, which binds to the binding site of an antibody that targets CD-19 with a T-cell receptor machinery. There are different technologies for this, but the bottom line is you’re binding a T-cell receptor machinery to a portion of antibody that targets a target and this example is an antibody that targets CD-19. So you have an antibody on T cells that is artificially expressed. B cells express antibodies and T cells don’t express antibodies. Now you have a T cell that is armed with an antibody to CD-19. So you go find CD-19, you stick to it and then activate T cells and the T cells then kill the CD-19-positive cells.

	One final nonclinical question. You are active on social media. How can this platform be effectively used in the field of oncology?

The technology is very fascinating. The advantage of it is that this is a patient’s own autologous T cells—you don’t need allogeneic. So this is a T-cell therapy, an immune therapy, that is from your own cells, making it more effective. So, if the therapy is proven to be effective, you don’t need to worry about finding a donor and you don’t need to worry about GVHD and toxicity of allogeneic transplant. You can potentially widen the pool of patients who are eligible for immune therapy (T-cell therapy) as a potential replacement of allogeneic transplant, maybe a potential replacement for autologous transplant in the future. So it’s not only widening the pool of patients who may be eligible, but it also may be a replacement therapy for patients who would have been eligible for more toxic allogeneic transplant. This opens the door mainly for elderly patients with lymphoma, where most of them would not be eligible for transplant. Patients with large cell lymphoma or MCL who fail frontline therapy are not candidates for transplant because they can’t tolerate it, whereas potentially they can tolerate their own T cells going in without the need for toxic conditioning regimens.

Social media is where everybody has a presence: patients, foundations, caregivers, doctors, hospitals— everybody is on social media. But the name social media is sort of a misnomer. People think that it is just following the pattern of Facebook: friendship, sharing what you ate, what party you went to, and so forth. It is more like a grass-root communication tool where you can communicate with anyone at anytime, anywhere, with ease and accessibility.

There are two major advantages of having an oncologist like myself—as well as my colleagues from institutions across the world&mdash;on social media platforms: You are providing reliable information that corrects a lot of misinformation on the Web, and you are providing a public service for people who need credible information who can now reach out to you and ask for guidance.

This is not for one-on-one consultation. It is not for someone to reach out to you and say, “My son has this diagnosis, his doctor told him this, and what do you think?” This is not for consultation. This is for general guidance—to refer patients to clinical trials or point out that there is something there that you should explore. That is where I see my role on social media: providing a presence that people can trust and offering general guidance as a public service.

At the 18th Annual International Congress on Hematologic Malignancies, Anas Younes, MD, sat down with Oncology & Biotech News to discuss trends in the management of hematologic malignances. 

Emerging Treatments and Trends in Hematologic Malignancies: A Q&A With Anas Younes, MD

		Lymphoma Division Chief John Theurer Cancer Center at HackensackUMC

		Chief Science Officer and Director of Research and Innovation Regional Cancer Care Associates

Medicine is undergoing a revolution that will transform the practice of healthcare, including oncology.

The palpable excitement generated by everything happening in cancer care is also associated with a sense of anxiety and uncertainty, given the complexity of the disease and current landscape. How and will the changing medical landscape alter our practice? Will the current changes in the economics of medicine allow us to move toward more complex but rationale therapeutics?

The Human Genome Project transformed biology through its integrated Big Science approach, combining the expertise of engineers, computer scientists, and mathematicians, with biologists. The Human Genome Project has already revolutionized many fields of science, including microbiology, virology, infectious disease, plant biology, and cancer. On the other hand, the mounting evidence of the diversity and adaptability of cancer is daunting and makes us question how we will be able to truly develop precision medicine in oncology.

The emergence of systems biology will likely radically transform our current paradigms. Systems biology represents an experimental approach that attempts to study biological systems in a holistic manner—ie, through global, integrative and dynamic analyses of systems and diseases. Systems medicine aims at integrating multiscale biological information into predictive and actionable models that will help reshape our perception, understanding, and treatment of diseases, including cancer.

In the foreseeable future, clinicians, researchers, and ultimately, consumers and patients, will be increasingly equipped with a deluge of personal health information— from biomarkers of disease behavior, to disease risk, and eventually, P4 medicine (predictive, preventive, personalized, and participatory)&mdash;through the proactive participation from all major stakeholders in the healthcare system. In cancer, systems biology integrated with novel computational techniques will help dissect processes and causal factors involved in cancer development, progression, and response to therapies.

The ultimate best stratification of patients with cancer (one size does not fit all) and development of rationale therapeutics should be and will be our mantra for years to come. Knowledge is the best medicine. Along these lines, our 

Emerging Technology Symposium at the John Theurer Cancer Center

 on May 12 will describe in more details how systems biology is changing and will transform cancer care!

Emerging Breakthroughs in Cancer Care: Toward a Revolution?

It is a decision that faces every successful startup biotech: sell to Big Pharma or head for IPO waters, and ultimately, independence. Epizyme, a Cambridge, Massachusetts-based biotech, opted for the latter, with a successful IPO in 2013.

From its inception in 2007, Epizyme has entered into several major development deals that have allowed the company to remain independent while advancing its proprietary platform. Epizyme has strategic collaborations with Celgene, Eisai, and GSK, and others.

On the clinical side, Epizyme says on its website that its development strategy is based on “the systematic identification of genetic alterations that create oncogenes, selecting patients where a genetic alteration is found using a companion diagnostic, and then designing small molecule therapeutics to inhibit the oncogene.”

Specifically, Epizyme focuses on developing small molecule inhibitors of histone methyltransferases (HMTs), a class of 96 enzymes. HMTs can become oncogenic through genetic alterations. Based on their individual oncogenic potential, Epizyme is specifically targeting 20 of the 96 HMTs through its proprietary platform.

The company’s two lead candidates are the small molecule inhibitors EPZ-5676 and EPZ-6438. EPZ-5676, which inhibits the HMT DOT1L, is being developed for the treatment of acute leukemias that have a rearrangement of the 

 gene. EPZ-6438 inhibits the HMT EZH2 and is being evaluated for the treatment of non-Hodgkin lymphoma, as well as for INI1-deficient tumors.

, Robert Gould, PhD, chief executive officer of Epizyme, commented on the company’s plan for its lead products this year. “In 2014, we plan to have clinical studies ongoing to assess the proof of concept of our EPZ-5676 and EPZ-6438 therapeutic candidates in five genetically defined cancers. We plan to disclose data from both of these programs in the second half of 2014, including phase I study dose escalation and expansion stage data for EPZ-5676 and phase I dose escalation study data for EPZ-6438.”

Epizyme believes that its phase I EPZ-5676 study (NCT01684150) that includes acute leukemias with 

 rearrangements is the first clinical trial to evaluate an HMT inhibitor. The other proof-of-concept programs Epizyme has planned for EPZ-5676 this year involve pediatric patients with 

 rearrangements resulting from a chromosomal translocation and adult patients with 

 rearrangements due to partial tandem duplication.

In August 2013, the FDA granted orphan drug designation to EPZ-5676. Epizyme is developing the drug through a partnership with Celgene that allows the company to maintain the US rights to market EPZ-5676.

With its EZH2-inhibitor platform, Epizyme has launched a phase I/II clinical trial (NCT01897571) of EPZ-6438 involving patients with advanced solid tumors or relapsed/refractory B-cell lymphomas. A proof-of-concept study for young adult patients with synovial sarcomas is also planned for this year.

		*Data disclosure in second half of 2014.

		**Gated to phase I dose escalation data.

		MLL-r indicates mixed lineage leukemia-rearranged; POC, proof of concept;

Epizyme is developing EPZ-6438 through a collaboration with Eisai, which refers to the agent as E7438. The agreement stipulates that Eisai has exclusive worldwide rights to market the product, while retaining for Epizyme the option to co-develop and market EPZ-6438 in the United States. Epizyme is also collaborating with Eisai and Roche on creating a companion diagnostic for identifying patients with 

Epizyme, a Cambridge, Massachusetts-based biotech, opted for independence, with a successful IPO in 2013.

Epizyme Maintains Independence, Advances HMT-Inhibitor Platform

	Improvement in Outcomes With High-Intensity Induction Chemotherapy

Lymphoma expert Andre Goy, MD, discussed the emerging landscape of mantle cell lymphoma (MCL) therapy at the 18th Annual International Congress on Hematologic Malignancies. Several novel agents are being tested in clinical trials for MCL. “This field is changing rapidly,” said Goy, who is chairman and director, and chief of the Lymphoma Division at John Theurer Cancer Center.

According to Goy, the progression-free survival (PFS) of more than 5 years that current patients with MCL can experience is attributed to intensive chemotherapy approaches, and particularly, regimens that incorporate a high-dose version of the chemotherapy agent cytarabine. A recent analysis of 167 patients aged <65 years treated with intense chemotherapy regimens who were not on a clinical trial showed that patients treated with a high-intensity regimen had improved PFS and overall survival (OS) compared with those treated with R-CHOP.

For those patients who are younger, several studies have shown that an induction regimen containing high-dose cytarabine improves outcomes, with a 5-year event-free survival of 56% to 65%. A recent large European trial demonstrated that high-dose cytarabine in addition to R-CHOP significantly increased complete response rates and prolonged time to treatment failure from 46 months to 88 months (

 “This trial showed that the benefit of cytarabine is related to patients achieving minimal residual disease sooner and faster,” said Goy.

Still, there is a great need for novel therapies, as about 50% of patients are not eligible for intensive chemotherapies, and a relatively high relapse rate and chemoresistance persists. The MCL treatment scheme of chemotherapy followed by a transplant and more chemotherapy for those who relapse or become chemorefractory is not sufficient, said Goy, as the median duration of response in relapsed MCL is only 6 to 8 months with chemotherapy. “The new landscape is growing enormously and we have new options,” said Goy. “Agents are now being tested and approved in the relapsed and refractory setting and are slowly being moved into frontline treatment.”

	MCL Frontline Therapies for Elderly Patients

	Novel Agents in Development in the Relapsed Setting

One goal of new trials is to test whether the addition of novel therapies, such as bortezomib (Velcade) or ibrutinib (Imbruvica), to a chemotherapy backbone will achieve an earlier and deeper response in MCL. The second goal is to prevent relapse with either consolidation or maintenance therapy. A recent frontline study showed that adding bortezomib as either a maintenance or consolidation therapy improved 3-year PFS from 59% to 67% (

“R-CHOP alone is not enough for these patients,” said Goy. Researchers are evaluating whether bortezomib has a role in the frontline setting for elderly patients. Bendamustine (Treanda) plus rituximab (Rituxan) may be a new backbone that can be combined with novel agents, including bortezomib. Ongoing studies, such as the ECOG 1411 trial and a GOELAMS trial, are testing these combinations. Goy said that he believes that maintenance approaches will be part of routine MCL regimens in the future, based on improvement in survival of patients receiving maintenance after R-CHOP.

The goal of studies with newer agents is to get away from using chemotherapy in MCL. Bortezomib has been approved by the FDA since 2006 for treating MCL patients who had received one prior therapy. In 2009, updated results of the phase II PINNACLE trial, which involved 134 relapsed/refractory MCL patients, showed that single-agent bortezomib had an overall response rate of 33%, a complete response rate of 8%, and a median duration of response of 10 months.

 Since then, combination trials, such as bortezomib with rituximab and dexamethasone, have been building on the initial efficacy of bortezomib as a single agent. Currently, second-generation proteasome inhibitors, including carfilzomib (Kyprolis), are also in clinical trials in MCL.

Another group of agents being evaluated in relapsed/ refractory MCL are mTOR inhibitors. In a 162-patient phase III trial, the median PFS with temsirolimus (175 mg weekly for 3 weeks followed by 75 mg weekly) was 4.8 months compared with 1.9 months in the investigator’s choice arm.

 “The benefit was marginal but sufficient enough for approval in Europe in a relapsed setting based on this trial,” said Goy. Temsirolimus combined with rituximab could be a new treatment option and trials are ongoing in the frontline setting.

The immunomodulatory agent lenalidomide was approved in 2013 for use in relapsed or refractory MCL patients. The approval was based on the single-arm EMERGE study, which involved 134 heavily pretreated patients (median of four prior therapies). The overall response rate with single-agent lenalidomide was 28% and the median duration of response was 16.6 months.

 A patient subset analysis showed that there were clear responses for all patient characteristics analyzed.

There are several ongoing trials combining lenalidomide with agents such as rituximab, bortezomib, or both in the relapsed MCL setting. “The most exciting of these combinations is rituximab plus lenalidomide,” Goy noted. In a phase II first-line, chemotherapy-free trial of 31 patients, the overall response rate with the combination was 77% and the complete response rate was 40%.

 “These are early results but are very promising,” said Goy.

Other agents in development are predominantly focused on targeting the B-cell receptor pathways important in MCL. Idelalisib, an oral PI3K delta isoform inhibitor, was tested in a phase I trial in relapsed/ refractory MCL and had a response rate of 69% in patients receiving a dosage of ≥150 mg twice daily.

ABT-199, an oral second-generation BH3 mimetic which inhibits BCL-2, is also being examined in MCL. In a single-agent phase I study, all eight relapsed MCL patients had a partial response to treatment with ABT-199.

Ibrutinib, an oral inhibitor of BTK, was approved by the FDA for MCL in November 2013 based on a phase II clinical trial showing a response rate of 68%, including a complete response rate of 21%, in patients who had received at least one prior therapy.

“It’s a very exciting time in MCL and we need to focus on new clinical trials to develop nonchemotherapy options for elderly patients,” Goy concluded.

			LaCasce A, et al. Comparative outcome of initial therapy for younger patients with mantle cell lymphoma: an analysis from the NCCN NHL Database. 

			Hermine O, et al. Alternating courses of 3x CHOP and 3x DHAP plus rituximab followed by a high dose Ara-C containing myeloablative regimen and autologous stem cell transplantation (ASCT) increases overall survival when compared to 6 courses of CHOP plus rituximab followed by myeloablative radiochemotherapy and ASCT in mantle cell lymphoma: final analysis of the MCL Younger Trial of the European Mantle Cell Lymphoma Network (MCL net). 2012 ASH Annual Meeting. Abstract 151.

			Kaplan LD, et al. Bortezomib maintenance (BM) versus consolidation (BC) following aggressive immunochemotherapy and autologous stem cell transplant (ASCT) for untreated mantle cell lymphoma (MCL): CALGB 5043. International Conference on Malignant Lymphoma. Abstract 89.

			Goy A, et al. Bortezomib in patients with relapsed or refractory mantle cell lymphoma: updated time-to-event analyses of the multicenter phase 2 PINNACLE study. 

			Hess G, et al. “Phase III study to evaluate temsirolimus compared with investigator’s choice therapy for the treatment of relapsed or refractory mantle cell lymphoma.” 

			Goy A, et al. Single-agent lenalidomide in patients with mantlecell lymphoma who relapsed or progressed after or were refractory to bortezomib: phase II MCL-001 (EMERGE) study. 

			Ruan J, et al. Combination biologic therapy without chemotherapy as initial treatment for mantle cell lymphoma: multi-center phase II study of lenalidomide plus rituximab. 2013 ASH Annual Meeting. Abstract 247.

			Spurgeon SEF, et al. Final results of a phase I study of idelalisib, a selective inhibitor of phosphatidylinositol 3-kinase P110δ (PI3Kδ), in patients with relapsed or refractory mantle cell lymphoma (MCL). 2013 ASCO Annual Meeting. Abstract 8519.

			Davids, MS et al. The single-agent Bcl-2 inhibitor ABT-199 (GDC-0199) in patients with relapsed/refractory (R/R) non- Hodgkin lymphoma (NHL): responses observed in all mantle cell lymphoma (MCL) patients. 2013 ASH Annual Meeting. Abstract 1789.

			Wang ML, et al. Targeting BTK with ibrutinib in relapsed or refractory mantle-cell lymphoma. 

Lymphoma expert Andre Goy, MD, provides insight into the rapidly changing treatment landscape for patients with mantle cell lymphoma. 

April 2014 | Oncology & Biotech News

Tissue Truly Is the Issue in Advanced Non-Small Cell Lung Cancer

Emerging Treatments and Trends in Hematologic Malignancies: A Q&A With Anas Younes, MD

Emerging Breakthroughs in Cancer Care: Toward a Revolution?

Epizyme Maintains Independence, Advances HMT-Inhibitor Platform

Treatment Landscape for Mantle Cell Lymphoma Continues to Evolve