Vijh Ashok K
Institut de Recherche d'Hydro-Québec, 1800 Blvd. Lionel-Boulet, Varennes, Que., Canada J3X 1S1.
Med Hypotheses. 2004;62(2):233-6. doi: 10.1016/S0306-9877(03)00339-6.
Sastry and Parikh [Med. Hypotheses 60(4) (2003) 573] have recently sought an explanation for the fact that the occurrence of a particular cancer in populations in a developing country such as India takes place at a younger age (about one decade) than in populations in Western countries. They have hypothesized that a higher infectious burden in India gives rise to repeated cell divisions leading to early senescence of immune cells, and, thence their reduced ability for immune surveillance against cancer, resulting in earlier onset of cancer. The analysis presented here points out to some difficulties with this interpretation, both on empirical and theoretical grounds. The reduced surveillance ability, caused by higher infectious burden, of the immune cells postulated by Sastry and Parikh [loc. cit.] would also mean that populations in India should suffer higher incidence of cancer, as compared to people in Western countries; the empirical data show that, in fact, quite the opposite is true - in the present communication shows that for many common cancers, typical cities in India show the lowest incidence. Theoretically, it is postulated here that repeated heavy infections in India, in fact, challenge the immune system, particularly the adaptive immune system and create an immunological memory: this trains and strengthens the immune system against the future battles. Also it is shown that the shortening of the telomeric cap by repeated cell divisions caused by heavy infectious attacks, as argued by Sastry and Parikh [loc. cit.], is not the cause of earlier onset of cancers among Indians; in fact, when telomeric caps become shortened to a critical point, a danger signal is generated arresting the cell cycle - thus, it provides a fundamental mechanism for ordering the cell to cease proliferation. It is suggested that the root of occurrence of cancers at an earlier age in India perhaps lies in the accumulation of mutations at an earlier age among Indians who do develop cancers; the factors responsible for these accelerated mutations are not clear at the present time and need further investigation.
萨斯特里和帕里克[《医学假说》60(4)(2003)573]最近试图解释这样一个事实：在印度这样的发展中国家，特定癌症在人群中的发病年龄比西方国家人群要早（约十年）。他们推测，印度较高的感染负担导致细胞反复分裂，进而导致免疫细胞过早衰老，从而其对癌症的免疫监视能力下降，导致癌症更早发病。本文所呈现的分析指出了这种解释在经验和理论层面上存在的一些困难。萨斯特里和帕里克[同前引文]所假设的因较高感染负担导致免疫细胞监视能力下降，这也意味着与西方国家的人相比，印度人群应患癌症的发病率更高；但经验数据表明，事实上情况恰恰相反——本文表明，对于许多常见癌症，印度的典型城市发病率最低。从理论上讲，本文推测，印度反复遭受严重感染实际上会挑战免疫系统，尤其是适应性免疫系统，并形成免疫记忆：这会训练并增强免疫系统应对未来的战斗。此外，研究还表明，如萨斯特里和帕里克[同前引文]所主张的，由严重感染攻击导致的细胞反复分裂使端粒帽缩短，并非印度人癌症更早发病的原因；事实上，当端粒帽缩短到临界点时，会产生一个危险信号使细胞周期停滞——因此，它提供了一种基本机制来命令细胞停止增殖。有人认为，印度癌症发病年龄较早的根源可能在于患癌症的印度人在较早年龄就积累了突变；目前尚不清楚导致这些加速突变的因素，需要进一步研究。
