Evidence map›Paper›PMID 17999161›Full record

ReviewFamilial cancer2008

Hereditary colorectal cancer syndromes: molecular genetics, genetic counseling, diagnosis and management.

Henry T Lynch, Jane F Lynch, Patrick M Lynch, Thomas Attard

Abstract readReview
PubMed Publisher
In one paragraph

Review in Familial cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

90 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Guideline
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Heme Oxygenase-1 and Its Role in Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Colorectal Cancer in Young and Older Adults in Uruguay: Changes in Recent Incidence and Mortality Trends.International journal of environmental research and public health · 2021
    Article
  18. Review
  19. Gastric cancer is highly prevalent in Lynch syndrome patients with atrophic gastritis.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2021
    Article
  20. Article

30 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Henry T LynchDepartment of Preventive Medicine and Public Health, Creighton University School of Medicine, Omaha, Nebraska 68178, USA. htlynch@creighton.edu
Jane F Lynch
Patrick M Lynch
Thomas Attard

Funding

EDRN--THE HEREDITARY CANCER CLINICAL CENTERU01CA086389 · NCI · CREIGHTON UNIVERSITY · PI LYNCH, HENRY T · 2000 to 2010
$6.2M
NCI NIH HHS 1U01 CA 86389
6 · The paper itself

Abstract

Hereditary forms of colorectal cancer, as is the case with virtually all forms of hereditary cancer, show extensive phenotypic and genotypic heterogeneity, a phenomenon discussed throughout this special issue of Familial Cancer. Clearly, the family physician, oncology specialist, genetic counselor, and cancer geneticist must know fully the complexity of hereditary cancer syndromes, their differential diagnosis, in order to establish a diagnosis, direct highly-targeted surveillance and management, and then be able to communicate effectively with the molecular geneticist so that an at-risk patient's DNA can be tested in accord with the syndrome of concern. Thus, a family with features of the Lynch syndrome will merit microsatellite instability testing, consideration for immunohistochemistry evaluation, and mismatch repair gene testing, while, in contrast, a patient with FAP will require APC testing. However, other germline mutations, yet to be identified, may be important should testing for these mutations prove to be absent and, therein, unrewarding to the patient. Nevertheless, our position is that if the patient's family history is consistent with one of these syndromes, but a mutation is not found in the family, we still recommend the same surveillance and management strategies for patients from families with an established cancer-causing germline mutation. Our purpose in this paper is to provide a concise coverage of the major hereditary colorectal cancer syndromes, to discuss genetic counseling, molecular genetic evaluation, highly targeted surveillance and management, so that cancer control can be maximized for these high hereditary cancer risk patients.

Indexed as

Genetic CounselingMolecular BiologyAdenomatous Polyposis ColiColorectal Neoplasms, Hereditary NonpolyposisGenetic Predisposition to DiseaseGenetic TestingGerm-Line MutationHumansPeutz-Jeghers SyndromeRisk Factors

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.