我記得很早以前看過有關端粒酶的網路醫藥新聞，
細胞尾端的端粒長度,
在複製後會變短,
印象中人細胞基因尾端的端粒是長的比較好,
擁有端粒長的基因人比較長壽. 

聯合新聞網 2007/07/12

學者首次發現，身上痣很多的人，生理年齡比痣很少的人年輕好幾歲。

對痣多的人而言，這是個好消息。因為既有研究顯示，痣多的人罹患惡性黑色素瘤（一種致命性皮膚癌）的機率也略高，這個新研究結論則指出痣多的人可享受老得較慢的好處。

由皮膚醫學專家維若妮卡‧巴塔耶領銜的倫敦國王學院研究團隊，分析了九百多對雙胞胎女性的染色體「端粒」（染色體末端的ＤＮＡ序列），希望透過端粒的長度，瞭解痣的數量與生理年齡的關係。

結果發現，有痣的人老化程度較低，較容易保持青春的外表，罹患心臟病與骨質疏鬆症等老年相關疾病的機率，也可能比沒有痣的人低。這篇研究已發表於「癌症流行病學生物標記與預防」期刊。

在學者眼中，染色體端粒類似「生物時鐘」。人體細胞隨時間逐漸分裂，端粒的長度也會縮短，如果端粒太短，細胞就會死亡。

新研究發現，皮膚上的痣超過一百顆的人，染色體端粒的長度比皮膚上的痣不到廿五個的人要長，生理年齡因此比較年輕。

巴塔耶說：「皮膚科醫師常說，不管自然給人什麼東西，一定有它的道理。如果身上長痣，只是為了增加得黑色素瘤的機率，那實在有點遜。」

文中提到醫學發現身上多痣的人,
其端粒比較長.
我從小身上就多痣,
臉上手上身體上,
衣服遮住的地方遮不住的地方,
大大小小痣真多,
我曾經花錢點掉一些.

我先生說他小時候,
碗裡的飯不吃乾淨,
他父親說 : "飯粒不吃乾淨, 以後娶的太太臉上長麻子(痣或黑斑)!"

我臉上的痣,
算命的說這叫做"孔子的墨汁",
我的紫微命盤命宮有文昌星,
也是主痣多,
代表有文藝的氣息.
所以我才注意到這個資訊.

如果這些關連性確實存在,
那在人小時候,
就可以取他的基因來量量看端粒的長度,
可能可以預知長大後他是否有文才!!

每隔一陣子取人體細胞量量端粒的長度,
可以預測壽命.

如果要收集或研究端粒及端粒酶,
就找一些痣多痣大又有文才的人來取樣,
豈不方便辨識?

後來我也就忘了,
再也沒有看過端粒或端粒酶的任何資訊.

直到昨天看到新聞,
美國科學家伊麗莎白．布萊克本、凱蘿．格蕾德與傑克．索斯塔克三人
因發現染色體如何被端粒telomere保護獲得諾貝爾醫學獎。
當細胞分裂時，
端粒中一個獨特的ＤＮＡ序列有保護染色體免於降解之效。
如果端粒酶telomerase的濃度高，
端粒長度得以維持，
這些發現，
一來有助於癌症治療的研究，
二來有助於長壽的研究。

這個新聞令我回想起之前看到的端粒與痣的文章,
搜尋了一下可否有文獻,
找到了,
特此部份轉載如下 :

Nevus Size and Number Are Associated with Telomere
Length and Represent Potential Markers of a
Decreased Senescence In vivo
Veronique Bataille,1,3 Bernet S. Kato,1 Mario Falchi,1 Jeffrey Gardner,4 Masayuki Kimura,4
Marko Lens,1 Ursula Perks,1 Ana M. Valdes,1 Dot C. Bennett,2
Abraham Aviv,4 and Tim D. Spector1
Twin Research and Genetic Epidemiology Unit, King’s College London, St. Thomas Hospital Campus; 2Division of Basic Medical
Sciences, St. George’s, University of London, Cranmer Terrace, London, United Kingdom; 3Dermatology Department, West
Hertfordshire NHS Trust, Hemel Hempstead General Hospital, Herts, United Kingdom; and 4Center of Human
Development and Aging, University of Medicine and Dentistry of New Jersey, Newark, New Jersey

Abstract
Nevus counts represent one of the strongest risk factors for
melanoma. They appear in childhood and adolescence and
involute from middle age onwards. Recent evidence has
shown that nevus cells undergo oncogene-induced senescence
involving the p16/retinoblastoma pathway. However,
telomere length also influences senescence in proliferative
somatic cells and varies between individuals. This study
explores whether telomere length measured in white cells is
associated with nevus count and size in 1,897 Caucasian
women ages 18 to 79 years. Total body nevus counts were
positively correlated with white cell telomere length (mean,
7.09 kbp; range, 5.09-9.37) after adjustment for age (P =
0.0001). Age-adjusted telomere length was also associated
with nevus count for nevi above 5 mm in diameter (P = 0.04).
Subjects in the top category for nevus count had an average
age-adjusted telomere length 150 bp longer than those in
the lowest category. The positive correlation between white
cell telomere length and nevi number and size may reflect
an increased replicative potential (reduced senescence) in
individuals with longer telomeres, which may not be
melanocyte specific. Understanding mechanisms influencing
the induction and involution of nevi will not only help
in understanding the pathophysiology of melanoma but
should also shed light on the complex relationship between
aging and cancer. (Cancer Epidemiol Biomarkers Prev
2007;16(7):1499–502)

Introduction
Nevus numbers vary greatly in any Caucasian populations
and undergo a significant reduction from middle age onwards
(1, 2). Mean total body nevus count in the United Kingdom is
30 and remains the most powerful predictive marker of risk for
melanoma (3-5). Nevus number is known to be significantly
influenced by genetic factors, with twin studies showing that
60% of the variation in nevus number is explained by additive
genetic factors (6-8). Furthermore, in families with a genetic
susceptibility to melanoma, affected individuals often have
large numbers of common and atypical nevi (9, 10). In these
melanoma-prone families, nevi continue to appear in large
numbers in adulthood and have a delayed involution with
large numbers of nevi still present in older age groups (10, 11).
The melanoma suppressor gene CDKN2A is now known
to encode the two cell cycle inhibitors p16 (INK4a) and
ARF (alternative reading frame), with the related p15 (INK4b;
ref. 12). Germ-line and somatic CDKN2A mutations and
deletions have been linked respectively to familial and sporadic
melanoma, and p16 carriers often show large numbers of nevi
(10, 13). p16 inhibits cell proliferation by binding to cyclindependent
kinases (cyclin-dependent kinases 4 and 6), preventing
phosphorylation of the retinoblastoma protein. p16 is
also known to be important in cell senescence in all cell types
(14). Another well known effector pathway for human
replicative cell senescence is attributed to telomere shortening
and a DNA damage response through other growth inhibitors,
such as p53 and p21 (15, 16).
Telomeres are specialized DNA-protein complexes that cap
the end of eukaryotic chromosomes and are essential for
maintaining genome stability and integrity. The human
telomeric complex is composed of TTAGGG repeated DNA
sequences with the enzyme telomerase where present and
several associated proteins controlling telomere length and
capping. Shortening of telomeres occurs naturally with
successive divisions in somatic cells, whereas in the germ-line
and most cancer cells, high telomerase activity allows cells to
maintain long telomeres and avoid senescence (17-19). Twin
and family studies have shown that telomere length in white
cells is partly heritable, although environmental factors, such
as inflammation, smoking, and obesity, are also important
(20-22). Shorter white cell telomere length has also been linked
to chronic diseases of aging, such as atherosclerosis, osteoarthritis,
and diabetes (18, 23-26). Telomere attrition causes cell
senescence via the p53 pathway, although p16 is also likely to
be involved as senescent cells overexpress p16 (14, 15, 17).
We speculate that telomere shortening may play a key role, as
well as the p16 pathway, in limiting nevus growth and may be
involved in the disappearance of nevi with age. The aim of this
study was to explore this hypothesis by correlating leukocyte
telomere length with total body nevus counts and nevus size in
a large population-based sample of adults.

以上原文轉貼自http://cebp.aacrjournals.org/content/16/7/1499.full.pdf

請繼續看端粒,痣,有文藝個性的關連(後記)