Coming home to roost: The self-seeding hypothesis of tumor growth

Written by Sharon Reynolds | 11 February 2011

Reprinted from NCI Cancer Bulletin for February 8, 2011

The spread of cancer cells from their original location to other sites in the body, known as metastasis, has long been thought of as a one-way journey. But some researchers also believe that metastatic cancer cells can fuel primary tumor growth, with potentially important implications for the timing and nature of cancer treatment.

The concept of tumor self-metastasis, or tumor “self-seeding,” originated at Memorial Sloan-Kettering Cancer Center, based on a series of studies led by Drs. Joan Massagué, head of the Metastasis Research Center, and Larry Norton, deputy physician-in-chief of the center’s breast cancer programs.

In studies of mice, Dr. Massagué observed that breast tumors expressing genes associated with metastasis were growing faster than tumors that didn’t express these genes, even though the genes had no apparent role in increased cell division or decreased cell death. “Moreover, the fraction of dividing cells was not higher in fast-growing tumors versus tumors that are slower growing,” explained Dr. Norton.

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Unexpected findings on Gallium-67 Scintigraphy

Written by Wu, Hsieh, Sun, Lo, Lin, Yang, Yen, Kao | 26 January 2011

Detection of Undifferentiated Endometrial Stromal Sarcoma

Wu YC, Hsieh TC, Sun SS, Lo WC, Lin TY, Yang CF, Yen KY, Kao CH.

From the *Department of Nuclear Medicine and PET Center, China Medical University Hospital, and †China Medical University, Taichung, Taiwan; ‡Department of Biomedical Imaging and Radiological Science, China Medical University, Taichung, Taiwan; §Division of Hematology and Oncology, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan; Department of Pathology, China Medical University Hospital, Taichung, Taiwan; ∥School of Medicine, China Medical University, Taichung, Taiwan.

Immunological Therapies Can Relieve Aromatase Inhibitor-Related Joint Symptoms in Breast Cancer Survivors

Written by Zhang, Qingyuan MD; Tang, Dabei MM; Zhao, Hong MM | 01 January 2011

Reprinted from American Journal of Clinical Oncology, December 2010 - Volume 33 - Issue 6 - pp 557-560, doi: 10.1097/COC.0b013e3181cae782

Objectives: Aromatase inhibitors can cause joint symptoms. The purpose of this pilot study was to evaluate the feasibility of immunologic therapies for this kind of joint symptoms.

Methods: A total of 16 postmenopausal women with stage I–III breast cancer with joint symptoms related to Aromatase inhibitors were enrolled. They received immunologic therapies of thymosin α1 1.6 mg, twice a week for 4 weeks. Outcome measures included the Brief Pain Inventory-Short Form, Western Ontario and McMaster Universities Osteoarthritis index, and the Functional Assessment of Cancer Therapy-General quality of life measure. Interferon-gamma and interleukin-4 were determined to evaluate immunomodulatory activity. Paired Samples Test and linear regression analysis were used to statistics the outcome measures.

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Immunohistochemical studies on uterine carcinosarcoma, leiomyosarcoma, and endometrial stromal sarcoma: expression and prognostic importance of ten different markers

Written by R Kolvisto-Korander, R Butzow, AM Kolvisto, A Leminen | 19 December 2010

Uterine sarcomas are rare and aggressive gynecologic malignancies. In this immunohistochemical (IHC) study, expression of Ki-67, p53, CD10, CD44, desmin, smooth muscle actin, estrogen receptor α (ERα), androgen receptor (AR), progesterone receptor A (PRA), and c-kit and their influence on survival in cases of uterine carcinosarcoma (CS), leiomyosarcoma (LMS), and endometrial stromal sarcoma (ESS) were evaluated. Medical records were reviewed and data collected concerning all uterine sarcomas treated during a 12-year period at Helsinki University Central Hospital. There was sufficient histological material for IHC analysis and slide review in 67 cases. Survival analysis was performed using the Kaplan-Meier method, and median survival times with 95% confidence intervals are given. Survival in cases of LMS was statistically significantly affected by the expression of p53, ERα, and PRA. Striking differences in expression of IHC markers when comparing results with those in earlier studies were the absence of AR immunoreactivity in all uterine sarcomas and low incidence of c-kit (15%; in endometrial stromal sarcoma). None of the markers was statistically significantly associated with survival of ESS and CS patients. The expression of p53, ERα, and PRA in uterine LMS may give prognostic information concerning the behavior of the disease. Hormonal therapy could be recommended as a treatment option in cases of hormone receptor-positive LMS.

Department of Obstetrics and Gynecology, University of Helsinki, P.O. Box 140, 00029, Helsinki, HUS, Finland. Abstract