Obesity and Cancer Risk تعريف السمنة والسرطان

دراسات عن علاقة السرطان بالبدانة او
السمنة:

Obesity and the Risk for a Hematological
Malignancy: Leukemia, Lymphoma, or Myeloma

1.
Marshall A. Lichtman

+ Author Affiliations

1.
University of Rochester Medical
Center, Rochester, New York, USA

1.
Correspondence: Marshall A.
Lichtman, M.D., University of Rochester Medical Center, 601 Elmwood Avenue,
Rochester, New York, 14642-0001, USA. Telephone: 585-275-2205; Fax: 585-271-1876;
e-mail: mal@urmc.rochester.edu

Received
June 27, 2010.

Accepted
August 27, 2010.

First
published online in THE ONCOLOGIST Express on October 7, 2010.

Disclosures:
Marshall A. Lichtman: Expert
testimony: Toxic tort but no relevance.

The content of this article has
been reviewed by independent peer reviewers to ensure that it is balanced,
objective, and free from commercial bias. No financial relationships relevant
to the content of this article have been disclosed by the independent peer
reviewers.

Abstract

The aggregate of epidemiological
studies indicates a significantly elevated risk for cancer in people with a
high body mass index (BMI); a “dose–response” effect exists with increasing
risk as BMI increases from the normal to overweight to obese categories.
Successful sustained weight loss decreases future risk. The relationship of
being overweight to the risk for leukemia in the aggregate has been supported
in several large cohort studies and two meta-analyses of cohort and case–control
studies. One meta-analysis found an elevated risk for each of the four major
subtypes of leukemia. A significant association between the risk for
non-Hodgkin's lymphoma and elevated BMI was supported by a meta-analysis of 13
cohort and nine case–control studies. The risk for diffuse large B-cell
lymphoma may be especially significant. A high BMI increases the risk for
myeloma, as judged by a meta-analysis of 11 cohort and four case–control
studies. The biological relationship of obesity to the risk for cancer
(biological plausibility) is unresolved. The two major causal final pathways
could be “inductive” or “selective.” The metabolic, endocrinologic,
immunologic, and inflammatory-like changes resulting from obesity may increase
the cell mutation rate, dysregulate gene function, disturb DNA repair, or
induce epigenetic changes, favoring the induction of neoplastic transformation
(inductive). Alternatively, obesity may create an environment in which
pre-existing clones that are dormant are permitted (selected) to emerge.

http://theoncologist.alphamedpress.org/content/15/10/1083.abstract

وهناك دراسة حديث اخرى قام بها((Lichtman,2010 عن علاقة السمنة والورم الموي الخبيث :
الوكيميا الغدد المفاوية و المايلوما:

وقد وجد ان اي تغيرات ناجمة عن الأصابة بالسمنة
سواء في التمثيل الغذائي، او جهاز المناعه ، او تحورات داخل الخلية قد يؤدي الى
تغيرر في وضيفة الجين كل ذالك قد يؤثر في
تحول الأورام . وبشكل عام تعتبر السمنة بيئة مناسبة تسمح في الحيوانات بتحول الاورام الساكنة او
الغير نشطة الى حالة نشطة وتبداء في الظهور.

Obesity and Cancer

1.
Kathleen Y. Wolin^a,^b,

2.
Kenneth Carson^b,^c and

3.
Graham A. Colditz^a ^c

+ Author Affiliations

1.
^aDepartment of Surgery, and

2.
^cDepartment of Medicine,
Washington University School of Medicine, St. Louis, Missouri, USA;

3.
^bAlvin J. Siteman Cancer Center,
Barnes Jewish Hospital, and Washington University School of Medicine, St.
Louis, Missouri, USA

1.
Correspondence: Kathleen Y.
Wolin, Sc.D., Washington University School of Medicine, Department of Surgery
and Siteman Cancer Center, 660 S Euclid Avenue, Campus Box 8100, St. Louis,
Missouri 63110, USA. Telephone: 314-454-7958; Fax: 314-454-7941; e-mail: wolink@wustl.edu

Received
November 19, 2009.

Accepted
April 14, 2010.

First
published online in THE ONCOLOGIST Express on May 27, 2010.

Disclosures:
Kathleen Y. Wolin:
None; Kenneth Carson: None; Graham A. Colditz: None.

The content of this article has
been reviewed by independent peer reviewers to ensure that it is balanced,
objective, and free from commercial bias. No financial relationships relevant
to the content of this article have been disclosed by the authors or independent
peer reviewers.

Abstract

Weight, weight gain, and obesity
account for approximately 20% of all cancer cases. Evidence on the relation of
each to cancer is summarized, including esophageal, thyroid, colon, renal,
liver, melanoma, multiple myeloma, rectum, gallbladder, leukemia, lymphoma, and
prostate in men; and postmenopausal breast and endometrium in women. Different
mechanisms drive etiologic pathways for these cancers. Weight loss,
particularly among postmenopausal women, reduces risk for breast cancer. Among
cancer patients, data are less robust, but we note a long history of poor
outcomes after breast cancer among obese women. While evidence on obesity and
outcomes for other cancers is mixed, growing evidence points to benefits of
physical activity for breast and colon cancers. Dosing of chemotherapy and
radiation therapy among obese patients is discussed and the impact on
therapy-related toxicity is noted. Guidelines for counseling patients for
weight loss and increased physical activity are presented and supported by
strong evidence that increased physical activity leads to improved quality of
life among cancer survivors. The “Five A’s” model guides clinicians through a
counseling session: assess, advise, agree, assist, arrange. The burden of
obesity on society continues to increase and warrants closer attention by
clinicians for both cancer prevention and improved outcomes after diagnosis

http://theoncologist.alphamedpress.org/content/15/6/556.abstract

دراسة
للعلاقة بين السرطان والسمنةقام بها(kATHLEEN
and ,etl, 2009 )

وجدوا
ان خفض الوزن وزياد النشاط البدني يحسن من جودة وكفائة الحياة لدى المرضى الناجين
من مرض السرطان.

الأستاذة نورا البكري