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ONCOLOGY Vol 28 No 9

I was recently consulted concerning a patient in the ICU at my hospital with advanced breast cancer, but I soon realized there were much larger issues at stake. This woman is in her 50s and was diagnosed approximately 1 year ago with metastatic triple-negative breast cancer.

Cognitive dysfunction during and following treatment for cancer, often referred to as “chemobrain,” is an adverse effect of cancer treatment that may interfere with patients’ ability to resume their precancer lifestyle, with subsequently reduced quality of life.

Much of the existing research into the phenomenon commonly referred to as “chemobrain” has been descriptive, and we know enough now to identify some patients at risk for cognitive changes after a diagnosis of cancer.

With the growing number of cancer survivors, there is increased interest in understanding and preventing post-treatment sequelae that may limit full recovery to prediagnosis health.

This review will focus largely on the effects of systemic cytotoxic treatment on cognitive function, reflecting what has been most extensively studied in the literature.

A 71-year-old woman presented with back pain and was incidentally found to have a left upper pole renal mass. She underwent left open partial nephrectomy; the pathology results revealed a 2.2-cm clear-cell renal cell carcinoma (RCC) with negative margins and a Fuhrman nuclear grade of 2.

While definitions of follicular lymphoma maintenance therapy in clinical trials and clinical practice have been somewhat variable, ideally maintenance therapy would be limited to patients in complete remission or with minimal residual disease following initial therapy

The rationale for maintenance therapy in indolent non-Hodgkin lymphoma was derived from historical data suggesting that despite robust response rates to standard therapy, most patients eventually relapse and disease-free intervals become progressively shorter.

Intratumor heterogeneity is one of the biggest challenges in cancer diagnosis and treatment. Despite morphologic and clinical recognition of tumor heterogeneity, an understanding of it at a molecular level has only begun to emerge in recent years.

It may be necessary to broaden our concept of the malignant process beyond that of a disease to be attacked—to one that reflects a deeper understanding of the fundamentals of living systems.

Cancer heterogeneity, long recognized as an important clinical determinant of patient outcomes, was poorly understood at a molecular level. Genomic studies have significantly improved our understanding of heterogeneity, and have pointed to ways in which heterogeneity might be understood and defeated for therapeutic effect.

Postpartum breast cancer represents a high-risk, under-recognized subset of young women’s breast cancer. The lack of clear identity for postpartum breast cancer is due in part to both the “dual effect” that pregnancy has on the incidence of breast cancer diagnosis.

In spite of recent encouraging developments in the setting of GI neuroendocrine tumors, many clinical questions remain to be answered and will be highlighted in this commentary.

The relative abundance of new data on the biological underpinnings of neuroendocrine tumors, combined with clinical trial data supporting new treatment options, is a clear sign of progress. Yet, as is so often the case, these recent studies have generated a multitude of new and different questions.

In this review, we summarize biologic, pathologic, and clinical aspects of gastroenteropancreatic-neuroendocrine tumors, focusing on recent advances in their treatment.

The issue of tumor heterogeneity is real, and it is present on several different levels. Without question, the presence of tumor heterogeneity has important clinical implications, and at this time, it represents a significant challenge to the success of cancer therapy.

 

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